Research Radar

New PubMed studies on repurposed drugs and natural compounds in cancer — summarized in plain language and reviewed by a person before posting.

How to read this page. These studies are automatically collected from PubMed and summarized by AI from the abstract, then reviewed by a human before publishing. Each summary describes only what that study reported — most are early lab, animal, or small human studies, and findings often conflict. This is educational information, not medical advice, and not a recommendation to take anything. Always talk with your oncologist.

Topic tags. Each study is filed under its main topic. Anticancer studies are the default; these tags flag the other dimensions:

Safety — Safety & interactionsAbsorption (PK) — How it's absorbed (PK)Formulation — Formulation & deliverySupportive care — Symptom & supportive careMetabolism — Metabolism & pathwaysTrial — Clinical trialMechanism — Biomarker & mechanism

Human onlyPositive outcomesSafety signalsTrials200 of 200 studies

Case reportReported negativeLimited evidenceTier 3 · early humann = 1

Primary High-Grade Intraperitoneal Sarcoma Mimicking a Germ Cell Tumor in an 8-Year-Old Girl in Somaliland: A Diagnostic Challenge

International medical case reports journal · Jul 2026 · case report

intra-abdominal sarcomaprimary high-grade intraperitoneal sarcomapediatric abdominal tumor

This case report describes an 8-year-old girl in Somaliland who presented with a large abdominopelvic mass initially suspected to be a germ cell tumor. Empiric germ cell chemotherapy produced no response; surgery and histopathology revealed a high-grade intra-peritoneal sarcoma (desmin+, myogenin-), and the patient died about three months after treatment. The report emphasizes the diagnostic challenges when biopsy and molecular testing are limited.

Reported effects: cycles without response 2, n=1 · time to death 3 mo, n=1

Key findings

Imaging suggested a germ cell tumor, and empiric germ cell tumor-directed chemotherapy was started.
No clinical or radiological response was observed after two cycles of empiric chemotherapy.
Exploratory laparotomy and cytoreductive surgery identified a large intra-peritoneal mass with omental and nodal involvement.
Histopathology showed a high-grade malignant neoplasm with pleomorphic round-to-spindle cells and rhabdoid features; immunohistochemistry was diffusely desmin positive and myogenin negative; INI1 testing was unavailable.
Despite postoperative chemotherapy the disease progressed and the patient died approximately 3 months after treatment.

Limitations: Single-patient case report (n=1).; Empiric therapy was given without pre-treatment histopathological confirmation.; Incomplete diagnostic work-up: INI1 testing and other molecular diagnostics were unavailable.; Short clinical follow-up (patient died ~3 months after treatment).; Findings from one case in a resource-limited setting may not generalize..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Meta-analysisTrialMixed resultsModerate evidenceTier 4 · clinical

Comparative effectiveness of immune checkpoint inhibitors in squamous vs. non-squamous cervical carcinoma: a systematic review and meta-analysis of randomized controlled trials

Translational cancer research · Jun 2026 · systematic review and meta-analysis of randomized controlled trials

metastatic cervical cancercervical squamous cell carcinoma (SCC)cervical non-squamous cell carcinoma (non-SCC)

The authors performed a systematic review and meta-analysis of four randomized controlled trials evaluating immune checkpoint inhibitors in metastatic cervical cancer, comparing outcomes in squamous versus non-squamous histologies. They report that ICI therapy improved progression-free and overall survival overall, but benefits varied by histology and by ICI class (anti-PD-1, anti-PD-L1, anti-PD-1/CTLA-4).

Reported effects: ORR anti-PD-1 in SCC vs control, p P<0.001 · ORR anti-PD-1 in non-SCC vs control, p P=0.23 · +9 more

Studied with: anti-PD-1/CTLA-4 combination.

Key findings

Four eligible randomized controlled trials were included in the meta-analysis.
ICI therapy significantly improved PFS and OS in both SCC and non-SCC patients compared with the control treatment.
Anti-programmed cell death protein 1 (anti-PD-1) monotherapy significantly increased the ORR in SCC patients (P<0.001), while no significant improvement was observed in non-SCC patients (P=0.23).
Subgroup analysis showed that anti-PD-1 and anti-PD-1/CTLA-4 combination therapies significantly prolonged PFS in SCC patients (both P<0.001), but not in non-SCC patients (P=0.13 and P=0.83, respectively).
Anti-programmed cell death ligand 1 (anti-PD-L1) therapy failed to improve PFS in SCC patients (P=0.22) but significantly enhanced PFS in non-SCC patients (P<0.001).
OS subgroup analysis revealed that anti-PD-1, anti-PD-L1, and anti-PD-1/CTLA-4 therapies all significantly prolonged OS in SCC patients.
In non-SCC patients, only the anti-PD-1 subgroup exhibited a significant OS benefit (P=0.006), with no statistically significant differences observed in the anti-PD-L1 and anti-PD-1/CTLA-4 subgroups (P=0.08 and P=0.83, respectively).

Limitations: Meta-analysis included only four randomized controlled trials (small number of trials).; Abstract provides no patient-level data, aggregate trial-level pooling may mask heterogeneity.; Different ICI classes and combination regimens were pooled and subgroup analyses may be underpowered.; Details on control treatments, exact effect sizes (HRs, ORs, rates), and sample sizes are not reported in the abstract..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewReported positiveLimited evidenceTier 4 · clinical

Relacorilant: First Approval

Drugs · Jun 2026 · regulatory approval summary

Relacorilantepithelial ovarian cancerfallopian tube cancerprimary peritoneal cancerpancreatic cancerprostate cancer

Relacorilant is a non-steroidal, selective glucocorticoid receptor antagonist being developed for several solid tumours and Cushing syndrome. The article reports that relacorilant received its first approval in the USA on 25 March 2026 for use in combination with nab-paclitaxel for adults with platinum-resistant epithelial ovarian, fallopian tube or primary peritoneal cancer after 1-3 prior systemic regimens (at least one including bevacizumab). The article summarizes development milestones leading to this approval.

Studied with: nab-paclitaxel.

Key findings

Relacorilant is a non-steroidal, selective glucocorticoid receptor II antagonist developed by Corcept Therapeutics.
Relacorilant received first approval in the USA on 25 March 2026.
Approval is for use in combination with nab-paclitaxel for adults with platinum-resistant epithelial ovarian, fallopian tube or primary peritoneal cancer who have received 1-3 prior systemic treatment regimens, at least one of which included bevacizumab.
Relacorilant is being developed for various solid tumours including ovarian, fallopian tube, peritoneal, pancreatic and prostate cancers, as well as for Cushing syndrome.
The article summarizes milestones in the development of relacorilant leading to this approval.

Limitations: Abstract provides no efficacy or safety outcome data or numeric results from trials.; No trial design, sample size, or methods are reported in the abstract.; This is an approval/summary article, not primary trial data.; Geographic scope limited to a USA approval; supporting evidence is not detailed in the abstract..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed

ReviewMechanismInconclusiveLimited evidenceTier 3 · early human

Mesonephric-like Adenocarcinoma of the Female Genital Tract: A Comprehensive Review of Clinicopathological, Immunophenotypic, Molecular Features, and Clinical Management

International journal of surgical pathology · Jun 2026 · comprehensive review

mesonephric-like adenocarcinoma (MLA)mesonephric adenocarcinoma (MA)female genital tractuterine cervix

This is a comprehensive review summarizing clinicopathologic, immunophenotypic, and molecular features of mesonephric-like adenocarcinoma (MLA) of the female genital tract. The authors report that MLA shows diverse histologic patterns, is typically negative or only focally positive for ER, is positive for TTF-1, CD10, and GATA3 immunostains, and often harbors KRAS mutations. They note that MLA resembles mesonephric adenocarcinoma histologically and molecularly but, unlike MA, is not associated with mesonephric remnants. The review aims to improve clinicians' and pathologists' recognition of this rare tumor type.

Key findings

MLA is a recently recognized rare malignancy of the female genital tract with histomorphology, immunohistochemistry, and molecular characteristics similar to mesonephric adenocarcinoma but not associated with mesonephric remnants.
Histologic patterns described for MLA include tubule-like, glandular, papillary, solid, sex cord-like, trabecular, retiform, cribriform, glomeruloid, and spindle cell patterns.
Immunohistochemically, most MLAs show negative or focal weak expression for ER and are positive for TTF-1, CD10, and GATA3.
Molecularly, these tumors often harbor KRAS gene mutations.

Limitations: This is a narrative review rather than primary original data.; No systematic review or meta-analytic methods are described in the abstract.; MLA is a rare tumor, so primary evidence summarized may be limited in quantity and quality.; The abstract does not report treatment or clinical outcome data..

Provides a clinicopathologic, immunophenotypic, and molecular summary intended to help pathologists and clinicians recognize and diagnose mesonephric-like adenocarcinoma.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

ReviewMechanismMixed resultsModerate evidenceTier 4 · clinical

Recent advances in characterizing the immune microenvironment and biomarkers of endometrial carcinoma

Frontiers in immunology · May 2026

endometrial carcinoma

This review used bioinformatics and cross-study analyses to screen immune-related biomarkers and prognostic models in the tumor microenvironment of endometrial carcinoma. The authors report five immune-related markers and two gene families that were repeatedly found across studies, validate their clinical prognostic significance, and summarize implicated oncogenic signaling pathways and functions of infiltrating immune cells.

Key findings

Performed a systematic bioinformatics cross-study screen of biomarkers and prognostic models related to immune infiltration in endometrial carcinoma.
Identified five immune-related markers and two gene families that were consistently reported across multiple studies.
Reported validation of the clinical prognostic significance of those markers (as stated in the abstract).
Summarized oncogenic signaling pathways in which the markers are involved.
Summarized functional implications of immune-infiltrating cells for tumor behavior to guide target identification and future immunopharmacological research.

Limitations: This is a review/synthesis and does not present new primary experimental data.; Methods and selection criteria for the bioinformatics screening and cross-study analysis are not detailed in the abstract, so risk of heterogeneity or selection bias across studies is possible.; Although the abstract states clinical prognostic validation, no sample sizes, cohorts, or validation methods are reported here.; Functional/mechanistic proposals appear to be inferred from existing studies and bioinformatics rather than demonstrated experimentally in this report..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewReported positivePreclinical onlyTier 1 · lab

Biological activities and therapeutic potential of soy isoflavones: a focus on anticancer activity

Molecular biology reports · May 2026 · narrative review

Genisteinbreast cancerovarian cancerprostate cancergliomaneuroblastomahepatocellular carcinomalung cancerbladder cancerosteosarcomarhabdomyosarcoma

This is a narrative review of the biological activities and potential therapeutic roles of soy isoflavones (including genistein and daidzein). The authors summarize proposed anticancer mechanisms (estrogen receptor modulation, apoptosis, anti-angiogenesis, epigenetic effects, etc.) and report that in vitro and in vivo studies have shown promising results across a range of tumor types. They conclude that further research—especially studies combining isoflavones with established chemotherapeutics—is needed.

Studied with: chemotherapeutic agents.

Key findings

Soy isoflavones (genistein, daidzein) have estrogenic and non-estrogenic activities including anti-inflammatory, antioxidant, and immunomodulatory effects.
Proposed anticancer mechanisms include modulation of estrogen receptors, copper ion-dependent induction of cell death, promotion of apoptosis, inhibition of angiogenesis and metastasis, regulation of epigenetic processes, and effects on platelet function.
Because of estrogen receptor interactions, isoflavones have been studied particularly in hormone-dependent cancers such as breast, ovarian, and prostate cancer.
In vitro and in vivo studies have reported promising results in multiple malignancies (gliomas, neuroblastoma, hepatocellular carcinoma, lung and bladder cancers, osteosarcoma, rhabdomyosarcoma).
Authors recommend further investigation, particularly combining isoflavones with established chemotherapeutics, to evaluate potential synergy.

Limitations: This article is a narrative review and does not present new clinical trial data.; The evidence summarized is primarily preclinical (in vitro and in vivo) with no clinical trial data provided in the abstract.; Mechanistic proposals are not proven clinical effects and require further experimental and clinical validation.; Safety and efficacy in patients, optimal dosing, and interactions with standard therapies are not established in this review..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Human · observationalMechanismMixed resultsLimited evidenceTier 3 · early humann = 21

HER2 and FOLR1 Expression in Mesonephric and Mesonephric-Like Adenocarcinomas in the Gynecologic Tract

International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists · May 2026

Trastuzumab-deruxtecan-t-dxdmesonephric adenocarcinoma (cervix)mesonephric-like adenocarcinoma (endometrium)mesonephric-like adenocarcinoma (ovary)

The authors measured HER2 and FOLR1 protein expression by immunohistochemistry in 21 mesonephric and mesonephric-like gynecologic adenocarcinomas (13 endometrial, 5 ovarian, 3 cervical). HER2 was detectable in 14 of 21 tumors (two cases scored 2+ and many scored 1+, with no 3+ cases), while FOLR1 met MIRV eligibility in one case and ten additional tumors had 5–70% expression. Most tumors did not meet current thresholds for HER2- or FOLR1-targeted monotherapy, but the authors suggest detectable expression could justify exploring T-Dxd and MIRV combinations in selected cases.

Reported effects: Total cases assessed 21 · endometrial cases 13, n=21 · +9 more

Studied with: trastuzumab deruxtecan + mirvetuximab soravtansine.

Key findings

HER2 expression was present in 14/21 tumors.
HER2 (2+) was seen in two cases by both EC and GaC criteria; no HER2 (3+) was identified.
Twelve other cases showed HER2 (1+) by endometrial cancer (EC) criteria; only four met 1+ by GaC criteria.
FOLR1 met current MIRV treatment criteria in one case; ten other cases showed FOLR1 expression ranging from 5% to 70%.
Most tumors did not meet current biomarker thresholds for trastuzumab (HER2) or MIRV monotherapy.

Limitations: Small sample size (21 cases).; Observational immunohistochemical study of archival tumors only — no treatment or clinical outcome data provided.; Heterogeneous primary sites (cervix, endometrium, ovary) which may affect biomarker distribution.; Use of different scoring criteria (EC vs GaC) produced discordant HER2 categorization, which may limit generalizability..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed

Case reportMechanismReported positiveLimited evidenceTier 3 · early humann = 1

Anthracotic Right Supraclavicular Lymph Node Mimicking Metastasis on FDG-PET/CT in Endometrial Carcinosarcoma: A Case Report

In vivo (Athens, Greece) · May 2026 · case report

endometrial carcinosarcomaendometrial neoplasm

This is a single-patient case report of an 80-year-old woman with endometrial carcinosarcoma whose FDG-PET/CT showed uptake in the uterus and multiple lymph nodes including the right supraclavicular node. Core-needle biopsy of that supraclavicular node showed extensive anthracotic pigment without malignancy, demonstrating a benign cause of FDG uptake that could mimic distant metastasis. The surgical pathology established FIGO stage IIC endometrial carcinosarcoma. The authors emphasize that histologic confirmation of suspicious nodes is essential to avoid misdiagnosis and inappropriate upstaging.

Key findings

FDG-PET/CT demonstrated FDG uptake in the uterus and right supraclavicular, mediastinal, and hilar lymph nodes.
Ultrasound-guided core needle biopsy of the right supraclavicular lymph node revealed extensive anthracotic pigment deposition without evidence of malignancy.
Final diagnosis after surgery was endometrial carcinosarcoma, FIGO stage IIC.
Authors suggest right supraclavicular nodal anthracosis can cause false-positive FDG-PET/CT findings and that histologic confirmation is essential to avoid misdiagnosis and inappropriate disease upstaging.

Limitations: Single-patient case report — findings may not generalize.; No systematic evaluation of frequency or diagnostic accuracy of anthracosis-related false positives.; No imaging-pathology correlation beyond the sampled supraclavicular node; mediastinal/hilar nodes not reported as biopsied.; No direct demonstration of the proposed variant thoracic duct anatomy (hypothesized mechanism) in this patient..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewInconclusiveLimited evidenceTier 4 · clinical

Modern Radiotherapy for High-Risk and Very-High-Risk Prostate Adenocarcinoma

The Urologic clinics of North America · May 2026

prostate adenocarcinomaprostate cancer

This review summarizes modern radiotherapy approaches for patients with high-risk or very-high-risk prostate adenocarcinoma, noting shorter courses, selectively higher radiation doses, and elective pelvic nodal irradiation. It also discusses combining radiotherapy with intensification of androgen-deprivation therapy and active studies using genomic risk stratification to guide treatment intensification or deintensification.

Studied with: androgen-deprivation therapy.

Key findings

Modern radiotherapy strategies include fewer treatments (shorter courses).
Approaches permit selectively higher radiation doses.
Elective pelvic nodal treatment is used in some modern strategies.
There is potential to intensify androgen-deprivation therapy alongside radiotherapy.
Active studies are evaluating tailoring radiotherapy and androgen-deprivation based on genomic risk stratification tools.

Limitations: Narrative review without primary data reported in the abstract.; Abstract provides no quantitative outcomes, effect sizes, or specific trial results.; Very brief abstract; details on methods, evidence quality, or recommendations are not provided..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 9

Expanded Histologic Lineage and Origin of Mesonephric-Like Adenocarcinoma: A Clinicopathologic Study of 9 Cases

International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists · May 2026 · retrospective clinicopathologic study

mesonephric-like adenocarcinomaovarian neoplasmuterine (corpus) neoplasmcervical mucosal neoplasmmesenteric tumor

This retrospective clinicopathologic study analyzed 9 cases of mesonephric-like adenocarcinoma (MLA). The authors report two previously unreported presentations (ovarian MLA coexisting with a benign mucinous cystadenoma and MLA on the cervical mucosal surface), additional atypical locations including a mesenteric MLA intermixed with clear cell carcinoma, associations with endometriosis/adenomyosis in several cases, and recurrent somatic mutations (KRAS in 5 of 7 sequenced cases; PTEN/BRAF and ERBB3 in 1 case each). The findings expand the known morphologic and anatomic spectrum of MLA and support a possible Müllerian epithelial origin.

Reported effects: number_of_cases 9, n=9 · unique_presentations_count 2, n=9 · +6 more

Key findings

Retrospective analysis of 9 MLA cases.
Two unique presentations reported for the first time: an ovarian MLA coexisting with a benign mucinous cystadenoma and an MLA on the cervical mucosal surface.
One case had a mesenteric MLA component intermixed with clear cell carcinoma; endometriosis was present around the tumor and in the adjacent ovary.
Of the remaining 6 cases, 3 were associated with endometriosis or adenomyosis.
Next-generation sequencing (NGS) performed on 7 cases identified KRAS mutations in 5 cases and mutations in PTEN/BRAF and ERBB3 in 1 case each.
Overall, the study broadens the morphologic and anatomic distribution of MLA and provides further support for a Müllerian epithelial origin.

Limitations: Small sample size (9 cases) limits generalizability.; Retrospective case series without controls.; Next-generation sequencing performed in only 7 of 9 cases (incomplete molecular sampling).; No clinical outcome, treatment, or prognostic data reported.; No functional experiments to confirm pathogenicity of reported mutations..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

ReviewReported positiveLimited evidenceTier 4 · clinical

Managing Clinical N1 Prostate Cancer

The Urologic clinics of North America · May 2026 · review

prostate adenocarcinomaclinical N1 prostate cancer (lymph node positive)

Clinical N1 prostate cancer means prostate adenocarcinoma with regional lymph node metastases identified before definitive therapy. The abstract emphasizes thorough diagnostic imaging to distinguish regional nodal disease from distant metastases. It states that multimodal therapy—typically combinations of surgery, radiation, and hormone (androgen deprivation) therapy—is the mainstay of management and that treatment should be individualized.

Studied with: surgery, radiation therapy, hormone therapy / androgen deprivation therapy.

Key findings

Clinical lymph node positive prostate cancer is prostate adenocarcinoma with metastasis to regional lymph nodes detected prior to definitive therapy.
This is an aggressive cancer with varying presentations and prognosis.
Thorough diagnostic imaging is key to establishing this stage and distinguishing it from distant metastatic disease.
The mainstay of therapy is multimodal treatment, typically surgery + radiation + hormone therapy or radiation therapy + hormone therapy.
Both surgery- and radiation-based strategies can be effective when appropriately combined with androgen deprivation therapy; treatment individualization is important.

Limitations: Review article without primary new patient-level data reported in the abstract.; No quantitative outcomes, effect sizes, or sample sizes are provided in the abstract.; No details on specific agents, doses, timing, or selection criteria for surgery versus radiation are provided.; Heterogeneity of presentations and prognosis is noted but not stratified or quantified in the abstract..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Case reportMechanismReported positiveLimited evidenceTier 3 · early humann = 1

Elevated PSMA Activity in Kimura Disease

Clinical nuclear medicine · May 2026 · case report

prostate adenocarcinoma

The authors report a case in which 68Ga-PSMA PET/CT showed elevated PSMA activity in a left axillary lesion of Kimura disease in a patient with prostate adenocarcinoma. The case indicates that Kimura disease can produce false-positive findings on PSMA PET used for staging prostate cancer.

Key findings

In a patient with prostate adenocarcinoma, 68Ga-PSMA PET/CT demonstrated elevated PSMA activity in a left axillary Kimura disease lesion.
The finding suggests Kimura disease may cause false-positive PSMA PET results during staging of prostate cancer.

Limitations: Single case report (n=1), so findings may not generalize.; No systematic evaluation of how often Kimura disease causes PSMA uptake.; No quantitative or comparative data provided in the abstract..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Human · observationalMixed resultsLimited evidenceTier 3 · early humann = 32

Fertility-Sparing Surgery for Ovarian Mucinous Tumors and Risk of Recurrence

Cureus · Apr 2026 · retrospective

ovarian mucinous tumorsmucinous borderline tumormucinous carcinoma

This single-center retrospective study reviewed 32 patients with mucinous ovarian tumors who underwent fertility-sparing surgery and followed them for a median of 18 months. Overall survival at 18 months was 100% and disease-free survival was 81.2%, but 6 patients (18.8%) experienced recurrence, more often in mucinous carcinoma and infiltrative borderline subtypes. Tumor markers CA-125 and CEA remained normal in all patients. The authors conclude FSS can be an option in selected patients but recurrence risk varies by histology and requires close follow-up.

Reported effects: sample_size 32, n=32 · median_follow-up 18 mo, n=32 · +12 more

Key findings

Study included 32 patients managed with fertility-sparing surgery.
Median follow-up was 18 months.
Median age was 25-26 years (range 18-40).
Histology: 20 patients (62.5%) had mucinous borderline tumors (including 12 infiltrative subtypes) and 12 (37.5%) had mucinous carcinoma.
Median tumor size in infiltrative tumors was 10 cm (range 4-30 cm).
Laparotomy was performed in 68.8% of cases.
At 18 months, overall survival (OS) was 100% and disease-free survival (DFS) was 81.2%.
Recurrence occurred in 6 patients (18.8%), predominantly in mucinous carcinoma (33.3%) and infiltrative borderline tumors (16.7%).
Tumor markers CA-125 and CEA remained normal in all patients.

Limitations: Retrospective design; Small sample size (n=32); Short median follow-up (18 months); Single-center study; No control or comparison group reported; Heterogeneous histology (mix of borderline and carcinoma subtypes).

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMechanismMixed resultsModerate evidenceTier 4 · clinical

Non-Small Cell Lung Cancer, Version 4.2026, NCCN Clinical Practice Guidelines In Oncology

Journal of the National Comprehensive Cancer Network : JNCCN · Apr 2026

non-small cell lung cancer

These NCCN guidelines summarize recommendations for diagnosis, primary management, surveillance, and subsequent treatment of patients with non-small cell lung cancer. The panel updated the list of recommended targeted therapies based on recent FDA approvals and clinical data. This selection focuses on treatment recommendations for advanced or metastatic NSCLC with actionable biomarkers.

Key findings

The guideline provides recommendations for diagnosis, primary disease management, surveillance, and subsequent treatment of NSCLC.
The panel updated the list of recommended targeted therapies based on recent FDA approvals and clinical data.
This selection focuses on treatment recommendations for advanced or metastatic NSCLC with actionable biomarkers.

Limitations: This is a clinical practice guideline summary, not primary research reporting new experimental data.; The abstract provides no quantitative outcomes, study methods, or details of evidence grading.; No single compound or specific treatment regimen is described in the abstract.; Details on how recommendations were derived (e.g., evidence review methods) are not provided in the abstract..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed

Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 11

Ovarian Sertoli-Leydig cell tumors with heterologous rhabdomyosarcoma: Clinicopathologic features and molecular analysis highlighting recurrent genetic alterations

Histopathology · Apr 2026 · case series

ovarian Sertoli-Leydig cell tumorrhabdomyosarcoma (heterologous component)ovarian neoplasms

This case series of 11 ovarian Sertoli-Leydig cell tumors with heterologous rhabdomyosarcoma describes clinicopathologic features and molecular findings. All 7 tumors analyzed by next-generation sequencing had DICER1 hotspot mutations, most (6/7) also had a second loss-of-function DICER1 mutation, and additional mutually exclusive TERT promoter or TP53 alterations were observed. Component-specific sequencing in two cases showed shared DICER1 hotspots between SLCT and RMS components, supporting a clonal origin.

Reported effects: n_cases 11, n=11 · embryonal_RMS_count 10, n=11 · +17 more

Key findings

We report clinicopathologic features of 11 ovarian SLCTs with heterologous RMS (positivity for desmin and myogenin);
Ten tumors were in keeping with embryonal RMS and 1 with pleomorphic RMS.
The patients showed a bimodal age distribution: seven patients (64%) were aged 33 years or younger (mean 20) and four patients (36%) were aged 52 years or older (mean 60).
All tumors were unilateral.
Eight of 11 cases (73%) contained other heterologous elements, including gastrointestinal-type mucinous epithelium (5 cases) and immature cartilage (3 cases).
Seven of 11 cases (64%) underwent next-generation sequencing analysis.
All tumors tested molecularly (7/7, 100%) harbored hotspot DICER1 mutations.
Of these, six cases (86%) also carried a second nonsense or frameshift loss-of-function DICER1 mutation.
In addition to DICER1 mutations, TERT c.-124C>T promoter (4 cases) or TP53 mutations (3 cases) were present in all cases and were mutually exclusive.
Component-specific analysis in two cases revealed shared common DICER1 hotspot mutations in both the SLCT and RMS components, supporting a clonal origin.
In one case, a TERT promoter c.-124C>T somatic mutation was present only in the RMS component; in the other case the TERT promoter mutation was found in both components while a BRAF p.V600E mutation was exclusive to the RMS component.

Limitations: Small sample size (11 cases).; Retrospective case series design without systematic clinical outcome data reported in the abstract.; Next-generation sequencing was performed in only a subset of cases (7/11).; Component-specific molecular analysis was limited to two cases.; The abstract does not report whether DICER1 mutations were somatic versus germline in all cases..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed

Human · observationalMechanismMixed resultsModerate evidenceTier 3 · early humann = 1389

Clinicopathologic and molecular predictors of survival in BRCA-deficient tubo-ovarian high-grade serous carcinoma

Nature communications · Apr 2026 · cohort study

tubo-ovarian high-grade serous carcinoma (HGSC)

Researchers analyzed a large cohort of patients with tubo-ovarian high-grade serous carcinoma (n=1389, including 282 with pathogenic germline BRCA variants) and performed multi-omic profiling on a subset of tumors. They found that residual disease after surgery had limited prognostic impact in germline BRCA carriers, prognostic effects varied by mutation location within BRCA genes, and co-occurring alterations (e.g., NF1 loss, PIK3CA/RAD21/MYC amplifications), HRD score, and immune/EMT features were associated with differences in overall survival.

Reported effects: cohort size (HGSC) 1389, n=1389 · germline BRCA pathogenic variants (gBRCApv) count 282, n=282 · +4 more

Key findings

Large HGSC cohort (n = 1389) included 282 individuals with pathogenic germline BRCA variants (gBRCApv).
Residual disease after primary surgery has limited prognostic effect in gBRCApv-carriers compared to non-carriers.
Prognostic outcomes differ based on the mutation location within functional domains of the BRCA genes.
Multi-omic profiling was performed on 154 tumors, enriched for patients with BRCA-deficient tumors that experienced short overall survival (<=3 years, n = 42).
Patients with BRCA2-deficient HGSC and loss of NF1 survive twice as long as those without NF1 loss.
PIK3CA, RAD21 and MYC amplification define BRCA2-deficient HGSC with exceptionally short survival.
Patients with BRCA1-deficient HGSC and a more elevated HRD score survive significantly longer.
BRCA1-deficient tumors in short survivors have evidence of immunosuppressive c-kit signaling and EMT.
Overall outcome is influenced by co-occurring genomic alterations, the extent of DNA repair deficiency, and the tumor-immune microenvironment, not BRCA status alone.

Limitations: Observational cohort design; associations reported are not evidence of causation.; Multi-omic profiling was performed on a selected subset of 154 tumors enriched for short survivors (selection bias).; Molecular analyses sample size (n=154, short survivor subset n=42) is substantially smaller than the full cohort.; Abstract does not report follow-up duration, detailed treatment information, or effect size statistics for many associations..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 216

Identification of Actionable Gene Variants in Pulmonary Large-Cell Neuroendocrine Carcinoma: A Real-World Analysis of a Polish Cohort

International journal of molecular sciences · Mar 2026 · retrospective cohort

pulmonary large-cell neuroendocrine carcinomaLCNEC

Researchers performed targeted next-generation sequencing on 216 pulmonary LCNEC tumor samples from a retrospective Polish cohort to look for actionable gene variants. They found 46 variants in 46/216 samples (21.3%), with 28/216 (13%) harboring at least one potentially actionable alteration; most common were KRAS and PIK3CA (each 5%), and a novel TMEM79::NTRK1 fusion was found in one case (0.5%). Several typical NSCLC alterations (classical EGFR exon 18–21, ALK, FGFR1/2/3, ROS1) were not detected.

Reported effects: variant_count 46, n=216 · variant_positive_rate 21.3%, n=216 · +8 more

Key findings

Overall, 46 variants were identified in 46/216 (21.3%) tumor samples.
28/216 (13%) LCNECs harbored at least one actionable molecular variant potentially targetable by registered or investigational agents.
KRAS variants were present in 5% of tumors (including G12C at 2%).
PIK3CA variants were present in 5% of tumors.
RET single-nucleotide variants were observed in 3% of tumors.
Uncommon EGFR variants were observed in 1% of tumors; BRAF class II and III variants were observed at <1%.
A novel in-frame gene fusion (TMEM79::NTRK1) was identified in a single tumor sample (0.5%).
No classical EGFR exon 18-21 mutations nor ALK, FGFR1/2/3, or ROS1 alterations (mutations or fusions) were detected.

Limitations: Retrospective study design.; Targeted NGS panel limited to 17 genes, so alterations outside the panel would not be detected.; Single-country (Polish) cohort which may limit generalizability.; No clinical outcome or treatment-response data reported in the abstract to link variants to patient benefit..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Animal studyReported positivePreclinical onlyTier 2 · animal

KRAShing pancreatic cancer before takeoff

Science (New York, N.Y.) · Mar 2026

pancreatic cancer

The authors report that drugs which inhibit KRAS signaling delayed the development of pancreatic cancer in mice. The abstract does not specify which drugs, doses, timing, sample size, or statistical measures were used. This is an animal study showing a preclinical anticancer effect of KRAS-pathway inhibition.

Key findings

In mice, drugs that inhibit KRAS signaling delayed the development of pancreatic cancer.

Limitations: Study was performed in mice (animal model) and results may not translate to humans.; Abstract provides no details on which specific drugs were used, doses, timing, sample sizes, control groups, or statistical significance.; No quantitative results or methodology are reported in the abstract..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

ReviewReported positiveLimited evidenceTier 3 · early human

Active surveillance for prostate cancer: current status and future directions

Current opinion in urology · Mar 2026 · review

prostate adenocarcinoma

This is a narrative review of active surveillance strategies for prostate adenocarcinoma, emphasizing patient selection and monitoring. The authors state that active surveillance is the recommended approach for very low-grade and low-grade prostate cancer and is being offered to some favorable intermediate-risk patients, relying on periodic PSA testing, digital rectal exam, imaging, and repeat needle biopsies. They report that with accurate selection and a comprehensive surveillance plan, active surveillance avoids overtreatment and reduces treatment-associated comorbidities.

Key findings

Active surveillance is considered the treatment of choice in very low-grade and low-grade prostate cancer.
New data show success in management of some intermediate-risk prostate cancer.
Active surveillance programs use periodic PSA assessments, digital rectal examination, imaging studies, and needle biopsies for monitoring.
Successful active surveillance depends on accurate patient selection, comprehensive surveillance planning, proper use of diagnostic tests, and continuous patient commitment.
Active surveillance can avoid overtreatment and reduce treatment-associated comorbidities when the patient population is accurately selected.

Limitations: Narrative review article with no original patient-level data reported in this abstract; Abstract does not describe systematic review methods or quantitative synthesis.

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed

Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 33

Serous borderline ovarian tumor and low-grade serous ovarian cancer

Abdominal radiology (New York) · Mar 2026

low-grade serous ovarian cancer (LGSOC)high-grade serous ovarian cancer (HGSOC)serous borderline ovarian tumor (SBOT)epithelial ovarian cancer (EOC)

This review summarizes the pathology, molecular biology, treatment options, and imaging appearances of low-grade serous ovarian cancer (LGSOC) and serous borderline ovarian tumors (SBOT). The authors present imaging of primary and metastatic LGSOC from a cohort of 33 pathologically proven patients and describe differences between LGSOC and high-grade serous ovarian cancer (HGSOC).

Key findings

Low-grade serous ovarian cancer (LGSOC) represents 2-5% of ovarian carcinomas and 5-10% of serous ovarian carcinoma.
LGSOC and HGSOC are now considered distinct entities with different molecular biology and clinical course.
Because LGSOC is uncommon, published data on its imaging findings are limited.
The paper presents imaging appearances of primary tumor and metastasis in a cohort of 33 patients with pathologically proven LGSOC.
Since LGSOC often arise from serous borderline ovarian tumors (SBOT), the imaging appearances of SBOT are described and contrasted with LGSOC.

Limitations: Review article with a small cohort (33 patients) reported — limited sample size.; Low prevalence of LGSOC leads to limited available data on imaging findings.; Abstract does not report prospective design or standardized imaging protocol, limiting generalizability.; No quantitative diagnostic performance metrics or outcomes reported in the abstract..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed

Case reportMechanismInconclusiveLimited evidenceTier 2 · animaln = 1

Encephalic fibrosarcoma in a dog

Journal of veterinary diagnostic investigation : official publication of the American Association of Veterinary Laboratory Diagnosticians, Inc · Mar 2026 · case report

encephalic fibrosarcomabrain neoplasmfibrosarcoma

A 9-year-old castrated male mixed-breed dog with a one-week history of neurologic signs was euthanized; necropsy found a 1.5-cm mass in the right ventral pons. Histology showed elongate neoplastic cells with moderate anisocytosis/anisokaryosis and 11 mitoses in 2.37 mm2; immunohistochemistry was vimentin-positive with patchy myoglobin, weak desmin, and rare myogenin labeling. Transmission electron microscopy supported a diagnosis of encephalic fibrosarcoma, and the myogenic differentiation suggested by immunohistochemistry was not confirmed by TEM.

Reported effects: mass_size 1.5 · percent_effaced 60% · +1 more

Key findings

A pale-tan, firm, 1.5-cm mass effaced ~60% of the right-ventral aspect of the pons grossly.
Histologically composed of elongate neoplastic cells in bundles with collagenous stroma; moderate anisocytosis and anisokaryosis.
Mitotic count reported as 11 mitoses in 2.379mm2 (10 FN22/40d7 fields).
Immunohistochemistry: widespread cytoplasmic immunolabeling for vimentin, patchy cytoplasmic immunolabeling for myoglobin, weak cytoplasmic immunolabeling for desmin, and rare cytoplasmic immunolabeling for myogenin.
Transmission electron microscopy showed bundles of neoplastic cells and abundant extracellular collagen; TEM findings were consistent with fibrosarcoma but did not confirm the myogenic differentiation suggested by IHC.

Limitations: Single-case report (n = 1), limiting generalizability.; No therapeutic intervention or follow-up outcomes reported beyond euthanasia.; Diagnosis based on histology, immunohistochemistry, and TEM from a single tumor; absence of additional molecular or ancillary testing in the abstract.; Descriptive study without control or comparative data..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMechanismMixed resultsLimited evidenceTier 4 · clinical

Ductal Adenocarcinoma of the Prostate: Evolution and Current State

Advances in anatomic pathology · Mar 2026

prostatic ductal adenocarcinomaacinar adenocarcinoma

This is a narrative review of prostatic ductal adenocarcinoma (PDA), a rare histologic subtype of prostate cancer. The authors summarize PDA's epidemiology, clinical presentation, distinctive morphology, molecular findings (including ERG rearrangements), prognosis, and therapeutic challenges, and they discuss whether PDA is a distinct entity versus a histologic variant of acinar adenocarcinoma.

Key findings

PDA is a rare histological subtype of prostate carcinoma first described in 1967.
PDA has distinctive morphology and can have an aggressive clinical course and unusual metastatic patterns.
PDA frequently coexists with acinar adenocarcinoma.
Molecular evidence (including overlapping ERG rearrangements and other genomic alterations) points to a shared clonal origin between PDA and acinar adenocarcinoma, raising the question whether PDA is a separate entity or a histologic variant.
The review covers epidemiology, clinical presentation, histopathology, molecular underpinnings, prognosis, and therapeutic challenges of PDA.

Limitations: PDA is rare, so primary data are limited and based largely on small case series.; Frequent coexistence with acinar adenocarcinoma complicates separation of pure PDA and limits clarity on whether it is a distinct entity.; This article is a review and does not present new primary data or prospective controlled evidence..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Human · observationalReported positiveModerate evidenceTier 3 · early humann = 675901

Longer-term aspirin use and subsequent ovarian cancer risk in the Ovarian Cancer Cohort Consortium

International journal of epidemiology · Feb 2026 · pooled analysis of 10 prospective cohort studies

ovarian cancer

Investigators pooled data from 10 prospective cohorts including 675,901 participants (5,528 ovarian cancer cases) to examine repeat self-reported aspirin use and ovarian cancer risk. Overall, ever frequent aspirin use was not associated with ovarian cancer, but long-term use (>6 years) was associated with a lower risk (OR 0.86). The reduction was stronger among people with at least three ovarian cancer risk factors and was observed for long-term low-dose aspirin use but not for regular-dose aspirin.

Reported effects: ever frequent aspirin use OR 0.97 [0.91–1.03], n=675901 · long-term aspirin use (>6 years) OR 0.86 [0.77–0.97], n=675901 · +6 more

Key findings

Ever frequent aspirin use was not associated with ovarian cancer (OR 0.97; 95% CI: 0.91-1.03).
Long-term aspirin use (>6 years) was associated with a 14% lower ovarian cancer risk (OR 0.86; 95% CI: 0.77-0.97).
The long-term use risk reduction was evident among individuals with at least three ovarian cancer risk factors (OR 0.65; 95% CI: 0.50-0.85) but not among those with fewer than three risk factors (OR 0.94; 95% CI: 0.82-1.08); P-interaction = .02.
Reduced risks were also observed for low-dose aspirin (ever low-dose OR 0.90; 95% CI: 0.80-1.01; long-term low-dose OR 0.75; 95% CI: 0.56-0.99) but not for ever regular-dose use (OR 1.09; 95% CI: 0.94-1.27).

Limitations: Observational design — cannot establish causality and subject to residual confounding.; Aspirin use was self-reported, which can lead to misclassification.; Definitions and numeric dosing of 'low-dose' versus 'regular-dose' are not specified in the abstract.; Although multiple time-updated exposure metrics were used, unmeasured or time-varying confounders may remain..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Human trialTrialReported positiveModerate evidenceTier 4 · clinicaln = 298

Tumor Treating Fields Therapy After Stereotactic Radiosurgery for Brain Metastases From Non-Small Cell Lung Cancer: Final Results of the Phase 3 METIS Study

International journal of radiation oncology, biology, physics · Feb 2026 · Phase 3 randomized controlled multicenter trial

non-small-cell lung cancer brain metastases (NSCLC BM)

This phase 3 randomized trial compared stereotactic radiosurgery (SRS) followed by Tumor Treating Fields (TTFields, 150 kHz) versus SRS alone in 298 adults with 1–10 newly diagnosed brain metastases from NSCLC. TTFields significantly delayed time to intracranial progression (HR 0.72) and reduced intracranial progression rates at multiple time points; device-related adverse events were mainly grade ≤2 skin events and there was no deterioration in quality of life or cognitive function. Subgroup analyses in patients receiving immune checkpoint inhibitors (n = 118) showed more pronounced delays in intracranial progression. Some analyses were reported post hoc and median follow-up was 8.6 months.

Reported effects: TTIP HR 0.72 [0.53–0.98], p P = .044, n=298 · Intracranial progression rate at month 2 13.6%, p P = .034, n=298 · +6 more

Studied with: stereotactic radiosurgery (SRS), immune checkpoint inhibitors.

Key findings

TTFields significantly delayed time to intracranial progression (TTIP) compared with SRS alone (HR 0.72, 95% CI 0.53-0.98; Fine-Gray P = .044).
Intracranial progression rates for TTFields versus SRS alone were 13.6% versus 22.1% at month 2 (P = .034), 33.7% versus 46.4% at month 6 (P = .018), 46.9% versus 59.4% at month 12 (P = .023), and 53.6% versus 65.2% at month 24 (P = .031; post hoc).
Time to distant intracranial progression favored TTFields but was not statistically significant (HR 0.76, 95% CI 0.51-1.12; log-rank P = .165; post hoc).
In the subgroup receiving immune checkpoint inhibitors (n = 118), TTIP delay had HR 0.63 (95% CI 0.39-1.0; Cox P = .049; Fine-Gray P = .055) and time to distant intracranial progression HR 0.41 (95% CI 0.21-0.81; log-rank P = .0087; post hoc).
Device-related adverse events were mainly grade ≤2 skin events.
TTFields did not cause quality-of-life deterioration, and post hoc analyses showed improvements in deterioration-free survival and time to deterioration for global health status, physical functioning, and fatigue domains.

Limitations: Median follow-up was relatively short (median 8.6 months, range 0.07–85.2).; Several analyses reported were post hoc (intracranial progression at 24 months, distant progression analyses, QoL domain analyses).; Subgroup analyses (patients receiving immune checkpoint inhibitors, n = 118) are smaller and may be underpowered or exploratory.; Abstract does not report long-term neurotoxicity beyond the follow-up range stated..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed

OtherFormulationMixed resultsPreclinical onlyTier 1 · lab

Radiative magneto-thermal modeling of tri hybrid nanofluid in blood: A Biomedical intelligent framework for hyperthermia cancer therapy

Journal of thermal biology · Feb 2026

This computational study developed an intelligent framework (unsupervised neural networks optimized by a hybrid GA-SQP scheme) to model radiative magneto-thermal behavior of a tri-hybrid nanofluid (copper oxide, titanium oxide, silicon oxide) suspended in human blood modeled as a Casson fluid. The model found a 14% decline in the thermal profile with higher Prandtl number and a 15% increase in temperature with increased radiation parameter; results were validated against an Adams numerical method and assessed with error and convergence analyses.

Reported effects: change in thermal profile with higher Prandtl number 14% · change in temperature with uplift in radiation parameter 15%

Key findings

Developed a radiative magneto-thermal model of a tri-hybrid nanofluid (CuO, TiO2, SiO2) in human blood modeled as Casson fluid using an intelligent ANN framework optimized by GA-SQP.
Observed a 14% decline in the thermal profile for higher values of the Prandtl number.
Observed a 15% growth in temperature with an uplift in the radiation parameter.
Results were compared to a reference solution obtained via the Adams numerical method and validated via numerical comparisons, statistical error estimation, and convergence analysis.

Limitations: Computational modeling study only; no in vitro, animal, or human experimental data presented.; Blood properties modeled (Casson fluid) rather than measured from biological samples.; Findings are parameter-dependent model outputs and may rely on assumptions not validated experimentally.; No reported biological or clinical validation of heating effects in tissue or tumors..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed

Human · observationalMechanismReported positiveModerate evidenceTier 3 · early human

IRF7 is a novel prognostic biomarker in kidney renal clear cell carcinoma

Scientific reports · Jan 2026 · Multi-omics retrospective analysis of public cohorts (TCGA, GTEx, CPTAC) with tissue microarray validation and bioinformatic functional analyses

kidney renal clear cell carcinoma (KIRC)

This study used multi-omics analyses of public datasets and tissue microarrays to evaluate IRF7 in cancers, focusing on kidney renal clear cell carcinoma (KIRC). IRF7 was dysregulated across cancers and higher IRF7 expression in KIRC was associated with worse survival; tissue microarrays confirmed higher IRF7 in tumors versus normal tissue. Functional analyses linked IRF7 to immune checkpoints, T-cell activity, methylation, fatty acid metabolism, oxidative phosphorylation, and drug sensitivity. A KIRC-specific prognostic nomogram including IRF7 predicted overall survival with high accuracy.

Reported effects: KIRC differential expression p-value, p p < 0.001 · Association of elevated IRF7 expression with poor survival, p p < 0.01 · +1 more

Key findings

IRF7 was dysregulated in 22 cancers (KIRC: p < 0.001).
Elevated IRF7 expression in KIRC correlated with poor survival (p < 0.01).
IRF7 expression associated with immune checkpoints, epigenetic modifiers, T-cell activity, and methylation.
Functional analyses implicated IRF7 in fatty acid metabolism, oxidative phosphorylation, and drug sensitivity.
A KIRC-specific nomogram predicted overall survival with high accuracy.
Tissue microarrays confirmed IRF7 overexpression in KIRC versus normal tissues (p < 0.001), linked to reduced survival.

Limitations: Observational, retrospective bioinformatic analysis without prospective validation.; Abstract does not report sample sizes, effect sizes, or metrics for the nomogram performance.; Association data cannot establish causality or therapeutic predictive value.; No functional in vivo experiments or interventional data reported in the abstract..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMechanismMixed resultsLimited evidenceTier 4 · clinical

Immune landscape and potential role of immune checkpoint inhibitors on uterine leiomyosarcoma: a review

International journal of gynecological cancer : official journal of the International Gynecological Cancer Society · Jan 2026

uterine leiomyosarcoma

This is a narrative review of the immune environment of uterine leiomyosarcoma and the potential role of immune checkpoint inhibitors. The authors report variable PD-L1 expression, heterogeneous lymphocytic infiltration, and interactions with tumor-associated macrophages, note modest response rates to checkpoint inhibitors in clinical trials, and discuss that dual PD-1/CTLA-4 blockade and chemotherapy-induced immunogenic cell death may enhance immune activation in select patients. They conclude that combinatorial and personalized strategies, improved immune profiling, and macrophage-targeted approaches merit further study.

Studied with: anti-CTLA-4 + anti-PD-1 dual checkpoint blockade, chemotherapy (to induce immunogenic cell death), targeted immunomodulation, macrophage-targeted therapies.

Key findings

Uterine leiomyosarcoma has a variable tumor immune microenvironment including variable PD-L1 expression and differential lymphocytic infiltration.
Interactions with tumor-associated macrophages shape immune responses in leiomyosarcoma.
Clinical trials of immune checkpoint inhibitors in leiomyosarcoma have produced modest response rates.
Molecular analyses suggest that specific sub-groups of leiomyosarcoma patients may derive greater benefit from checkpoint inhibition.
Dual-checkpoint blockade combining anti-PD-1 and anti-CTLA-4 has demonstrated enhanced immune activation in select patients.
Chemotherapy-induced immunogenic cell death has been explored as a complementary approach to immunotherapy.
Authors recommend innovative combinatorial strategies, improved patient selection, enhanced macrophage-targeted therapies, and optimized immune profiling for future research.

Limitations: Narrative review only—no new primary experimental or patient-level data are presented.; Conclusions are based on heterogeneous published studies and molecular analyses rather than definitive randomized trial evidence.; Abstract reports only 'modest response rates' in trials without quantitative pooled estimates or meta-analysis.; Leiomyosarcoma heterogeneity and rarity limit generalizability of existing trial results (as noted by authors)..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

ReviewMechanismInconclusiveModerate evidenceTier 4 · clinical

Neuroendocrine tumours of the urinary bladder: recent advances

Histopathology · Jan 2026

neuroendocrine tumour of the urinary bladdersmall cell carcinomalarge cell neuroendocrine carcinomawell-differentiated neuroendocrine tumourparaganglioma

This review summarizes recent advances in the pathology and molecular understanding of neuroendocrine tumours of the urinary bladder. It reports that small cell carcinoma is the most commonly encountered bladder NET and may occur alone or alongside urothelial carcinoma or other histologies. Large-cell neuroendocrine carcinoma is being increasingly recognized but remains incompletely characterized, whereas well-differentiated NETs and paragangliomas of the bladder are rare. The authors state that molecular characterization advances have improved biological understanding and may enable better classification and risk stratification.

Studied with: urothelial carcinoma, other histological subtypes.

Key findings

Small cell carcinoma is the most frequently encountered neuroendocrine tumour of the urinary bladder and may present as either pure or in combination with urothelial carcinoma or other histological subtypes.
Large cell neuroendocrine carcinoma is increasingly recognized in this location, but it is not yet fully characterized.
Well-differentiated NET and paraganglioma of the bladder are rare neuroendocrine neoplasms.
Advances in the molecular characterization of these tumours have enhanced our understanding of their biology and can provide better classification and more accurate risk stratification for clinical decision-making.

Limitations: Narrative review format (no methods, search strategy, or systematic synthesis described in the abstract).; Abstract does not present new primary data or quantitative results.; Abstract provides no details on specific molecular markers, study cohorts, or clinical outcome data..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

ReviewMechanismInconclusiveModerate evidenceTier 4 · clinical

Histopathology and Molecular Pathology of Pineal Region Tumors

Advances and technical standards in neurosurgery · Jan 2026

pineal region tumorsgerm cell tumorspineal parenchymal tumorspineocytomapineal parenchymal tumor of intermediate differentiation (PPTID)pineoblastomagerminomapapillary tumor of the pineal region

This review chapter summarizes the histopathological features and molecular alterations of pineal-region tumors. It describes the main tumor groups (germ cell tumors and pineal parenchymal tumors), lists PPT subtypes (pineocytoma, PPTID, pineoblastoma), and highlights molecular findings such as microRNA biogenesis and RB pathway alterations in pineoblastoma, KBTBD4 insertions in PPTIDs, MAPK pathway mutations in germinomas, and chromosome 10 loss in papillary tumor of the pineal region.

Key findings

Pineal region tumors are rare, accounting for about 1% of central nervous system tumors.
The two most common pineal-region tumor types are germ cell tumors (GCTs) and pineal parenchymal tumors (PPTs).
PPTs include pineocytomas (well-differentiated), PPTIDs (intermediate differentiation), and pineoblastomas (poorly differentiated/high-grade).
Pineoblastoma molecular pathogenesis involves alterations in microRNA biogenesis and the retinoblastoma (RB) pathway.
PPTIDs are characterized by small in-frame insertions in KBTBD4.
Pineal germ cell tumors likely originate from overmigrated primordial germ cells and show the same histopathological spectrum as gonadal counterparts; germinomas frequently present mutations in the MAPK pathway.
Papillary tumor of the pineal region is a distinct ependymal-type tumor that shows loss of chromosome 10 in most cases.

Limitations: This is a narrative review/chapter and does not present original experimental or patient-level data.; Pineal-region tumors are rare (≈1%), so underlying studies and evidence are limited by tumor rarity.; The abstract provides no methodological details, sample sizes, or systematic review methods.; The abstract summarizes molecular associations but does not provide prognostic or therapeutic outcome data..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

ReviewReported positiveLimited evidenceTier 4 · clinical

Pineal Tumors and Pineal Region Tumors

Advances and technical standards in neurosurgery · Jan 2026 · narrative review

pineal region tumorspineal parenchymal tumors (PPTs)pineocytomapineal parenchymal tumor of intermediate differentiation (PPTID)pineoblastoma (PB)papillary tumor of the pineal region (PTPR)desmoplastic myxoid tumor, SMARCB1-mutantgerminomanon-germinomatous germ cell tumor (NGGCT)

This narrative review summarizes current radiotherapy principles for pineal region tumors (various pineal parenchymal tumors and germ cell tumors). It reports recommended radiation approaches and doses by subtype (e.g., adjuvant RT 50-54 Gy for some PPTs, CSI with boost for pineoblastoma, WVI 24 Gy + boost for germinomas) and notes survival outcomes reported in the literature (e.g., >90% 5-year OS for germinoma; >70% 5-year OS for older children with pineoblastoma). The authors highlight use of conformal and particle techniques and call for further dose-volume and biomarker-driven refinement.

Reported effects: adjuvant RT dose (pineocytoma) · adjuvant RT dose (PPTID) · +8 more

Studied with: surgery, chemotherapy.

Key findings

For pineocytoma (WHO grade I), gross total resection (GTR) provides excellent outcomes; adjuvant radiotherapy (50-54 Gy) or stereotactic radiosurgery (SRS) is reserved for subtotally resected cases.
PPTIDs (grades II-III): GTR is the main prognostic factor; adjuvant RT (50-54 Gy) improves overall survival; CSI (23-36 Gy + boost) is indicated for disseminated disease.
Pineoblastoma requires multimodal therapy: CSI (36 Gy + boost to 54-55.8 Gy) combined with chemotherapy yields 5-year OS rates >70% in children ≥3 years, but outcomes are poorer in younger or metastatic patients.
Papillary tumor of the pineal region (PTPR) often recurs locally; adjuvant focal RT (~50 Gy) is recommended.
Desmoplastic myxoid tumor, SMARCB1-mutant: limited data, but focal RT ≥54 Gy has been used.
Pure germinomas are highly radiosensitive and achieve >90% 5-year OS; reduced-volume RT (whole-ventricular irradiation, WVI, 24 Gy + boost) has replaced historical CSI for many cases.
Non-germinomatous germ cell tumors (NGGCTs) require combined chemotherapy and RT; CSI + boost achieves 70-90% 5-year OS.
Proton therapy and other particle techniques are increasingly used to reduce long-term neurocognitive and secondary malignancy risks.
Overall management relies on an integrated approach combining surgery, radiotherapy, and chemotherapy, with growing use of molecular classification to guide risk-adapted treatment.

Limitations: This is a narrative review (no original patient-level data or meta-analytic synthesis reported in the abstract).; Pineal region tumors are rare and heterogeneous, limiting the quality and quantity of evidence for some subtypes.; For some entities (e.g., desmoplastic myxoid tumor, SMARCB1-mutant) the abstract notes limited data supporting management recommendations.; Recommendations appear to be based on aggregated/prior literature rather than prospective randomized data (noted indirectly by review format)..

This review summarizes radiotherapy approaches and reported outcomes for pineal region tumors and is directly relevant to clinical radiotherapy planning for these neoplasms.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

ReviewMechanismInconclusiveLimited evidenceTier 3 · early human

Mesonephric-like Adenocarcinoma (MLA) Diagnostic Criteria and Controversies: Perspectives and Guidance From Pathologists in the MLA Consortium

International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists · Jan 2026

endometriumovaryextrauterine sites (often associated with endometriosis)

This is a review by members of the Mesonephric-like Adenocarcinoma (MLA) Consortium summarizing the literature on MLA diagnostic criteria. The authors describe MLA as a rare, aggressive gynecologic cancer that arises in the endometrium, ovaries, and other extrauterine sites, note its morphologic, immunohistochemical, and molecular similarities to cervical mesonephric adenocarcinoma as well as features suggesting mfcllerian derivation, and provide practical guidance while acknowledging ongoing controversies.

Key findings

MLA is a rare and aggressive gynecologic malignancy recognized in the last decade.
MLA arises in the endometrium, ovaries, and extrauterine sites often associated with endometriosis.
MLA closely mimics a variety of other tumor types in these locations.
MLA shows significant morphologic, immunohistochemical, and molecular homology with cervical mesonephric adenocarcinoma.
Clinicopathologic features suggest mfcllerian derivation despite similarities to cervical mesonephric adenocarcinoma.
An international MLA Consortium was convened to refine diagnostic criteria, improve treatment options, and facilitate research; the consortium's pathologists provide a comprehensive evaluation of the literature and practical diagnostic guidance.
Controversies remain regarding the morphologic, immunohistochemical, and molecular criteria for diagnosing MLA.

Limitations: Review article without presentation of new primary patient-level data.; MLA is a rare entity, so published evidence is limited and heterogeneous.; Ongoing controversies indicate lack of universally accepted diagnostic criteria.; Conclusions rely on existing literature and expert opinion, not prospective validation..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMechanismInconclusiveLimited evidenceTier 3 · early human

DICER1 -Associated Gynecologic Neoplasms: An Update and Review

Advances in anatomic pathology · Jan 2026 · narrative review

gynecologic neoplasmsembryonal rhabdomyosarcomaSertoli-Leydig cell tumorpleuropulmonary blastoma-like peritoneal sarcomaadenosarcomagynandroblastomajuvenile granulosa cell tumorSertoli cell tumorDICER1-related Wilms-like uterine tumor

This narrative review summarizes how germline and somatic DICER1 mutations are associated with a range of benign and malignant gynecologic neoplasms and describes their shared morphologic features. The authors note that a germline loss-of-function DICER1 mutation is often followed by a somatic hotspot (second-hit) mutation in tumors, and they recommend that recognition of characteristic morphology should prompt genetic testing and surveillance for patients and families. The review proposes the term "DICER1-related primitive polyphenotypic neoplasm" to encompass the diverse histologic features of these tumors.

Key findings

DICER1 is crucial for microRNA biogenesis and maturation.
Germline DICER1 mutations are associated with increased risk of a wide range of benign and malignant neoplasms; the same tumors can also arise sporadically via somatic DICER1 mutations.
In syndromic patients, a germline loss-of-function DICER1 mutation is usually followed by a somatic hotspot mutation in the tumor as a second hit.
DICER1-associated gynecologic neoplasms most commonly include embryonal rhabdomyosarcoma and moderately to poorly differentiated Sertoli-Leydig cell tumor, with several less frequent tumor types also described.
DICER1-mutant gynecologic neoplasms frequently share characteristic morphology (primitive mesenchyme, fetal-type epithelium/cartilage, rhabdomyoblastic and/or neuroectodermal differentiation, osteoid formation, and anaplasia).
Recognition of these distinctive morphologic features should prompt consideration of DICER1-associated neoplasm and genetic testing to facilitate surveillance for patients and families.
The morphologic spectrum of most DICER1-mutant gynecologic neoplasms appears wider than that of any known type of sarcoma.
The authors propose the term "DICER1-related primitive polyphenotypic neoplasm" to better capture the diverse histologic features.

Limitations: Narrative review without description of systematic search or methods — potential selection bias in included reports.; No primary data or quantitative synthesis (no new experimental or cohort data presented).; Extent of evidence, frequency estimates, and outcomes are not quantified in the abstract..

Summarizes the association between DICER1 mutations and a spectrum of gynecologic tumors and highlights implications for pathologic recognition and genetic testing.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Human · observationalMechanismReported positiveLimited evidenceTier 3 · early human

Exploring the tumor-promoting function and prognostic value of ESPL1 in prostate adenocarcinoma

Urologic oncology · Jan 2026 · Bioinformatic analysis of TCGA and GEO datasets, immunohistochemistry on tissues, Gene Set Enrichment Analysis, and in vitro functional assays (colony formation, CCK-8, EdU, TUNEL, flow cytometry, cell cycle) in prostate cancer cell lines

prostate adenocarcinoma

The study analyzed ESPL1 (encoding Separase) expression in prostate adenocarcinoma using public datasets and tissue IHC, performed pathway analysis, and tested ESPL1 function in prostate cancer cell lines. ESPL1 was higher in tumor versus normal tissue, associated with more advanced disease and worse survival, and GSEA linked it to cell division and DNA repair pathways. In vitro suppression of ESPL1 reduced cell growth and induced apoptosis. The authors propose ESPL1 as a prognostic marker and a potential target for further study.

Key findings

ESPL1 expression was markedly elevated in PRAD tissues compared to normal prostate samples.
High ESPL1 expression correlated with advanced disease features (higher T and N stages and residual tumor presence).
Survival analysis associated high ESPL1 levels with reduced overall survival (OS) and progression-free interval (PFI).
GSEA showed enrichment of pathways related to cell division and DNA repair in samples with high ESPL1.
Suppressing ESPL1 in prostate cancer cell lines reduced cell growth and induced apoptosis in vitro.

Limitations: Observational analysis of public datasets and IHC provides correlation but not proof of causation in patients.; Functional experiments were performed in vitro only; no in vivo (animal) or clinical validation was reported.; Sample sizes and cohort details are not provided in the abstract.; Prognostic utility was demonstrated retrospectively; prospective validation is needed..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Human · observationalMechanismReported positiveLimited evidenceTier 3 · early human

Transcriptomic landscape of coexisting ovarian clear cell carcinoma and endometriosis: Insights into malignant transformation

Cancer treatment and research communications · Jan 2026 · Spatial transcriptomics profiling integrated with single-cell RNA sequencing (scRNA-seq) of tissues containing coexisting endometriosis and ovarian clear cell carcinoma regions

endometriosisovarian clear cell carcinomahigh-grade serous ovarian cancer

This study used spatial transcriptomics combined with single-cell RNA sequencing to compare molecular profiles of coexisting endometriosis and ovarian clear cell carcinoma (OCCC) regions in human tissue. The authors report shared molecular features between EMS and OCCC, greater transcriptomic similarity of severe uterine EMS to OCCC than to HGSOC, and classification of OCCC-specific genes into EMS epithelial cell-specific and tumor microenvironment-related groups that are associated with pathways linked to progression, invasion, and metabolic reprogramming.

Key findings

Spatial transcriptomic profiling revealed shared molecular features between OCCC and EMS, including overexpression of genes related to tissue development and apoptosis.
Integration with scRNA-seq data showed severe uterine EMS exhibited greater transcriptomic similarities to OCCC than to non-EAOC ovarian cancer subtypes such as HGSOC.
OCCC-specific genes were classified into EMS epithelial cell-specific and tumor microenvironment-related categories.
Identified gene sets and categories are associated with pathways implicated in tumor progression, invasion, and metabolic reprogramming.
Findings support a transcriptomic progression pathway from EMS to OCCC and provide molecular insights relevant to etiology, diagnostics, and potential targeted strategies.

Limitations: Sample size and cohort details are not reported in the abstract.; Observational, transcriptomic profiling only — correlative data that cannot establish causal malignant transformation.; No functional validation experiments (e.g., in vitro/in vivo perturbation) are reported in the abstract to confirm mechanistic roles of identified genes or pathways.; Generalizability is unclear because the abstract does not describe the number or diversity of patients/tissues analyzed..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Human · observationalMechanismReported positiveLimited evidenceTier 3 · early human

Identification of a Prognostic ceRNA Network Regulating TMBIM6 in Prostate Adenocarcinoma via Integrated Bioinformatic Analysis

International journal of molecular sciences · Dec 2025 · integrated bioinformatic analysis of TCGA and GEO datasets

prostate adenocarcinoma

The authors performed integrated bioinformatic analyses of TCGA and GEO datasets to investigate TMBIM6 in prostate adenocarcinoma. They identified a putative DHRS4-AS1 / hsa-miR-222-3p / TMBIM6 ceRNA axis that was associated with prognosis and found correlations with co-expression pathways and immune infiltration (notably epithelial cell abundance). The study proposes this axis as a potential prognostic biomarker and calls for experimental validation.

Key findings

Identification of a proposed TMBIM6/hsa-miR-222-3p/DHRS4-AS1 ceRNA axis associated with prostate adenocarcinoma prognosis.
The network was supported by differential expression, correlation, and survival analyses in TCGA and GEO datasets.
Co-expression analysis identified pathways potentially involved in tumor progression linked to TMBIM6.
Immune infiltration analysis suggested a correlation between TMBIM6 expression and the abundance of epithelial cells.
Authors propose the DHRS4-AS1/hsa-miR-222-3p/TMBIM6 axis may act as a prognostic biomarker and recommend further experimental validation.

Limitations: Computational/bioinformatic analysis only — no experimental (in vitro or in vivo) validation reported in the abstract.; Associations reported are correlative and do not establish causation.; Abstract does not report sample sizes, independent validation cohorts, or adjustment for potential confounders.; Clinical utility and prognostic performance metrics are not provided; further experimental and clinical validation required..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewReported positiveLimited evidenceTier 4 · clinical

Surgery in NF2-Schwannomatosis

Familial cancer · Dec 2025 · review

vestibular schwannomameningiomaspinal schwannomaspinal ependymomaperipheral schwannomacentral and peripheral nervous system tumorsNF2-Schwannomatosis

This is a clinical review of surgical management in NF2-Schwannomatosis. The authors summarize therapeutic indications for vestibular schwannomas, meningiomas, spinal schwannomas and meningiomas, spinal ependymomas and peripheral schwannomas. They note surgical decisions are individualized and that multidisciplinary teams and centralized care can improve outcomes in this rare disease. The review explains why a single comprehensive generic decision tree is difficult to provide.

Key findings

Surgery remains an important treatment option for NF2-Schwannomatosis, sometimes performed urgently but usually planned within complex multi-tumour burden and morbidity.
The review details therapeutic indications for each tumor type: vestibular schwannomas, meningiomas, spinal schwannomas and meningiomas, spinal ependymomas and peripheral schwannomas.
A comprehensive generic decision tree is difficult because each patient has a unique disease burden.
Experience of the multidisciplinary team impacts outcomes, and centralized care has been shown to improve the disease course in this rare disease.

Limitations: Narrative review rather than presentation of new primary data.; Authors state a comprehensive generic decision tree is difficult due to individual patient variability.; Focus is on a rare disease, which may limit generalizability of recommendations.; Abstract does not specify whether review methodology was systematic..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Human · observationalMechanismInconclusiveLimited evidenceTier 3 · early human

Spatial patterns of glioblastoma

Cancer cell · Dec 2025 · spatial profiling of glioblastoma specimens

glioblastoma

The authors spatially profiled human glioblastoma specimens. They report uncovering cellular mechanisms that govern the extent of gene expression heterogeneity in malignant cells.

Key findings

The study performed spatial profiling of glioblastoma specimens.
The authors uncovered cellular mechanisms that govern the extent of gene expression heterogeneity in malignant cells.

Limitations: Abstract provides no sample size or details on patient cohorts.; Only descriptive spatial profiling of specimens is reported in the abstract; no therapeutic intervention or clinical trial data.; The abstract does not provide mechanistic details, validation experiments, or quantitative results..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed

ReviewInconclusiveLimited evidenceTier 4 · clinical

Genomics of ovarian cancers and the potential of precision medicine

Therapeutic advances in medical oncology · Dec 2025 · review

epithelial ovarian cancerhigh-grade serous ovarian cancerovarian clear cell carcinomaendometrioid ovarian carcinomamucinous ovarian carcinomalow-grade serous ovarian carcinomaovarian carcinosarcoma

This review describes the main genomic subtypes of epithelial ovarian cancer and how those differences may help match patients to targeted therapies. It highlights PARP inhibitors, MAPK pathway inhibitors, cell cycle checkpoint inhibitors, immune checkpoint inhibitors, and antibody-drug conjugate approaches that are being investigated for specific ovarian cancer types. The article also notes that resistance to PARP inhibitors remains a problem and that more evidence is needed for effective combination therapies.

Key findings

High-grade serous ovarian cancer is linked mainly to homologous recombination repair gene alterations such as BRCA1 and BRCA2.
Ovarian clear cell carcinoma is associated with ARID1A and PIK3CA alterations; endometrioid ovarian carcinoma with PIK3CA and KRAS; mucinous ovarian carcinoma with CDKN2A and KRAS; and low-grade serous ovarian carcinoma with MAPK pathway genes such as BRAF and KRAS.
PARP inhibitor therapy has improved survival for women with homologous recombination repair defects in high-grade serous ovarian cancer, but acquired resistance remains an issue.
The review emphasizes that genomically targeted combination therapies are urgently needed and that some reported responses are preliminary.

Limitations: Review article only; no new experimental or clinical data presented in the abstract.; No quantitative outcomes or effect sizes are reported in the abstract.; The abstract is broad and does not provide trial-level details, sample sizes, or follow-up durations.; Some therapies discussed are preliminary and require further evidence..

The article is about ovarian cancer genomics and targeted therapies, not a single compound experiment.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMixed resultsModerate evidenceTier 4 · clinical

Surgery for Recurrent Ovarian Cancer

Hematology/oncology clinics of North America · Dec 2025 · literature review

ovarian cancer

This review summarizes evidence about secondary cytoreductive surgery before chemotherapy for recurrent ovarian cancer. It reports that complete gross resection is the most important factor associated with benefit and that selection criteria to predict this outcome have been developed and validated. Three recent multicenter randomized trials reported mixed results, but a meta-analysis suggests a benefit, particularly in patients with complete gross resection.

Studied with: chemotherapy.

Key findings

Use of secondary cytoreductive surgery before standard chemotherapy in recurrent ovarian cancer is controversial.
Patient and disease factors that correlate with benefit from surgery have been identified.
Complete gross resection of disease is the most important factor for benefit.
Selection criteria have been developed and validated to predict likelihood of complete gross resection.
Three parallel multicenter randomized controlled trials of secondary cytoreduction have shown mixed results.
A meta-analysis suggests a benefit, particularly in those with complete gross resection of disease.

Limitations: This is a literature review rather than primary experimental data.; The randomized controlled trials summarized are reported as having mixed results, reducing certainty.; Apparent benefit is concentrated in patients achieving complete gross resection, which may limit generalizability to all recurrent ovarian cancer patients.; No quantitative results or trial details (sample sizes, effect sizes, p-values) are provided in the abstract..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed

ReviewMechanismMixed resultsModerate evidenceTier 4 · clinical

Molecular Pathology of Ovarian Endometrioid Carcinoma: A Review

Oncology research · Nov 2025 · narrative review

ovarian endometrioid carcinomaepithelial ovarian cancer

This narrative review summarizes contemporary evidence about ovarian endometrioid carcinoma (OEC), applying the endometrial cancer molecular taxonomy (POLE‑ultramutated, MMRd, p53‑abnormal, NSMP) to OEC. The authors report that OEC is enriched for Lynch syndrome and recommend routine MMR testing; POLEmut/MMRd tumors generally have favorable outcomes and may be candidates for de‑escalation or immunotherapy, while p53‑abnormal/high‑grade tumors have poorer prognosis and may need intensified management or HRD‑directed strategies.

Reported effect: proportion_of_epithelial_ovarian_cancers 10%

Studied with: immune checkpoint inhibitors, HRD-directed strategies.

Key findings

Ovarian endometrioid carcinoma (OEC) accounts for ~10% of epithelial ovarian cancers and displays broad morphologic diversity that complicates diagnosis and grading.
The endometrial cancer molecular taxonomy (POLE‑ultramutated, MMRd, p53‑abnormal, NSMP) also applies to OEC.
OEC is enriched for Lynch syndrome‑associated tumors, supporting routine MMR testing.
Integrating morphology with molecular classification refines diagnosis and prognostication.
POLEmut/MMRd subsets generally have excellent outcomes and are candidates for de‑escalation or immunotherapy.
p53abn/high‑grade tumors carry a poorer prognosis and may warrant intensified management and trials of HRD‑directed strategies.
Routine MMR immunohistochemistry with reflex germline testing improves Lynch detection.
Future priorities include prospective validation and multi‑omics to refine NSMP and identify new targets.

Limitations: Narrative review rather than primary research; no new patient‑level data reported.; Recommendations (e.g., de‑escalation, therapeutic strategies) lack prospective validation in OEC as noted by the authors.; Broad morphologic diversity and diagnostic/grading challenges in OEC may limit generalizability of some recommendations.; NSMP group remains heterogeneous and requires further molecular refinement per the authors..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewInconclusiveLimited evidenceTier 4 · clinical

Pancreatic cancer in 2025: Have we found a solution?

World journal of gastroenterology · Nov 2025 · narrative review

pancreatic neoplasmspancreatic cancer

This is a narrative review summarizing recent progress in pancreatic cancer up to 2025. The authors discuss advances in prevention and early detection, better molecular understanding, more effective systemic therapies, improved quality of life and surgical outcomes, and the role of artificial intelligence.

Key findings

Pancreatic cancer continues to have a very poor prognosis due to late presentation, aggressive biology, and resistance to chemotherapy.
Areas of progress highlighted include prevention and early detection strategies.
The review notes refinements in molecular understanding of pancreatic cancer that may inform therapy.
Identifying more effective systemic therapies and improving quality of life and surgical outcomes are described as progress areas.
The authors emphasize the importance of technological advances, particularly artificial intelligence.

Limitations: Narrative review; no original experimental or clinical data are reported in the abstract.; Abstract provides no methods, selection criteria, or systematic search details.; No quantitative results or specific studies/metrics are reported in the abstract.; Broad scope limits detail on any single intervention, biomarker, or therapy..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMechanismReported positivePreclinical onlyTier 1 · lab

Glioblastoma hijacks cholinergic networks

Cancer cell · Nov 2025

glioblastoma

This Cancer Cell piece summarizes work by Yang et al. showing that glioblastoma co-opts cholinergic neural circuits. The authors describe mechanisms by which the tumor exploits cholinergic signaling to disrupt the hierarchical organization of brain networks and note that these findings change how we think about tumor–brain interactions and suggest potential therapeutic directions.

Key findings

Glioblastoma alters normal brain function by hijacking neural circuits.
Yang et al. elucidate mechanisms by which glioblastoma exploits cholinergic signaling pathways.
This hijacking disrupts the hierarchical organization of brain networks.
The analysis reframes tumor–brain interactions and is said to open new therapeutic avenues.

Limitations: Abstract is a short commentary/review and provides no experimental details or methods.; No species, model system, sample sizes, or quantitative results are reported in the abstract.; Unable to assess primary data, study design, or statistical strength from this abstract alone..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed

ReviewReported positiveModerate evidenceTier 4 · clinical

Processed Meat Health Risks: Pathways and Dietary Solutions

The Journal of nutrition · Nov 2025 · review

colorectal cancerbreast cancerendometrial cancerlung cancer

This review summarizes epidemiologic evidence linking red and processed meat consumption with higher risks of multiple chronic diseases, including colorectal, breast, endometrial, and lung cancers, type 2 diabetes, cardiovascular disease, and all-cause mortality. It reports that processed meats show stronger associations than unprocessed red meat, with dose-response relationships indicating elevated risks even at moderate intakes. The authors describe plausible biological mechanisms (carcinogen formation, inflammation, gut microbiome changes, heme iron, TMAO, and metabolic effects) and note inconsistencies such as short-term randomized trial biomarker findings and modification of risk by overall diet, lifestyle, and genetics. The review concludes that minimizing processed meat and replacing red/processed meats with plant proteins, poultry, or fish is expected to reduce disease risk, and it calls for further research on causality, mechanisms, and population diversity.

Studied with: plant proteins, poultry, fish.

Key findings

Observational studies and meta-analyses show positive associations between red/processed meat consumption and multiple chronic diseases, including colorectal, breast, endometrial, and lung cancers, type 2 diabetes, cardiovascular disease, and all-cause mortality.
Dose-response relationships indicate elevated risks even at moderate intakes.
Processed meats consistently show stronger detrimental associations than unprocessed red meats.
Mechanistic pathways discussed include carcinogen formation, proinflammatory effects, gut microbiome dysbiosis, heme iron, trimethylamine N-oxide (TMAO), saturated fats, and effects on lipid metabolism and insulin resistance.
Replacing red/processed meats with plant proteins, poultry, or fish is associated with reduced disease risk according to the review.
Evidence complexities include inconsistent randomized controlled trial findings on short-term biomarkers and substantial modification of risk by processing, cooking methods, overall diet, lifestyle, and genetic factors.

Limitations: Predominantly observational epidemiologic evidence, which is susceptible to confounding and cannot establish causality.; Inconsistent randomized controlled trial findings limited to short-term biomarkers rather than clinical endpoints.; Heterogeneity introduced by differences in processing methods, cooking techniques, and definitions of processed versus unprocessed meat.; Potential modification of associations by overall diet, lifestyle, and genetic factors, complicating interpretation.; Identified gaps include need for greater mechanistic specificity, more diverse populations, and integrated health-environment assessments..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed

Human · observationalMixed resultsModerate evidenceTier 3 · early humann = 661

Prognosis and Follow-Up Recommendations for Subcutaneous and Dermal Leiomyosarcoma: Local Recurrence, Metastasis, and Overall Survival in a Danish Nationwide Cohort of 661 Patients

Journal of surgical oncology · Nov 2025 · nationwide population-based cohort study (patients diagnosed 1980–2022)

cutaneous leiomyosarcomasubcutaneous leiomyosarcomadermal leiomyosarcomaleiomyosarcomaskin neoplasms

This nationwide Danish cohort study (1980–2022) compared outcomes in 196 patients with subcutaneous and 465 patients with dermal cutaneous leiomyosarcoma (total n=661). At 10 years the local recurrence rates were similar (15% vs 11%, p=0.13), but subcutaneous tumors had a much higher 10-year metastasis risk (25% vs 2.7%, p<0.001) and lower 10-year overall survival (56% vs 64%, p=0.02). The authors conclude that grade 2–3 subcutaneous leiomyosarcoma should be considered high-risk and recommend 5 years of follow-up including clinical exam plus PET/CT or chest CT, while dermal leiomyosarcoma can have clinical follow-up for 4 years.

Reported effects: 10-year local recurrence 15%, p 0.13, n=196 · 10-year risk of metastasis 25%, p <0.001, n=196 · +1 more

Key findings

Cohort included 196 patients with subcutaneous leiomyosarcoma and 465 with dermal leiomyosarcoma (total n=661).
The 10-year local recurrence rate was similar: subcutaneous 15% and dermal 11% (p = 0.13).
The 10-year risk of metastasis was substantially higher for subcutaneous leiomyosarcoma (25%) versus dermal (2.7%), p < 0.001; metastases were primarily observed in grade 2 and 3 tumors.
Ten-year overall survival was lower for subcutaneous compared with dermal leiomyosarcoma (56% vs. 64%), p = 0.02.
Authors recommend classifying grade 2–3 subcutaneous leiomyosarcoma as high-risk and performing clinical examinations plus PET/CT or CT thorax for 5 years; dermal leiomyosarcoma follow-up can focus on clinical exams for 4 years given very low metastasis risk.

Limitations: Observational, registry-based cohort (potential for residual confounding and unmeasured variables).; Long study period (1980–2022) during which diagnostic methods, staging, and treatments likely changed, which may affect outcomes.; Abstract does not report details on treatments, adjuvant therapy, or timing of interventions that could influence recurrence, metastasis, or survival.; Potentially incomplete or variable clinical data quality across decades and centers (not detailed in abstract).; Findings are from Denmark and may not generalize to other healthcare settings or populations..

Provides 10-year estimates of local recurrence, metastasis, and overall survival for dermal versus subcutaneous cutaneous leiomyosarcoma and gives follow-up recommendations.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 48

Napsin-A Expression in Mesonephric and Mesonephric-like Adenocarcinomas: Implications for Distinction From Clear Cell Carcinoma

International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists · Nov 2025 · case series

mesonephric adenocarcinomamesonephric-like adenocarcinomaclear cell carcinomamesonephric carcinosarcoma

The authors performed Napsin-A immunohistochemistry on whole-slide sections from 48 mesonephric and mesonephric-like adenocarcinomas and carcinosarcomas. Napsin-A was positive in 17/48 cases (35.4%), with focal granular cytoplasmic staining in 1–40% of cells; positivity occurred in 13/32 MLAs, 2/13 MAs, and 2/3 carcinosarcomas. The study concludes that Napsin-A is expressed in a substantial subset of these tumors and that reliance on a single marker could lead to misclassification as clear cell carcinoma.

Reported effects: Napsin-A positive overall 35.4%, n=48 · Range of focal granular cytoplasmic expression · +3 more

Key findings

Napsin-A staining was positive in 17 of 48 cases (35.4%), with focal granular cytoplasmic expression ranging from 1% to 40%.
13/32 (40.6%) mesonephric-like adenocarcinomas (MLAs) were Napsin-A positive.
2/13 (15.4%) mesonephric adenocarcinomas (MAs) were Napsin-A positive.
2/3 (66.7%) mesonephric or mesonephric-like carcinosarcomas were Napsin-A positive.
Because of morphologic and immunohistochemical overlap, Napsin-A expression in MA/MLA may contribute to misclassification as clear cell carcinoma.

Limitations: Observational pathology series without reported clinical outcome correlation; Relatively small overall sample size and very small subgroup sizes (e.g., n=3 carcinosarcomas); Findings are based solely on immunohistochemistry on tissue sections; no clinical or molecular correlation reported in the abstract.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Human · observationalMechanismMixed resultsLimited evidenceTier 3 · early humann = 9

Elucidating divergent biology in uterine carcinosarcoma

Translational oncology · Nov 2025

uterine carcinosarcoma

The authors performed multi-omic profiling (whole-genome sequencing, RNA-seq, and enzymatic methylation sequencing) on microdissected epithelial and mesenchymal components from uterine carcinosarcoma samples, and assessed the tumour microenvironment with multiplex immunohistochemistry and computational pathology. They found low median tumor mutation burden, frequent TP53 mutations and recurrent copy-number amplifications, broadly similar genomic and epigenomic profiles between epithelial and mesenchymal regions, global hypomethylation with different pathway enrichment in each component, and higher tumour-associated macrophage and PD-L1+ cell density in the mesenchymal component. The study is descriptive and based on a small number of cases.

Reported effects: median TMB 0.97, n=18 · TP53 mutation frequency 94%, n=18 · +9 more

Key findings

WGS and EM-seq of 18 samples from 9 patients revealed a low tumor mutation burden (TMB; median = 0.97 mutations/Mb) and no evidence of microsatellite instability (MSI).
Driver mutations were identified in TP53 (94 %), PIK3CA (33 %), and PPP2R1A (22 %).
Copy-number analysis revealed recurrent amplifications of MYC (67 %), PIK3CA (61 %), CCNE1 (56 %), AKT2 (44 %), and SMARCA4 (39 %).
Comparative analysis of the epithelial (C) and mesenchymal (S) regions revealed no significant differences in mutation frequency, copy-number, transcriptomic and methylomic profiles.
Both regions exhibited global hypomethylation, with functional enrichment for xenobiotic metabolism pathways in C and epithelial-to-mesenchymal transition pathways in S regions.
Comparative mIHC performed on 21 cases showed similar T cell and B cell densities, but a higher density of tumour-associated macrophages and PD-L1+ cells in the S component.
Computational morphologic analysis showed substantial histomorphologic heterogeneity within and across UCS cases.

Limitations: Small sequencing sample size (18 samples from 9 patients) limits generalizability.; Observational, descriptive study without functional validation of genomic/epigenomic findings.; No clinical outcome or treatment-response data reported to link molecular features to prognosis or therapy response.; mIHC analysis was performed on a separate/expanded cohort of 21 cases but remains limited in size.; Heterogeneity within tumors may limit ability to generalize findings from microdissected regions..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Animal studyMechanismReported positivePreclinical onlyTier 2 · animal

Now you serine, now you don't

Trends in pharmacological sciences · Nov 2025 · commentary/review of a study

glioblastomabrain neoplasms

This article discusses a study in glioblastoma showing that tumor cells took up more serine. It also reports that limiting serine uptake made chemoradiation work better in preclinical models. The abstract is mainly a commentary on emerging research rather than a full original trial report.

Studied with: chemoradiation.

Key findings

Tumor metabolism in glioblastoma patients showed increased import of serine.
Limiting serine uptake enhanced the effectiveness of chemoradiation in preclinical models of glioblastoma.

Limitations: This is not a full original study report; it is a commentary/review-style article.; The abstract does not provide methods, sample size, or quantitative results.; The sensitization finding is preclinical, so human clinical benefit is unproven..

Discusses a metabolic vulnerability in glioblastoma and preclinical chemoradiation sensitization.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Animal studyReported positivePreclinical onlyTier 2 · animal

The effectiveness of anti-PD-L1 treatment and the underlying regulatory mechanism in ovarian clear cell carcinoma

International immunopharmacology · Oct 2025 · in vitro cell experiments and mouse in vivo experiments with molecular assays (western blot, RT-PCR, RNA pull-down, RIP)

ovarian clear cell carcinoma

This laboratory study used cell-based assays and mouse models to test anti-PD-L1 treatment in ovarian clear cell carcinoma (OCCC). The authors report that anti-PD-L1 showed effectiveness in OCCC, that PD-L1 is highly expressed and associated with proliferation, invasion and metastasis, and that the lncRNA ZFPM2-AS1 binds HNRNPC and the ZFPM2-AS1/HNRNPC axis modulates the response to anti-PD-L1. The work is preclinical and uses molecular, cellular and animal experiments.

Key findings

The study identified effectiveness of anti-PD-L1 treatment in OCCC (reported in vitro and in vivo).
PD-L1 was highly expressed in OCCC and was closely related to proliferation, invasion and metastasis in vitro and in vivo.
ZFPM2-AS1 was overexpressed in OCCC and can bind HNRNPC.
The ZFPM2-AS1/HNRNPC axis participates in regulating the effectiveness of anti-PD-L1 treatment.

Limitations: Preclinical study only (cellular assays and animal models); no human trial or clinical data reported in the abstract.; Abstract does not report sample sizes, numerical effect sizes, or statistical significance.; Details of experimental controls, doses, and treatment schedules are not provided in the abstract..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

ReviewMechanismInconclusivePreclinical onlyTier 1 · lab

Purinergic Signaling in Ovarian Carcinoma

Advanced pharmaceutical bulletin · Oct 2025 · review

ovarian carcinoma

This review discusses purinergic signaling in ovarian carcinoma and summarizes experimental evidence about how ATP and adenosine-related pathways may affect the tumor microenvironment. It describes roles in metastatic behavior, cell proliferation, metabolic changes, and suppression of anti-tumor immune responses. The article does not report new experimental or clinical results.

Key findings

ATP released by tumor cells can act in the tumor microenvironment through autocrine-paracrine signaling.
Extracellular ATP is converted to adenosine by CD39 and CD73.
The review links purinergic signaling to metastatic phenotype, proliferation, metabolic adaptations, and immune suppression in ovarian carcinoma.

Limitations: Review article; no original experimental data.; No human or animal intervention was performed.; No quantitative effect estimates were reported..

The article is about purinergic signaling pathways in ovarian carcinoma and discusses them as potential therapeutic targets, but it is a review rather than a study of a specific compound's effect.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewInconclusiveLimited evidenceTier 4 · clinical

Ovarian Cancer: Many Diseases Under One Name

Journal of insurance medicine (New York, N.Y.) · Oct 2025

ovarian cancer

This narrative review summarizes current knowledge about ovarian cancer, noting it is a heterogeneous group of diseases with the most common subtype being high-grade serous epithelial tumors. It highlights genetic risk factors (BRCA1/BRCA2 and mismatch repair genes), the lack of effective screening leading to advanced-stage diagnosis, and that management commonly involves specialized surgery and combination chemotherapy; prognosis varies by stage, grade, and histologic subtype.

Studied with: surgery, combination chemotherapy.

Key findings

Ovarian cancer is heterogeneous with multiple types and subtypes.
The most common variety is the high-grade serous epithelial tumor (reported as 70%-80% of cases).
Positive family history and susceptibility genes (BRCA1, BRCA2, and mismatch repair genes) increase risk.
Effective screening tools are lacking, so most cancers are diagnosed at advanced stages.
Diagnosis and accurate staging usually require tissue sampling and extensive debulking surgery performed by gynecologic oncology specialists.
Combination chemotherapy is commonly used before or after surgery, or as primary treatment for advanced disease.
Mortality rates vary by stage, grade, and tumor type; some less common subtypes (sex cord stromal, germ cell, borderline epithelial) have better survival.

Limitations: Narrative review rather than original research; no new primary data reported in the abstract.; Abstract does not specify methods (systematic search, inclusion criteria), so potential for selection bias in reviewed literature.; No quantitative outcomes, effect sizes, or detailed evidence levels are provided in the abstract..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed

Human · observationalMechanismMixed resultsLimited evidenceTier 3 · early human

Tumor treating fields alter local coagulation dynamics in glioblastoma patients

Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · Oct 2025

glioblastoma

The authors analyzed blood, tumor cells, and plasma-derived extracellular vesicles from glioblastoma patients and healthy donors to assess how Tumor Treating Fields (TTFields) affect coagulation-related biology. They report that short-term TTFields exposure prolonged blood coagulation and reduced clot rigidity by decreasing Factor II/FXIII activity and platelet count, while patient-derived GBM cells showed increased tissue factor (TF) abundance and changes in coagulation-related gene expression. Co-culture experiments indicated TTFields modulate pro- and anticoagulant factors and inflammatory pathways in the tumor microenvironment. The study does not report quantitative sample sizes or clinical thromboembolic outcomes.

Studied with: radiochemotherapy.

Key findings

Short-term TTFields exposure significantly prolongs blood coagulation in GBM patients and healthy donors by altering tissue factor (TF) expression and disrupting the extrinsic coagulation pathway.
TTFields reduced clot rigidity by decreasing Factor II/FXIII activity and platelet count, without impairing fibrinogen function.
Patient-derived GBM cells exposed to TTFields exhibited increased TF abundance.
RNA microarray of GBM cells after TTFields exposure showed upregulation of platelet adhesion marker ITGA2 and downregulation of THBS1.
TXNIP, described as a coagulation-modulating gene linked to immune regulation, was downregulated after TTFields exposure.
In an allogeneic co-culture model of patient-derived GBM cells and peripheral blood, TTFields modulated coagulation and immune responses, suggesting rebalancing of pro- and anticoagulant factors and alteration of inflammatory pathways.

Limitations: No sample size or detailed patient cohort characteristics are reported in the abstract.; Study reports short-term exposure effects; duration and long-term consequences are not defined.; Observational and ex vivo/in vitro analyses; causality in patients in vivo is not established.; No clinical outcome data on thromboembolic events or patient-level clinical endpoints are provided.; Findings include mixed pro- and anticoagulant signals (e.g., increased TF in tumor cells vs prolonged blood coagulation), complicating interpretation..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Case reportMechanismInconclusiveLimited evidenceTier 3 · early humann = 3

High-grade endometrioid carcinomas with pilomatrix-like features lacking CTNNB1 Mutations: Clinicopathologic characteristics and novel molecular events

Human pathology · Oct 2025 · case series

endometrial carcinomaendometrioid carcinomapilomatrix-like high-grade endometrioid carcinoma (PiMHEC)

The authors report three human cases of high-grade endometrioid carcinoma with pilomatrix-like features (PiMHEC) that lacked CTNNB1 exon 3 mutations and nuclear β-catenin by IHC. All tumors had characteristic pilomatrix-like morphology, presented at advanced stage, showed aggressive clinical behavior (two recurrences within 12 months), and targeted NGS identified alternative likely oncogenic alterations including FGFR4 p.T259A, TSC2 mutations, KRAS p.G12D, and MYC amplification.

Reported effects: number_of_cases 3, n=3 · patients_presenting_with_advanced_stage_disease 3, n=3 · +6 more

Key findings

Three cases of high-grade endometrioid carcinoma with pilomatrix-like features were analyzed.
All tumors demonstrated two components: a high-grade basaloid component with solid sheets of atypical basaloid cells, geographic necrosis, and focal "ghost" cells, and an associated low-grade FIGO grade 1 endometrioid carcinoma component.
None of the three cases showed nuclear β-catenin expression by IHC, and all lacked CTNNB1 exon 3 mutations.
All the patients presented with advanced-stage disease (stages IIC-IVB).
Two patients had a recurrence within 12 months.
NGS revealed no CTNNB1 mutations, but identified alternative likely oncogenic alterations: one tumor harbored an FGFR4 p. T259A mutation, two tumors had pathogenic TSC2 mutations, one had a KRAS p.G12D mutation, and two showed MYC amplification.

Limitations: Very small sample size (n=3) and single case-series design.; Case reports are descriptive and cannot establish causal relationships between identified mutations and the PiMHEC phenotype.; No functional validation provided to show that the alternative oncogenic alterations drive the pilomatrix-like phenotype.; Limited follow-up data reported (recurrence noted within 12 months for two patients), limiting assessment of long-term outcomes and prognostic significance..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Human trialTrialMixed resultsModerate evidenceTier 4 · clinicaln = 77

Phase 3 randomized trial of high-dose methotrexate for young children with high-risk embryonal brain tumors: A report from the Children's Oncology Group

Neuro-oncology · Oct 2025 · phase 3 randomized controlled trial

Methotrexateembryonal brain tumorsmedulloblastomaGroup 3 medulloblastomaSHH medulloblastomaembryonal tumor with multilayered rosettespineoblastoma

This phase 3 randomized trial tested adding high-dose methotrexate to induction chemotherapy in children ≤36 months with high-risk embryonal brain tumors. Overall complete response rates were similar between arms, but in medulloblastoma patients methotrexate was associated with higher CR (63% vs 30%) and improved 5-year event-free survival in Group 3 medulloblastoma (70% vs 33.3%). No benefit was seen for embryonal tumor with multilayered rosettes or pineoblastoma.

Reported effects: eligible patients 77, n=77 · patients evaluated for response 59, n=59 · +8 more

Studied with: induction chemotherapy, high-dose consolidation chemotherapy with hematopoietic stem-cell infusion.

Key findings

Of 77 eligible patients, 59 with detectable disease were evaluated for response and 28 (47.5%) achieved CR; 15/30 (50%) treated with methotrexate compared to 13/29 (45%) without methotrexate (P = 0.35).
For medulloblastoma (MB), CR was 12/19 (63%) with methotrexate compared to 6/20 (30%) without methotrexate (P = 0.039).
All SHH subtype MB (n = 11) were survivors (molecular characterization retrospective).
Five-year event-free survival (EFS) for Group 3 MB was 70% (90% CI: 39.6-87.2) with methotrexate versus 33.3% (90% CI: 15.0-52.9) without (P = 0.037).
In other embryonal tumors, CR was 3/11 (27%) with methotrexate compared to 7/9 (78%) without (P = 0.99).
No benefit observed for Embryonal Tumor with Multilayered Rosettes (n = 14; EFS 20.0% [90% CI: 1.8-52.5] with methotrexate versus 33.3% [90% CI: 10.8-58.1] without, P = 0.58) or pineoblastoma (n = 9; EFS 16.7% [90% CI: 1.6-46.1] with methotrexate versus 0% without, P = 0.52).

Limitations: Relatively small overall sample size (77 eligible) with smaller numbers in histologic/molecular subgroups; Molecular characterization was conducted retrospectively; Some subgroup analyses involve very small n (e.g., Group 3 MB: 10 vs 15; SHH MB n=11); Tests of significance were one-sided (as stated); Confidence intervals reported are 90% rather than the more conventional 95%.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Human · observationalMixed resultsLimited evidenceTier 3 · early humann = 97

Endometrial carcinosarcoma without myoinvasion

International journal of gynecological cancer : official journal of the International Gynecological Cancer Society · Oct 2025 · multicenter retrospective study

uterine carcinosarcomaendometrial carcinosarcomaendometrial neoplasms

This multicenter retrospective study looked at 97 people with very early uterine carcinosarcoma that had not invaded the muscle layer of the uterus. The researchers compared outcomes by where the tumor was found and by whether patients received chemotherapy. Recurrence was common, mostly at distant sites, and the study did not find statistically significant survival differences with chemotherapy.

Reported effects: 5-year recurrence-free survival 63.5% [53.4–75.4], n=97 · overall survival 72% [62.6–82.9], n=97

Key findings

29 of 97 patients (29.9%) had a recurrence, mostly with a distant pattern of relapse.
The 5-year recurrence-free survival was 63.5% and overall survival was 72.0%.
No significant differences were observed in recurrence-free survival and overall survival based on tumor status.
The difference in recurrence-free survival and overall survival was not statistically significant based on receipt of chemotherapy.

Limitations: Retrospective observational design; Rare disease with small sample size; Non-randomized treatment selection; Follow-up for survival analysis was limited to 5 years; Potential confounding by indication; No chemotherapy regimen, dose, or timing details provided in the abstract.

This study evaluates outcomes in a rare endometrial cancer subtype and compares adjuvant chemotherapy versus no chemotherapy after surgery.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Case reportInconclusiveLimited evidenceTier 3 · early humann = 1

Primary ovarian rhabdomyosarcoma: A diagnostic dilemma in an uncommon tumor

Journal of cancer research and therapeutics · Oct 2025 · case report

Cyclophosphamide Actinomycin-d Vincristineovarian rhabdomyosarcoma

This case report describes a 17-year-old girl with a very rare ovarian rhabdomyosarcoma. The tumor was diagnosed by imaging, pathology, and immunohistochemistry, and it came back within 3 months after surgery. The authors report that she then received VAC chemotherapy (vincristine, actinomycin D, and cyclophosphamide), and they emphasize the need for earlier diagnosis and more standardized treatment approaches.

Studied with: vincristine, actinomycin D, cyclophosphamide.

Key findings

Imaging showed a large solid-cystic pelvic mass.
Histopathology and immunohistochemical markers (desmin, myogenin, WT1) confirmed ovarian rhabdomyosarcoma.
Recurrence occurred within 3 months after surgical resection.
VAC chemotherapy was given after early relapse.

Limitations: Single-patient case report.; No control group.; No quantitative treatment outcome data reported.; Cannot determine effectiveness of VAC from this report alone.; Focus is diagnostic and descriptive rather than evaluative..

Describes a rare ovarian cancer case and subsequent chemotherapy, but does not evaluate a compound's anticancer effect in a comparative way.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Case reportMechanismReported negativeLimited evidenceTier 3 · early humann = 2

Rectal large cell neuroendocrine carcinoma

Oxford medical case reports · Sep 2025 · case report (two patients)

rectal large cell neuroendocrine carcinoma (LCNEC)

This report describes two patients initially thought to have rectal adenocarcinoma who were re-diagnosed after surgery as having rectal large cell neuroendocrine carcinoma (LCNEC) by immunohistochemistry. The authors report that both patients received neo-adjuvant chemotherapy yet nonetheless developed metastatic disease, and they argue for routine early IHC to improve diagnosis and guide management.

Key findings

Rectal LCNEC is described as an exceedingly rare, aggressive neoplasm with poor prognosis (background statement).
Diagnosis is challenging due to clinical overlap with colorectal adenocarcinoma and relies on histology with immunohistochemistry (IHC).
Neuroendocrine markers cited as major determinants for diagnosis include synaptophysin, CD56, chromogranin A and Ki-67.
Two patients initially assumed to have rectal adenocarcinoma were re-diagnosed with rectal LCNEC via post-surgical IHC.
Both patients received neo-adjuvant chemotherapy but still developed metastatic disease.
Authors recommend routine early IHC as a critical diagnostic tool to guide management planning.

Limitations: Case report of only two patients (very small sample size); No control or comparison group; Clinical outcomes and follow-up details are limited in a short report; Findings are observational and not generalizable; No therapeutic efficacy data to support management recommendations.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Human trialTrialReported positiveModerate evidenceTier 4 · clinicaln = 31

Efficacy and safety of adjuvant TTFields plus pembrolizumab and temozolomide in newly diagnosed glioblastoma: A phase 2 study

Med (New York, N.Y.) · Sep 2025 · Phase 2, single-arm with case-matched control comparison

Pembrolizumab Temozolomideglioblastoma

This phase 2 clinical trial enrolled 31 patients with newly diagnosed glioblastoma after chemoradiation to test adding pembrolizumab to TTFields plus temozolomide. Among 26 patients treated per protocol, median progression-free survival was 12.0 vs. 5.8 months (HR 0.377; p = 0.0026) and median overall survival was 24.8 vs. 14.6 months (HR 0.522; p = 0.0477) compared to case-matched controls. Patients who had biopsy only showed larger PFS and OS benefits than those with maximal resection. Immune analyses suggested TTFields induced a T1IFN-driven clonal T cell expansion while pembrolizumab supported adaptive replacement and sustained T cell activation; severe treatment-related adverse events were reported as 7.5%.

Reported effects: median PFS 12 mo · PFS hazard ratio 0.377 [0.217–0.653], p=0.0026 · +7 more

Studied with: pembrolizumab, temozolomide.

Key findings

Among 26 patients treated per protocol, median PFS was 12.0 vs. 5.8 months in controls (HR 0.377, 95% CI 0.217-0.653; p = 0.0026).
Among 26 patients treated per protocol, median OS was 24.8 vs. 14.6 months in controls (HR 0.522, 95% CI 0.301-0.905; p = 0.0477).
Patients undergoing biopsy had longer PFS (27.2 vs. 9.6 months; HR 0.37, 95% CI 0.16-0.85; p = 0.014) and OS (31.6 vs. 18.8 months; HR 0.4, 95% CI 0.17-0.92; p = 0.023) compared to maximal resection.
Severe adverse events constituted 7.5% of treatment-related toxicities.
Immune correlates: TTFields promoted clonal T cell expansion via a T1IFN-driven trajectory, while pembrolizumab supported adaptive replacement of these clones, sustaining T cell activation and memory formation, especially in biopsy-only patients.

Limitations: Small sample size (31 enrolled; 26 treated per protocol).; Phase 2, non-randomized, single-arm design with case-matched controls rather than a randomized control group.; Potential selection or matching biases inherent to case-matched control comparisons.; Follow-up duration not specified in the abstract.; Funded by Novocure (industry support) which may present a conflict of interest..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed

Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 56

Human epidermal growth factor receptor-2, nectin-4, and trophoblast cell surface antigen-2 expression in endometrial carcinosarcoma

Gynecologic oncology reports · Sep 2025 · retrospective pathology series

endometrial carcinosarcoma

This retrospective immunohistochemical study examined HER2, nectin-4, and TROP2 expression in 56 endometrial carcinosarcomas. HER2 3+ was present in 7.1% of cases and HER2 2+/3+ expression was associated with serous carcinoma differentiation and largely confined to the carcinomatous component. Nectin-4 was detected in 39.3% (mostly weak) and TROP2 in 62.5% of cases; both were predominantly expressed in the carcinomatous component. The authors note HER2-directed antibody-drug conjugates could be of interest for ECS with serous differentiation and recommend further study of nectin-4 and TROP2 relevance.

Reported effects: HER2 3+ prevalence 7.1%, n=56 · HER2 2+ (equivocal) prevalence 10.7%, n=56 · +5 more

Key findings

HER2 overexpression (3+) was identified in 4 cases (7.1%).
An additional 6 cases (10.7%) showed equivocal (2+) HER2 staining.
HER2 2+/3+ expression was significantly associated with serous carcinoma differentiation (31.0% vs. 3.7%, P = 0.012).
HER2 2+/3+ expression was largely confined to the carcinomatous component (P < 0.001).
Nectin-4 was expressed in 39.3% of cases, predominantly weak in intensity, with significantly higher expression in the carcinomatous than in the sarcomatous component (P < 0.001).
TROP2 expression was observed in 62.5% of cases and was confined to the carcinomatous component, with no strong expression detected.
No significant correlations were found between marker expression and other clinicopathological variables beyond serous differentiation.

Limitations: Retrospective design; Modest sample size (n=56); Semi-quantitative immunohistochemistry without functional or clinical outcome data; Observational/correlative study — does not assess treatment response to targeted agents.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewSupportive careReported positiveStrong evidenceTier 4 · clinical

Exercise oncology comes of age

Journal of the National Cancer Institute. Monographs · Sep 2025

Supportive care

This monograph reviews the development of exercise oncology, noting the field has more than 30,000 peer-reviewed citations and multiple guidelines from major institutions based on randomized trial evidence. It documents progress in research and practice and outlines the formation of an International Society of Exercise Oncology to promote integrating exercise into oncology care.

Reported effect: peer-reviewed citations 30000

Key findings

Exercise oncology has accumulated more than 30,000 peer-reviewed citations in the scientific literature.
Multiple guidelines have been published by major medical institutions based on evidence from randomized controlled trials.
The monograph documents the progression of exercise oncology research and practice.
A new International Society of Exercise Oncology is being formed to organize the field and promote use of exercise in oncology care.

Limitations: This is a monograph/review rather than primary research and does not present new patient-level data.; Abstract provides no methods (e.g., systematic search strategy) or quantitative synthesis details.; Potential for advocacy or organizational bias given focus on forming a new society; no conflicts/funding disclosed in abstract..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewSupportive careReported positiveLimited evidenceTier 4 · clinical

History informing the future of exercise oncology

Journal of the National Cancer Institute. Monographs · Sep 2025

Supportive careadult cancerspediatric cancers

This narrative review / viewpoint summarizes roughly four decades of exercise oncology research in adults and children and describes the creation of the International Society of Exercise Oncology (ISEO). It briefly reviews early studies, larger randomized trials, and biological-mechanism research, discusses strengths/weaknesses/opportunities/threats for ISEO, and suggests ISEO could support research, education, and translation to practice. The authors note exercise is increasingly recognized as an important component of cancer care and propose this work may ultimately improve quality and quantity of life for people with cancer.

Key findings

Exercise is increasingly recognized by patients, clinicians, and allied health professionals globally as an important component of cancer care.
The paper provides a viewpoint on developments in exercise oncology over the past 4 decades leading to creation of the International Society of Exercise Oncology (ISEO).
The authors briefly review research in adult and pediatric cancers, from early foundational studies to larger randomized controlled trials and biological-mechanism work.
The paper discusses potential strengths, weaknesses, opportunities, and threats facing ISEO as a global forum for exercise oncology.
ISEO is presented as an opportunity to support research, collaborations, education and training, increase awareness, and support translation of research to clinical practice with the goal of improving quality and quantity of life for people with cancer.

Limitations: Narrative viewpoint / review rather than a systematic review or primary research; no new experimental or trial data presented.; Abstract indicates a brief review and perspective, so selection bias and lack of systematic methods are possible.; No quantitative synthesis or new effect estimates are reported in this paper..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewReported positiveModerate evidenceTier 4 · clinical

Tumor treating fields for glioblastoma: opportunities and drawbacks

Expert review of medical devices · Sep 2025 · review

glioblastomabrain neoplasms

This review summarizes tumor treating fields (TTFields), an alternating electric-field therapy for glioblastoma that uses dielectrophoresis to disrupt mitosis in dividing cells. The authors state that clinical trials have shown TTFields added to standard adjuvant treatments significantly improved progression-free and overall survival. They also note unresolved questions about neuropsychological effects and management of postoperative motor deficits and call for further research.

Studied with: standard adjuvant treatments.

Key findings

TTFields therapy applies alternating electric fields and, via dielectrophoresis, selectively disrupts mitotic processes in replicating cells.
Clinical trials reported that TTFields significantly improved progression-free and overall survival rates when combined with standard adjuvant treatments.
Unanswered questions remain about the impact of TTFields on neuropsychological functioning and the management of postoperative motor deficits.

Limitations: This publication is a review rather than primary clinical trial data.; The abstract provides no numeric trial results or detailed quantitative outcomes.; The review notes unresolved clinical questions (neuropsychological effects, motor deficit management), indicating incomplete evidence.; Safety and long-term outcome details are not provided in the abstract..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed

ReviewInconclusiveLimited evidenceTier 4 · clinical

Cancer of the corpus uteri: A 2025 update

International journal of gynaecology and obstetrics: the official organ of the International Federation of Gynaecology and Obstetrics · Sep 2025

Endometrial neoplasms

This is a 2025 narrative review updating current knowledge about cancer of the corpus uteri (endometrial cancer). The article states that incidence and mortality from endometrial cancer are increasing and summarizes topics including histopathology, staging, surgical and non-surgical management, follow-up, and management of recurrent disease.

Key findings

Incidence of endometrial cancer is increasing, as is mortality from endometrial cancer.
The article provides an update covering histopathology and staging of endometrial cancer.
The article reviews surgical and non-surgical management approaches.
The article discusses follow-up and management of recurrent endometrial cancer.

Limitations: Narrative review: no new primary data reported in the abstract.; Abstract does not describe search methods, inclusion criteria, or evidence synthesis approach.; No quantitative results, effect sizes, or levels of evidence are reported in the abstract..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Human · observationalMechanismReported negativeModerate evidenceTier 3 · early humann = 6036

Real-world clinical outcomes of patients with high-risk endometrial cancer or endometrial carcinosarcoma in England: A retrospective cohort study

The journal of obstetrics and gynaecology research · Sep 2025 · retrospective cohort study

endometrial cancerendometrial carcinosarcoma

This retrospective, population-based cohort study of 6,036 women in England described real-world outcomes after initiation of first adjuvant therapy for high-risk endometrial cancer or endometrial carcinosarcoma. Median real-world disease-free survival (rwDFS) was 4.56 years and median overall survival (OS) was 8.85 years; 45% experienced recurrence and 39% died during follow-up. Recurrence was associated with a 3.23-fold higher risk of death, and rwDFS correlated with OS (Kendall's τ = 0.75).

Reported effects: sample_size 6036, n=6036 · mean follow-up 48 mo, n=6036 · +10 more

Key findings

6036 women were included (mean age 67 years; 86% White) with mean follow-up of 48 months.
45% of patients experienced recurrence and 39% of patients died due to any cause.
Median rwDFS from initiation of adjuvant therapy: 4.56 years (95% CI: 4.14-5.12).
Median OS from initiation of adjuvant therapy: 8.85 years (95% CI: 8.15-9.82).
Estimated 2-year and 5-year probabilities: rwDFS 0.64 (95% CI: 0.63-0.65) and 0.49 (95% CI: 0.48-0.50); OS 0.78 (95% CI: 0.77-0.79) and 0.60 (95% CI: 0.58-0.61).
Disease recurrence was associated with a 3.23-fold higher risk of death (p < 0.001).
Kendall's τ between rwDFS and OS was 0.75 (95% CI: 0.69-0.80, p < 0.001), supporting rwDFS as a surrogate for OS.

Limitations: Retrospective observational design (potential for confounding and bias).; Use of registry data (NCRAS) may limit availability of detailed clinical variables and introduces potential data-recording limitations).; rwDFS was operationalized as time to next treatment or death, a surrogate endpoint rather than confirmed radiographic/pathologic recurrence.; Findings are from England and may not generalize to other settings or populations..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewReported positiveModerate evidenceTier 4 · clinical

Cancer of the ovary, fallopian tube, and peritoneum: 2025 update

International journal of gynaecology and obstetrics: the official organ of the International Federation of Gynaecology and Obstetrics · Sep 2025 · narrative review

ovarian cancerfallopian tube cancerperitoneal cancerepithelial ovarian cancersovarian germ cell malignanciesovarian stromal malignancies

This is a narrative review updating FIGO staging and summarizing current knowledge on ovarian, fallopian tube, and peritoneal cancers. It describes the 2014 FIGO staging revisions (including subdivisions of Stage IC and IIIC/IIIA) and summarizes genetics, surgical management, chemotherapy, targeted therapies, and aspects of germ cell and stromal ovarian malignancies. The review notes that high-grade serous carcinoma is the most common histology and that no feasible screening strategies currently exist.

Key findings

FIGO's 2014 staging revision groups ovarian, fallopian tube, and peritoneal cancers in the same system and subdivides Stage IC into IC1 (surgical spill), IC2 (preoperative capsule rupture or tumor on surface), and IC3 (malignant cells in ascites or peritoneal washings).
Stage IIIC was revised to include a category for spread to retroperitoneal lymph nodes without intraperitoneal dissemination, subdivided into IIIA1(i) (metastasis ≤10 mm) and IIIA1(ii) (metastasis >10 mm); Stage IIIA2 is now defined as microscopic extrapelvic peritoneal involvement with or without positive retroperitoneal lymph nodes.
Most of these malignancies are high-grade serous carcinomas (HGSCs).
There are currently no feasible screening strategies for ovarian cancer.
Diagnosis, treatment, surveillance, and survival have improved due to advances in radiology, pathology, genomics, and molecular biology, and individualized care emphasizes precision surgery to limit morbidity.
Germline genetic analysis and identification of somatic mutations in tumor tissue provide data informing the use of targeted agents and immunotherapy; the review also covers chemotherapy and management of germ cell and stromal ovarian malignancies.

Limitations: Narrative review with no original patient-level data presented; Abstract does not report review methods, search strategy, or criteria for evidence selection (not identified as a systematic review or meta-analysis); No new primary quantitative data or pooled estimates provided in this abstract.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 21

Mucinous cystic neoplasms of the pancreas and liver share a similar DNA methylation profile with mucinous ovarian tumors

The Journal of pathology · Sep 2025

pancreatic mucinous cystic neoplasmhepatic mucinous cystic neoplasmmucinous ovarian carcinomamucinous borderline ovarian tumor

Researchers performed immunohistochemistry, targeted DNA sequencing, and genome-wide DNA methylation profiling on a cohort of pancreatic and hepatic mucinous cystic neoplasms. They found that both pancreatic and hepatic MCNs have distinct methylation profiles within their organ landscapes and that both group with mucinous ovarian tumors in combined methylation analyses, suggesting possible shared origins.

Reported effects: pancreatic MCNs in cohort 15 · hepatic MCNs in cohort 6 · +9 more

Key findings

Immunohistochemistry and targeted DNA sequencing were used to confirm MCN diagnoses in the studied cohort.
Unsupervised DNA methylation analysis placed MCN-P predominantly as a distinct group within the pancreatic tumor methylation landscape.
MCN-L demonstrated a specific methylation profile within the liver tumor methylation landscape compared with other entities.
Both MCN-P and MCN-L grouped with mucinous ovarian carcinoma and mucinous borderline ovarian tumors (mBOTs) in the ovarian tumor methylation landscape.
Low-grade MCNs showed greater DNA methylation similarity to mBOTs, whereas high-grade or invasive MCNs associated primarily with mucinous ovarian carcinomas.
Across all samples (19 tumor types and four normal tissue types, n=430), MCNs grouped with mucinous ovarian tumors and normal ovarian tissue.
Network analysis of differentially methylated probes showed MCN-P and MCN-L share significant methylation traits resembling mucinous ovarian tumors.

Limitations: Small cohort of primary interest (15 pancreatic MCNs and only 6 hepatic MCNs).; Observational, cross-sectional molecular profiling — cannot establish lineage or causality.; Findings are based on DNA methylation patterns alone (no functional or lineage-tracing experiments reported).; Potential heterogeneity and differences between reference sample sets used for comparative landscapes..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMechanismInconclusiveLimited evidenceTier 4 · clinical

Modeling large cell neuroendocrine carcinoma of the lung for molecular, therapeutic and microenvironmental inferences: current knowledge and future perspectives

Expert review of anticancer therapy · Sep 2025 · narrative review

large cell neuroendocrine carcinoma of the lung

This narrative review summarizes current knowledge about large cell neuroendocrine carcinoma (LCNEC) of the lung, focusing on diagnostic criteria, molecular alterations, the tumor microenvironment including immune components, and ongoing clinical trials including immuno-oncology. The authors emphasize that LCNEC is a heterogeneous disease with distinct developmental trajectories that complicate diagnosis and clinical decision-making. They suggest this heterogeneity may provide a rationale for personalized targeted approaches or immunotherapy in patient subsets, but conclude that further studies using a holistic framework are needed.

Key findings

LCNEC of the lung is described as a high-grade non-small cell carcinoma with neuroendocrine morphology and neuroendocrine markers.
Diagnosis and therapeutic decision-making are challenging, likely because LCNEC comprises a heterogeneous mix of genetic and epigenetic alterations intertwined with the host microenvironment.
The review structures LCNEC knowledge across three outlooks: (i) diagnostic criteria and molecular alterations; (ii) microenvironmental changes, including the immune system; and (iii) available clinical trials, including immune-oncology studies.
Different developmental trajectories of LCNEC may explain diagnostic and treatment difficulties and may offer a rationale for personalized targeted therapies or immunotherapy in subsets of patients.
The authors call for future studies to frame LCNEC within a broader, holistic context among lung cancers rather than viewing it as a single, isolated tumor type.

Limitations: Narrative review that does not present original experimental or clinical data.; Abstract emphasizes heterogeneity and diagnostic challenges, which limit definitive clinical recommendations.; No quantitative synthesis or meta-analysis is reported in the abstract.; Authors state that readiness for a major change in understanding LCNEC is unresolved and further studies are needed..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Case reportMechanismInconclusiveLimited evidenceTier 3 · early humann = 1

High-grade Endometrial Endometrioid Carcinoma: A Case Report of Complete Transdifferentiation to Pilomatrix-like Carcinoma

International journal of surgical pathology · Sep 2025 · Case report

Endometrial endometrioid carcinomaPilomatrix-like high-grade endometrioid carcinoma

This is a single-patient case report of a 56-year-old woman whose high-grade endometrial endometrioid carcinoma showed complete transdifferentiation to a pilomatrix-like carcinoma pattern, with metastases to ovaries and lymph nodes. Pathology showed basaloid cells with ghost cell keratinization, aberrant cytoplasmic and nuclear β-catenin expression, focal CDX2, absent PAX8 and ER/PR, and NGS identified a CTNNB1 (p.Ser37Phe) mutation with a variant allele frequency of 18.6%. The authors note this tumor is rare, diagnostically challenging, presented at high stage, and it is unknown whether standard adjuvant therapies are effective for this subtype.

Reported effect: CTNNB1 variant allele frequency 18.6%, n=1

Key findings

Hysterectomy specimen confirmed high-grade endometrioid carcinoma with secondary involvement of both ovaries, left tubo-ovarian ligament and obturator lymph nodes.
Microscopically the tumor had a solid, nested/insular pattern with peripheral basaloid cells, central ghost cell keratinization, and extensive geographic necrosis.
No low-grade endometrioid carcinoma component was identified in the primary tumor or metastases after extensive sampling.
Immunohistochemistry showed aberrant cytoplasmic and nuclear expression of β-catenin, focal CDX2 expression, and negativity for PAX8 and estrogen and progesterone receptors (ER/PR).
Next-generation sequencing found a CTNNB1 pathogenic mutation (p.Ser37Phe, c.110C > T) with a variant allele frequency of 18.6%.
Based on morphology, immunohistochemistry and NGS analysis, the diagnosis of pilomatrix-like high-grade endometrioid carcinoma was established.

Limitations: Single-patient case report — findings may not be generalizable.; No data presented on treatment given or therapeutic outcomes for this patient.; Follow-up and clinical outcome details are not reported in the abstract.; Unable to assess effectiveness of standard adjuvant therapies for this subtype from this report..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

OtherMixed resultsModerate evidenceTier 4 · clinical

NCCN Guidelines® Insights: Non-Small Cell Lung Cancer, Version 7.2025

Journal of the National Comprehensive Cancer Network : JNCCN · Sep 2025 · Practice Guideline

non-small-cell lung cancer (NSCLC)

This document summarizes recent updates to the NCCN Guidelines for non-small cell lung cancer (NSCLC). The updates focus on systemic therapy options for patients with nonmetastatic NSCLC and on corresponding molecular testing considerations.

Key findings

The NCCN Guidelines Insights present recent updates for NSCLC management.
The discussion emphasizes systemic therapy options for nonmetastatic NSCLC.
The guidance highlights molecular testing considerations that correspond to systemic therapy choices.

Limitations: Abstract provides no details on specific therapies, recommended regimens, or testing algorithms.; No primary data, numerical results, or methods are reported in the abstract.; As a guideline summary, it synthesizes evidence rather than presenting new experimental or clinical trial data..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Lab · in vitroReported positivePreclinical onlyTier 1 · lab

Chrysin induces cell death and inhibits migration and invasion in squamous cervical carcinoma using a three-dimensional cell culture model

Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas · Aug 2025

squamous cell cervical carcinomacervical cancer

This laboratory study used a 3D spheroid model of the HPV-16-positive SiHa cervical cancer cell line to test the natural flavonoid chrysin. Chrysin caused concentration-dependent reductions in cell viability and spheroid size, and inhibited spheroid migration and invasion; these effects were associated with decreased MMP-2 and VEGF production. The authors state these results support further in vivo preclinical studies.

Key findings

Chrysin treatment exhibited concentration-dependent cytotoxic and cytostatic effects, reducing cell proliferation and decreasing SiHa spheroid size.
Chrysin inhibited cell migration and invasion in spheroid assays.
Chrysin decreased production of MMP-2 and VEGF, which the authors link to the observed anti-migratory and anti-invasive effects.
Experiments were performed in a 3D spheroid culture using the SiHa (HPV-16-positive) human cervical cancer cell line.

Limitations: In vitro study only (3D cell culture); no animal or human data reported.; Single cell line (SiHa) studied, limiting generalizability across cervical cancers.; Abstract provides no quantitative dose levels, sample sizes, statistical values, or detailed methods.; Mechanistic detail limited to measured decreases in MMP-2 and VEGF; causal pathways not fully established in this report..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Animal studyReported positivePreclinical onlyTier 2 · animal

Bifidobacterium animalis suppresses non-small cell lung cancer progression and modulates tumor immunity through indole-3-acetic acid

Cell reports · Aug 2025 · mouse models and NSCLC cell lines; gut microbiota comparison in patients with NSCLC and healthy controls

Indole-3-acetic-acidnon-small cell lung cancer

This study looked at gut bacteria and a bacterial metabolite in non-small cell lung cancer. The authors found that Bifidobacterium animalis was lower in patients with NSCLC, and in mouse models and cell lines it was associated with less tumor progression. They identified indole-3-acetic acid as a key metabolite and reported that it affected AHR/METTL3/STAT3 signaling and immune cells in ways linked to reduced tumor growth.

Key findings

Bifidobacterium animalis was markedly decreased in patients with NSCLC compared with healthy controls.
B. animalis suppressed tumor progression in two NSCLC mouse models and NSCLC cell lines.
Indole-3-acetic acid was identified as the pivotal metabolite of B. animalis with anti-NSCLC properties.
B. animalis and IAA activated AHR and suppressed METTL3 and STAT3 m6A methylation.
B. animalis and IAA reduced M2 macrophage polarization and enhanced CD8+ T cell functions by suppressing IL-6.

Limitations: Preclinical findings dominate the study; the anticancer effects were shown in mouse models and cell lines, not in a human trial.; Human data were observational/comparative microbiome profiling only, so causality cannot be established.; The abstract does not provide sample sizes, doses, or follow-up duration.; The abstract does not report clinical outcomes in patients..

The study links a gut bacterium and its metabolite to NSCLC progression and antitumor immunity in preclinical models.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

ReviewReported positiveLimited evidenceTier 4 · clinical

Mistletoe in Cancer Cell Biology: Recent Advances

Current issues in molecular biology · Aug 2025 · review

non-small-cell lung cancercancer cells (general)

This review summarizes research from 2020–2025 on mistletoe (Viscum album) in cancer biology, covering new molecular mechanisms, immunomodulatory effects, and clinical observations. It reports preclinical findings of immunogenic cell death (calreticulin exposure, ATP release) and immune changes (IL-6/IL-10 shifts), cites real-world data in >400 NSCLC patients suggesting longer median overall survival when mistletoe is combined with PD-1/PD-L1 inhibitors, and notes a Phase I trial reporting IV safety at 600 mg three times weekly. The authors call for further standardized clinical research and advanced mechanistic studies.

Reported effects: calreticulin exposure (% of cancer cells) · ATP release (fold change) 7 · +5 more

Studied with: PD-1/PD-L1 inhibitors.

Key findings

Mistletoe extracts trigger endoplasmic reticulum stress, leading to calreticulin exposure in 18-51% of cancer cells and a 7-fold increase in adenosine triphosphate (ATP) release.
Three-dimensional culture models showed a 15.8% increase in pro-inflammatory IL-6 and a 26.4% reduction in immunosuppressive IL-10, indicating macrophage reprogramming effects.
Real-world evidence from over 400 non-small-cell lung cancer patients shows that combining mistletoe with PD-1/PD-L1 inhibitors doubles median overall survival (6.8 to 13.8 months).
Biomarker-selected populations in the cited real-world data experienced up to a 91.2% reduction in death risk.
The Johns Hopkins Phase I trial established intravenous administration safety at 600 mg three times weekly.
Authors report that advanced analytics (metabolomics, chronobiology, machine learning) are being used to enable precision-medicine applications.

Limitations: This publication is a review (secondary synthesis) rather than a single prospective randomized trial.; The real-world evidence cited is observational (over 400 NSCLC patients) and may be subject to confounding and selection bias.; The Phase I trial reported safety but does not establish efficacy.; Many findings summarized are preclinical (cell culture, 3D models), limiting direct clinical inference.; Heterogeneity of included studies and lack of standardized clinical protocols are noted as issues..

Review synthesizes preclinical mechanisms and limited clinical/real-world evidence on mistletoe in cancer, including combination with immune checkpoint inhibitors.

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMechanismInconclusiveLimited evidenceTier 3 · early human

HER2/neu as a Signaling and Therapeutic Marker in Uterine Serous Carcinoma

Cells · Aug 2025 · review

uterine serous carcinomaendometrial cancerbreast cancer

This is a narrative review of HER2/neu as a signaling and therapeutic marker in uterine serous carcinoma (USC). It summarizes HER2 expression and amplification in USC, compares USC HER2 features to breast cancer, evaluates preclinical and clinical evidence for HER2-directed therapies (including monoclonal antibodies and ADCs), and discusses possible mechanisms of resistance.

Studied with: monoclonal antibodies, antibody-drug conjugates, chemotherapy.

Key findings

HER2/neu coordinates cell growth and differentiation and when overexpressed and/or amplified its downstream tyrosine kinase can become constitutively activated, causing dysregulated gene transcription.
HER2/neu has been successfully targeted in breast cancer with monoclonal antibodies and antibody-drug conjugates.
Use of HER2-directed therapies in gynecologic malignancies has been slower, in part due to unique characteristics of HER2 protein expression and gene amplification in USC such as major heterogeneity and lack of apical staining compared to breast cancer.
Optimal testing algorithms for HER2/neu status in USC may have important implications for developing targeted therapies.
The review evaluates efficacy of HER2-directed therapies in both preclinical and clinical settings and discusses possible mechanisms of resistance.

Limitations: Narrative review rather than original experimental or systematic/meta-analytic data.; Abstract contains no quantitative results or study-level sample sizes.; Conclusions depend on heterogeneous preclinical and clinical studies in the literature rather than a single controlled dataset.; Field limitations noted (e.g., heterogeneity of HER2 expression in USC) may limit generalizability of testing and therapeutic approaches..

Reviews HER2/neu expression and the potential of HER2-directed therapies in uterine serous carcinoma, with attention to diagnostic testing and resistance.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Human · observationalMechanismMixed resultsLimited evidenceTier 3 · early humann = 590

Integrated molecular and clinical characterization of pulmonary large cell neuroendocrine carcinoma

Nature communications · Aug 2025 · cohort study (two independent clinical/genomic cohorts)

pulmonary large cell neuroendocrine carcinoma (LCNEC)small cell lung cancer (SCLC)non-small cell lung cancer (NSCLC)

The authors analyzed clinical and molecular data from 590 patients with pulmonary large cell neuroendocrine carcinoma across two cohorts. They identified two genomic subtypes (NSCLC-like with KEAP1/KRAS/STK11 mutations and SCLC-like with RB1/TP53 mutations) and report that 80% of tumors aligned with SCLC transcriptional profiles. The study found elevated FGL-1 and SPINK1 expression in NSCLC-like LCNECs and higher DLL3 in SCLC-like LCNECs, and noted fewer tumor-infiltrating lymphocytes in LCNEC compared with other lung cancers. Overall survival was comparable across chemotherapy, chemoimmunotherapy, and immunotherapy in this cohort.

Reported effect: proportion aligning with SCLC transcriptional profiles 80%, n=590

Key findings

Study cohort: 590 patients across two independent cohorts.
Comparable overall survival across treatment regimens (chemotherapy, chemoimmunotherapy, immunotherapy) without unexpected adverse events.
Genomic analysis identified two LCNEC subtypes: NSCLC-like (KEAP1, KRAS, STK11 mutations) and SCLC-like (RB1, TP53 mutations).
80% of LCNEC tumors aligned with SCLC transcriptional profiles.
Serial sampling showed stable mutational landscapes but shifting transcriptomic profiles over time.
Elevated FGL-1 (a LAG-3 ligand) and SPINK1 expression were observed in NSCLC-like LCNECs; DLL3 levels were higher in SCLC-like LCNECs.
Immunofluorescence confirmed FGL-1 expression in NSCLC-like LCNECs.
H&E analyses indicated fewer tumor-infiltrating lymphocytes in LCNECs versus other lung cancers.
Authors suggest these immunogenomic features support future investigation of LAG-3, SPINK1, and DLL3-targeted approaches.

Limitations: Observational cohort design — no randomized comparison of treatments reported in the abstract.; Abstract provides no quantitative survival or subgroup outcome measures (no effect sizes or statistical details reported).; Molecular associations (expression of FGL-1, SPINK1, DLL3) are descriptive and do not demonstrate therapeutic efficacy.; Functional or clinical validation of proposed targets is not presented in the abstract.; H&E-based assessment of tumor-infiltrating lymphocytes is a histologic surrogate and may lack detailed immunophenotyping..

Identifies immunogenomic subtypes and candidate targets (FGL-1/LAG-3, SPINK1, DLL3) in LCNEC that may guide future therapeutic investigations.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewInconclusiveLimited evidenceTier 4 · clinical

Small cell carcinoma of the bladder: Review of pathogenesis, presentation, and management

Bladder cancer (Amsterdam, Netherlands) · Aug 2025 · narrative review

small cell carcinoma of the bladder (SCCB)

This is a narrative review of small cell carcinoma of the bladder (SCCB), a rare and aggressive subtype that represents under 1% of bladder cancers. The authors summarize clinical presentation, staging, local and systemic management, and molecular insights, noting most treatment regimens are extrapolated from small cell lung cancer and that novel agents are in development. They call for greater preclinical research and increased patient participation in clinical trials.

Key findings

SCCB is a rare, aggressive malignancy accounting for less than 1% of bladder cancers.
The review summarizes epidemiology, cystoscopic and imaging findings, staging methods, local and systemic treatment approaches, and molecular mechanisms underlying SCCB.
Most treatment regimens for SCCB are extrapolated from small cell lung cancer due to shared neuroendocrine features and aggressive phenotype.
Novel agents for SCCB are in clinical development.
The authors recommend increased preclinical research and greater participation of SCCB patients in clinical trials to expand treatment options.

Limitations: Review article with no new primary data reported.; Evidence base is limited and heterogeneous because SCCB is rare (<1% of bladder cancers).; Many treatment recommendations are extrapolated from small cell lung cancer rather than SCCB-specific trials.; Likely lack of large, randomized clinical trials specific to SCCB..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Animal studyReported positivePreclinical onlyTier 2 · animal

A humanized anaplastic lymphoma kinase (ALK)-directed antibody-drug conjugate with pyrrolobenzodiazepine payload demonstrates efficacy in ALK-expressing cancers

Nature communications · Aug 2025 · xenograft antitumor assays

neuroblastomarhabdomyosarcomacolorectal carcinomamelanomaovarian carcinomabreast carcinoma

This study tested a humanized antibody-drug conjugate called CDX0239-PBD in ALK-expressing cancer models. In cell lines, it was taken up by ALK-positive neuroblastoma cells and killed them in a way that depended on surface ALK expression. In mouse xenograft models, it produced strong antitumor activity and complete responses were maintained in several ALK-expressing cancers.

Key findings

ALK RNA, protein, and tumor cell surface expression was elevated in multiple pediatric and adult malignancies with minimal expression in childhood normal tissues.
CDX0239-PBD was internalized in ALK-expressing neuroblastoma cell lines with cell surface expression-dependent cytotoxicity.
CDX0239-PBD exhibited potent antitumor efficacy including maintained complete responses in ALK-expressing patient and cell line-derived neuroblastoma, fusion-positive rhabdomyosarcoma, and colorectal carcinoma xenograft models.

Limitations: Preclinical study only; no human treatment data are reported in the abstract.; Efficacy was shown in cell lines and xenograft mouse models, which may not predict clinical benefit.; No quantitative effect sizes, dosing details, or toxicity results are provided in the abstract..

The abstract describes a preclinical anticancer antibody-drug conjugate targeting ALK-expressing tumors.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

OtherMechanismReported positiveLimited evidenceTier 3 · early human

Immune memory shapes ovarian cancer recurrence

Cancer cell · Aug 2025

ovarian cancer

The paper reports that Ghisoni et al. integrated multiomic and functional analyses related to ovarian cancer. They propose a roadmap for biomarker-driven therapy and suggest immune phenotyping could be used in clinical stratification to address recurrence.

Key findings

Ghisoni et al. integrated multiomic and functional analyses in ovarian cancer.
The authors provide a roadmap for biomarker-driven therapy in ovarian cancer.
They suggest that immune phenotyping could be incorporated into clinical stratification to address recurrence.

Limitations: Abstract provides no methodological details, sample sizes, or quantitative results.; Findings are presented as a proposed roadmap/suggestion; clinical validation is not described in the abstract.; Unclear which specific datasets, cohorts, or experimental models were analyzed from the abstract alone..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed

ReviewMechanismInconclusiveLimited evidenceTier 4 · clinical

Recent Therapies and Biomarkers in Mucinous Ovarian Carcinoma

Cells · Aug 2025 · review

mucinous ovarian carcinomaovarian cancer

This review summarizes recent treatment ideas and biomarkers for mucinous ovarian carcinoma, a rare type of ovarian cancer. It discusses targeted therapies such as HER2 inhibitors and KRASG12C inhibitors, as well as checkpoint inhibitors and other newer strategies. The abstract does not report results from a new experiment or clinical trial, only a synthesis of the literature.

Key findings

Mucinous ovarian carcinoma is described as having frequent KRAS mutations and HER2 amplifications.
The review highlights HER2 inhibitors and KRASG12C inhibitors as targeted therapy options under discussion.
Checkpoint inhibitors are noted as potentially useful in tumors with high PD-L1 expression or tumor mutational burden.
The abstract mentions antibody-drug conjugates, synthetic lethality approaches, and Wnt/β-catenin pathway inhibitors as emerging strategies.

Limitations: Review article only; no original patient, animal, or cell-line data in the abstract.; No quantitative outcomes, response rates, or survival data are reported.; The abstract is broad and does not specify which therapies were tested in which settings.; Potential clinical benefit is discussed as promising or potential, not demonstrated in this abstract..

This is a review of therapies and biomarkers in a specific ovarian cancer subtype, not a primary efficacy study.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMechanismMixed resultsLimited evidenceTier 4 · clinical

Hallmark discoveries in the biology of non-Wilms tumour childhood kidney cancers

Nature reviews. Urology · Aug 2025

clear-cell sarcoma of the kidneycongenital mesoblastic nephromamalignant rhabdoid tumour of the kidneyrenal-cell carcinomarenal medullary carcinomaWilms tumourother rare renal histologies

This review summarizes major discoveries in the biology of non-Wilms childhood kidney tumours, a heterogeneous group that makes up about 20% of paediatric and AYA renal tumours. It describes how clinicopathological observation, immunohistochemistry, molecular cytogenetics and next-generation sequencing improved tumour recognition and risk stratification, and how new models (cell lines, organoids, xenografts, genetically engineered mouse models) have aided understanding and target identification. The authors note that despite these advances, patients with these rare tumours still die at higher rates than those with Wilms tumour and call for international coordinated efforts to address unresolved questions.

Key findings

Approximately 20% of paediatric and adolescent/young adult patients with renal tumours are diagnosed with non-Wilms tumours.
Differential diagnosis evolved from clinicopathological observation to immunohistochemistry, molecular cytogenetics and next-generation sequencing, enabling near-definitive recognition and risk stratification.
New renal-tumour models (cell lines, organoids, xenografts and genetically engineered mouse models) have improved understanding of tumour development and facilitated identification of new therapeutic targets.
Despite these advances, patients with these rare cancers continue to die at higher rates than patients with Wilms tumour.
The authors recommend international coordinated efforts to answer unresolved questions and improve outcomes.

Limitations: Review article summarizing prior work rather than presenting new primary data.; Subject focuses on a heterogeneous group of rare tumours, limiting generalizability across all non-Wilms histologies.; Abstract indicates unresolved questions remain and that outcomes are still poor, implying limited definitive clinical evidence for improved outcomes..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Human · observationalSupportive careMixed resultsModerate evidenceTier 3 · early humann = 267586

Risk of atherosclerotic cardiovascular disease after cancer diagnosis: findings from 3 prospective cohort studies

Journal of the National Cancer Institute · Aug 2025 · prospective cohort study

Supportive carecervical cancerHodgkin lymphomaprostate cancerbreast cancercolorectal cancerlung cancerendometrial canceroral cavity and pharynx cancerkidney cancerovarian cancersarcomamelanomaleukemia

Researchers followed participants in three large prospective cohorts for up to 36 years to examine whether a cancer diagnosis was associated with later atherosclerotic cardiovascular disease (ASCVD). They documented 4,334 new ASCVD events among 49,603 incident cancer cases and found that cervical cancer and Hodgkin lymphoma were associated with higher ASCVD risk, prostate cancer with slightly lower risk, and that ASCVD risk trajectories over time varied by cancer type (for example, breast cancer survivors had lower ASCVD risk for the first 7.5 years, then risk increased).

Reported effects: new-onset ASCVD events among incident cancer cases 4334, n=49603 · cervical cancer HR 1.56 [1.06–2.29] · +6 more

Key findings

During up to 36 years of follow-up, 4,334 new-onset ASCVD events among 49,603 incident cancer cases were documented.
Cervical cancer was associated with increased ASCVD incidence (HR = 1.56, 95% CI = 1.06 to 2.29).
Hodgkin lymphoma was associated with increased ASCVD incidence (HR = 2.80, 95% CI = 1.89 to 4.15).
Prostate cancer was associated with lower ASCVD incidence (HR = 0.91, 95% CI = 0.85 to 0.97).
Breast cancer survivors experienced lower ASCVD risk during the first 7.5 years after diagnosis, but risk gradually increased afterward (Pnonlinearity = .01).
ASCVD risk increased over time among patients with cancers of the colorectum (P = .003), lung (P = .002), and endometrium (P = .04).
No statistically significant association with ASCVD risk was observed for cancers of the oral cavity and pharynx, kidney, or ovary; sarcoma; melanoma; or leukemia.

Limitations: Observational cohort design cannot establish causality.; Potential for residual confounding despite multivariable adjustment.; Cohorts consist of nurses and health professionals, which may limit generalizability to other populations.; Abstract does not report details on cancer stage or treatments, which could influence ASCVD risk..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Human trialTrialReported positiveStrong evidenceTier 4 · clinicaln = 571

Tumor Treating Fields With Gemcitabine and Nab-Paclitaxel for Locally Advanced Pancreatic Adenocarcinoma: Randomized, Open-Label, Pivotal Phase III PANOVA-3 Study

Journal of clinical oncology : official journal of the American Society of Clinical Oncology · Jul 2025 · randomized, open-label, phase III, multicenter

Gemcitabine Sodium-butyratelocally advanced pancreatic adenocarcinomapancreatic adenocarcinoma

This randomized phase III trial assigned 571 patients with unresectable locally advanced pancreatic adenocarcinoma to gemcitabine/nab-paclitaxel with or without Tumor Treating Fields (TTFields). Adding TTFields significantly prolonged median overall survival (16.2 vs 14.2 months; HR 0.82; P = .039), and also improved pain-free survival and distant progression-free survival; PFS, local PFS, and overall response rate were not improved. Device-related skin adverse events occurred in 76.3% of patients (mostly mild-to-moderate) with 7.7% reporting grade 3 skin AEs.

Reported effects: median OS 16.2 mo [15–18], n=571 · OS HR 0.82 [0.68–0.99], p=0.039, n=571 · +6 more

Studied with: gemcitabine/nab-paclitaxel.

Key findings

Overall survival (OS) was significantly longer with TTFields plus gemcitabine/nab-paclitaxel versus gemcitabine/nab-paclitaxel alone (median 16.2 months v 14.2 months; HR 0.82; P = .039).
Pain-free survival was significantly prolonged with TTFields (median 15.2 months v 9.1 months; HR 0.74; P = .027).
Distant progression-free survival (distant PFS) was significantly prolonged with TTFields (median 13.9 months v 11.5 months; HR 0.74; P = .022); this analysis was reported post hoc.
Progression-free survival (PFS), local PFS, and overall response rate (ORR) were not improved with TTFields.
Device-related skin adverse events occurred in 76.3% of patients, mostly mild-to-moderate, with 7.7% experiencing grade 3 skin AEs.
The abstract reports no additive systemic toxicity with the addition of TTFields.

Limitations: Open-label design (not blinded).; Distant PFS outcome was analyzed post hoc.; Device-related skin adverse events were common (76.3%), including 7.7% grade 3 events.; Abstract provides limited detail on duration of follow-up and per-arm event counts.; Findings apply to patients with unresectable locally advanced pancreatic adenocarcinoma and may not generalize to other stages..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed

Human · observationalMechanismMixed resultsLimited evidenceTier 3 · early humann = 300

Unveiling histotype-specific biomarkers in ovarian carcinoma using proteomics

Molecular therapy. Oncology · Jul 2025 · proteomic analysis of tumor and control tissue samples

epithelial ovarian cancerovarian carcinomaborderline ovarian tumorbenign ovarian tumor

The authors performed proteomic analysis on 300 patient samples across four main epithelial ovarian cancer histotypes, plus borderline and benign tumors, to find differentially abundant proteins and candidate biomarker panels. They report multiple proteins (e.g., SNCG, S100A1, VWA2, AGR2, CTH, SPINK1) that distinguish tissues, and survival analyses that linked GLYR1, RPL12, GDPGP1, and POLR2M to more favorable outcomes and SDF4, PPP3CC, EIF2AK2, and STX6 to worse outcomes. The study presents histotype-specific protein attributes that the authors propose could inform diagnosis and prognosis, but these candidates require further validation.

Key findings

Proteomic data from 300 patient samples were used to identify differentially abundant proteins (DAPs) across EOC histotypes and control tissues.
Identified DAPs included SNCG, S100A1, VWA2, AGR2, CTH, and SPINK1 that contributed to biomarker panels stratifying tissues.
Enrichment of biological processes was observed to profile histotypes and involve the identified DAPs.
Survival analysis identified candidate prognostic biomarkers with histotype-specific associations: GLYR1, RPL12, GDPGP1, and POLR2M were associated with favorable outcomes.
Survival analysis also linked SDF4, PPP3CC, EIF2AK2, and STX6 with unfavorable outcomes.

Limitations: Observational proteomic profiling without interventional or functional validation experiments reported in the abstract.; No independent external validation cohort is mentioned in the abstract.; Abstract does not report adjustment for clinical confounders in the survival analyses.; Clinical utility of identified biomarkers is not established by this study; further validation is required..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Lab · in vitroMechanismReported positivePreclinical onlyTier 1 · lab

Aurora kinase-a expression heterogeneity and potential benefit of combination therapy in prostate adenocarcinoma

Frontiers in cell and developmental biology · Jul 2025 · Integrative analysis of TCGA/GEO multi-omics and single-cell RNA-seq with in vitro experiments on prostate cancer cells

prostate adenocarcinoma

This study used public multi-omics datasets and single-cell RNA sequencing, plus in vitro experiments, to examine heterogeneity of Aurora kinase A (AURKA) expression in prostate adenocarcinoma. High-AURKA epithelial subpopulations were associated with proliferation and DNA repair programs, while low-AURKA subpopulations activated TNF-alpha and androgen receptor pathways linked to drug resistance. The authors report that AURKA may compensate after androgen receptor inhibition and that computational drug-sensitivity analyses suggest AURKA inhibitors could have benefit in combination with targeted therapies, ADCs, or immunotherapy; TMB and CD274 were identified as potential biomarkers for AURKA-high patients.

Studied with: targeted therapy, antibody-drug conjugate (ADC) therapy, immunotherapy, androgen receptor (AR) inhibition.

Key findings

Pan-cancer analysis showed AURKA expression heterogeneity among urological tumors across multiple molecular levels.
AURKA alteration positively correlated with MYC and E2F pathways in pan-cancer analysis.
Single-cell analysis identified epithelial subpopulations with high AURKA expression (epi3/4/6) that promoted proliferation via cell cycle and DNA repair regulation.
Low AURKA expression subsets (epi1/2/7) activated TNF-alpha and androgen receptor pathways associated with drug resistance.
AURKA may act as a compensatory pathway supporting tumor activity after androgen receptor (AR) inhibition in prostate cancer.
Clinical analysis associated AURKA overexpression with poorer prognosis in patients with low Gleason scores or high PSA.
Drug-sensitivity co-analysis suggested AURKA inhibitors may have benefit when combined with targeted therapy, ADC therapy, and immunotherapy.
Tumor mutational burden (TMB) and CD274 (PD-L1) expression were identified as biomarkers in AURKA high-expression prostate adenocarcinoma patients for clinical outcome.

Limitations: Primary evidence is computational (TCGA/GEO integration and single-cell analysis) and in vitro; no in vivo (animal) or clinical trial validation reported in the abstract.; Abstract does not report sample sizes, cohorts, or statistical details for prognostic associations.; Drug-sensitivity co-analysis appears to be predictive/correlative and not validated experimentally in vivo or clinically.; Prognostic associations may be confounded and are not demonstrated to be independent of other clinical variables in the abstract..

This preclinical and computational study characterizes AURKA expression heterogeneity in prostate adenocarcinoma and proposes molecular subtyping to guide combination strategies involving AURKA inhibitors and other therapies.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Case reportMechanismReported positiveLimited evidenceTier 3 · early humann = 1

Plasma epigenomic profiling reveals treatment-emergent squamous transformation in prostate cancer

NPJ precision oncology · Jul 2025 · Serial plasma epigenomic (circulating chromatin) profiling from a single patient case report

prostate adenocarcinomametastatic prostate cancer

The authors performed serial plasma circulating chromatin (epigenomic) profiling in a single patient with metastatic prostate cancer who developed squamous transformation. They detected dynamic changes in gene regulation in circulating chromatin that reflected emergence of squamous differentiation, enabling non-invasive diagnosis and monitoring of this resistance phenotype. The abstract notes potential therapeutic implications but provides no validation data.

Key findings

Circulating chromatin (plasma epigenome) showed dynamic changes corresponding to squamous differentiation in a patient with metastatic prostate cancer.
These plasma epigenomic changes enabled non-invasive detection and monitoring of treatment-emergent squamous transformation.
Authors state the findings have potential therapeutic implications.

Limitations: Single-patient case report (n=1), limiting generalizability.; No validation cohort or independent replication reported in the abstract.; No quantitative results or performance metrics provided in the abstract.; Observational profiling; cannot establish clinical utility or impact on outcomes from the data presented..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

OtherMechanismReported positiveLimited evidenceTier 3 · early humann = 21

Large language models-enabled digital twins for precision medicine in rare gynecological tumors

NPJ digital medicine · Jul 2025 · Proof-of-concept computational digital-twin development integrating institutional/published cases and literature-derived data

rare gynecological tumorsuterine carcinosarcoma

The authors developed a proof-of-concept large language model (LLM)-enabled digital twin that integrates clinical and biomarker data from 21 cases and 655 publications to generate tailored treatment plans. Applied to metastatic uterine carcinosarcoma, the system identified therapeutic options that might be missed by single-source analyses and efficiently modeled individual patient trajectories. The authors argue that defining tumors by biology rather than organ could enable more personalized care for rare gynecological tumors.

Reported effects: integrated_cases_n 21 · literature_publications_n 655

Key findings

Developed an LLM-enabled digital twin integrating clinical and biomarker data from institutional and published cases (n = 21) and literature-derived data (n = 655 publications).
Created tailored treatment plans for metastatic uterine carcinosarcoma using multi-source data integration.
Identified treatment options potentially missed by traditional, single-source analysis.
LLM-enabled digital twins can efficiently model individual patient trajectories.
Shifting to a biology-based rather than organ-based tumor definition could enable more personalized care for rare gynecological tumors.

Limitations: Proof-of-concept computational study without prospective clinical validation.; Small number of integrated cases (n = 21).; No clinical outcomes or patient-level efficacy/safety data reported.; Relies on literature-derived data and published cases which may have heterogeneity and publication bias.; Abstract does not report external validation or comparison to standard-of-care decision processes..

Demonstrates a computational approach for biomarker-driven treatment matching in rare gynecological tumors using LLMs; clinical impact not evaluated in this study.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewInconclusivePreclinical onlyTier 4 · clinical

Metabolic reprogramming in melanoma therapy

Cell death discovery · Jul 2025

melanoma

This is a review summarizing recent studies on how metabolic reprogramming supports melanoma growth, proliferation, metastasis, and resistance to therapy. It discusses metabolic pathways involved in melanoma progression and considers targeting these pathways alone or combined with existing therapeutic inhibitors as a potential strategy.

Studied with: established therapeutic inhibitors.

Key findings

Melanoma exhibits metabolic reprogramming that supports energy production, biosynthesis, tumor progression, and therapy resistance.
The review summarizes recent studies elucidating metabolic pathways involved in melanoma progression, therapeutic response, and resistance.
The authors discuss potential of targeting metabolic pathways, alone or in combination with established therapeutic inhibitors, to block melanoma progression.

Limitations: Review article with no original experimental or clinical data reported.; Abstract does not state systematic-review methods or provide search strategy, so selection bias is possible.; Conclusions are narrative and may be speculative without new experimental validation presented in this paper..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Human · observationalReported positiveLimited evidenceTier 3 · early human

Health effects associated with consumption of processed meat, sugar-sweetened beverages and trans fatty acids: a Burden of Proof study

Nature medicine · Jul 2025 · meta-analysis (Burden of Proof meta-regression)

colorectal cancer

This Burden of Proof meta-regression analyzed associations between processed meat, sugar-sweetened beverages (SSBs), and trans fatty acids (TFAs) and risks of type 2 diabetes, ischemic heart disease (IHD) and colorectal cancer. The authors reported conservative estimates that processed meat intake was associated with at least an 11% increase in type 2 diabetes risk and a 7% increase in colorectal cancer risk; SSBs with at least an 8% increase in type 2 diabetes risk and a 2% increase in IHD risk; and TFAs with at least a 3% increase in IHD risk. The associations were given two-star ratings indicating weak or inconsistent input evidence, and the authors note further research is needed while recommending limiting consumption given disease burden.

Reported effects: average increase in type 2 diabetes risk (processed meat, 0.6-57 g/day) 11% · average increase in colorectal cancer risk (processed meat, 0.78-55 g/day) 7% · +3 more

Key findings

Processed meat (0.6-57 g/day) was associated with at least an 11% average increase in type 2 diabetes risk (relative to zero consumption).
Processed meat (0.78-55 g/day) was associated with at least a 7% average increase in colorectal cancer risk (relative to zero consumption).
SSB intake (1.5-390 g/day) was associated with at least an 8% average increase in type 2 diabetes risk (relative to zero consumption).
SSB intake (0-365 g/day) was associated with at least a 2% average increase in ischemic heart disease (IHD) risk (relative to zero consumption).
TFA consumption (0.25-2.56% of daily energy intake) was associated with at least a 3% average increase in IHD risk (relative to zero consumption).
Each association received two-star ratings reflecting weak relationships or inconsistent input evidence; authors recommend further research and continuing recommendations to limit consumption given high chronic disease burden.

Limitations: Findings are based on meta-regression of existing studies rather than randomized trials, so causal inference is limited.; The authors rate the associations as two-star, indicating weak or inconsistent input evidence.; Dose-response characterization is described as limited and the results are presented as conservative estimates relative to zero consumption..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed

ReviewReported positiveLimited evidenceTier 4 · clinical

Radiation Therapy for Metastatic Melanoma

Dermatologic clinics · Jul 2025 · narrative review

metastatic melanomabrain metastases

This narrative review summarizes how radiation therapy (RT) is being used in metastatic melanoma and how its role has evolved. The authors describe RT's value for local control, palliation, and management of brain metastases, and discuss emerging evidence of synergy between RT and immune checkpoint inhibitors, including the abscopal effect.

Studied with: immune checkpoint inhibitors.

Key findings

Metastatic melanoma is aggressive with a low 5-year survival rate of 27%.
Melanoma was historically considered radioresistant, but responses to radiation therapy have evolved, particularly when combined with systemic therapies such as immune checkpoint inhibitors.
Radiation therapy is now recognized for utility in local control, palliative care, and management of brain metastases in metastatic melanoma.
Emerging evidence indicates synergy between radiation therapy and immune checkpoint inhibitors, with mechanisms such as the abscopal effect under investigation.

Limitations: This is a review article and does not present original trial data.; Abstract provides no details on radiation doses, schedules, or specific clinical trial results.; Evidence for synergy with immune checkpoint inhibitors is described as emerging, indicating limited or early-stage data.; The abstract does not state this is a systematic review or meta-analysis, so the review methodology and comprehensiveness are unclear..

Discusses the clinical role of radiation therapy in metastatic melanoma and its integration with immune checkpoint inhibitors.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Human · observationalMechanismReported positiveModerate evidenceTier 3 · early human

Construction of a prostate adenocarcinoma molecular classification: integrating spatial transcriptomics with retrospective cohort validation

Journal of translational medicine · Jul 2025 · Spatial transcriptome analysis; Monocle 2 trajectory analysis; TCGA-PRAD cohort prognostic analysis (Kaplan-Meier and univariate Cox); Consensus clustering to define subtypes; retrospective cohort validation with immunohistochemistry and follow-up

prostate adenocarcinoma

The authors integrated spatial transcriptomics, TCGA-PRAD prognostic analyses, and a retrospective clinical cohort to define malignant cell differentiation-related prognostic genes and build a three-subtype molecular classification (MDPC) for prostate adenocarcinoma. They identified three malignant spot types and 33 MDPGs, produced three MDPC subtypes (DPP4+MSMB+, NHP2+NVL+, COL1A1+MYLK+), and validated that the COL1A1+MYLK+ subtype was associated with markedly worse overall survival and progression-free survival in their cohort. The COL1A1+MYLK+ subtype was also linked to higher Gleason/WHO grades, prior bone metastasis, and treatment history.

Reported effects: OS hazard ratio 20.72, p=0.0018 · PFS hazard ratio 117, p=0.0036 · +3 more

Key findings

Three malignant spot types were identified through spatial transcriptome analysis.
Thirty-three malignant cell differentiation-related prognostic genes (MDPGs) were defined.
A malignant cell differentiation-based PRAD classification (MDPC) with three subtypes was constructed: DPP4+MSMB+, NHP2+NVL+, and COL1A1+MYLK+.
MDPC correlated with tumor genomics and immunomics and had prognostic predictive value.
In the retrospective cohort, the COL1A1+MYLK+ MDPC subtype was an independent risk factor for overall survival (HR = 20.720, P = 0.0018) and progression-free survival (HR = 117.00, P = 0.0036).
The COL1A1+MYLK+ subtype was closely correlated with Gleason grade, WHO/ISUP grade, radiotherapy, chemotherapy, endocrinotherapy, bone metastasis before treatment, and progression after treatment.

Limitations: Retrospective cohort design for validation (potential for selection and confounding biases).; Abstract does not report sample sizes for spatial transcriptomics, TCGA-PRAD subanalyses, or the retrospective cohort.; No prospective or external prospective validation reported in the abstract.; Abstract-level report lacks detail on cohort composition, methods for controlling confounders, and reproducibility metrics..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewFormulationReported positiveLimited evidenceTier 4 · clinical

Nanomedicine in Immunotherapy for Non-Small Cell Lung Cancer: Applications and Perspectives

Small methods · Jul 2025 · review

non-small cell lung cancer

This is a review article summarizing how nanomedicines are being developed to support immunotherapy for non-small cell lung cancer. The authors survey core features and the current clinical status of strategies such as immune checkpoint blockade, antibody-drug conjugates, cell engagers, adoptive cells, and cancer vaccines, and emphasize recent nanomedicine developments that may boost these approaches. The abstract highlights advantages of nanomedicines including tumor targeting, improved bioavailability, reduced systemic toxicity, and potential to overcome immune resistance. No new experimental data or quantitative results are reported in the abstract.

Studied with: immune checkpoint blockade, antibody-drug conjugates, cell engagers, adoptive cells, cancer vaccines.

Key findings

Nanomedicines may offer advantages including specific targeting of tumor cells, improved drug bioavailability, reduced systemic toxicity, and overcoming of immune resistance.
The review surveys the core features and current clinical status of NSCLC immunotherapy strategies: immune checkpoint blockade, antibody-drug conjugates, cell engagers, adoptive cells, and cancer vaccines.
Particular emphasis is placed on recent developments of nanomedicines that boost these immunotherapy strategies.

Limitations: This is a review article; no new experimental or clinical trial data are presented in the abstract.; Abstract provides no quantitative results, sample sizes, doses, or outcome metrics.; Species, specific clinical trial identifiers, and funding sources are not specified in the abstract..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Human · observationalMechanismMixed resultsLimited evidenceTier 3 · early humann = 51

Molecular diversity in uterine carcinosarcoma: Beyond TP53

Gynecologic oncology · Jul 2025 · observational genomic profiling of tumor samples

uterine carcinosarcoma

The authors performed next-generation sequencing of tumor DNA from 51 uterine carcinosarcoma patients, analyzing mutations, copy-number changes, microsatellite instability, tumor mutational burden, and homologous recombination deficiency. They found TP53 alterations were most frequent (88%), with PIK3CA (35%) and CCNE1 (33%) also common; most cases had a TP53-mutant profile, 11 were HR-deficient, and 7 samples had high TMB (≥16). Carcinoma and sarcoma components showed concordant gene variants but divergent copy-number changes, supporting a monoclonal origin. No molecular variables were statistically significant in survival analysis, but 45 cases (88%) harbored alterations that the authors considered potentially targetable by existing therapies.

Reported effects: n_included 51, n=51 · TP53_alteration_frequency 88%, n=51 · +9 more

Key findings

Among 51 included patients, TP53 was most frequently altered (88%), followed by PIK3CA (35%) and CCNE1 (33%).
Separate analysis of carcinoma and sarcoma components revealed concordant gene variants but divergent copy number variations.
Based on molecular classification, the majority of the cases 44 (84.6%) had a TP53-mutant profile.
Eleven cases were homologous recombination (HR) deficient.
Seven samples (14%) had high tumor mutational burden (TMB ≥16).
Key altered pathways were TP53, RTK/RAS, PI3K, and cell cycle pathways.
Alterations that could serve as possible molecular targets for existing therapies were identified in 45 cases (88%).
No molecular variables were statistically significant in the survival analysis.

Limitations: Observational genomic profiling without an interventional component.; Modest sample size (51 patients), limiting statistical power.; Survival analysis found no statistically significant molecular associations.; Carcinoma and sarcoma components were analyzed separately only "when possible," implying incomplete paired-component data in some cases.; Clinical impact of the identified potentially targetable alterations was not tested in patients (no interventional/therapeutic data)..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

ReviewMechanismInconclusiveLimited evidenceTier 4 · clinical

Carcinosarcoma of the Endometrium-Pathology, Molecular Landscape and Novel Therapeutic Approaches

Medicina (Kaunas, Lithuania) · Jun 2025 · review

endometrial carcinosarcomaendometrial cancercarcinosarcoma of the endometrium

This is a narrative review of endometrial carcinosarcoma (ECS), a rare, aggressive biphasic endometrial cancer. The authors summarize epidemiology, pathology including that ECS arises from epithelial components undergoing epithelial-to-mesenchymal transition, prognosis, molecular characteristics, and current and novel therapeutic approaches, noting a poor prognosis and limited high-quality trial evidence.

Reported effects: proportion_diagnosed_early 50% · proportion_with_metastatic_lymph_nodes 33% · +1 more

Key findings

ECS is a rare, aggressive biphasic metaplastic carcinoma with a monoclonal origin composed of epithelial and mesenchymal components.
The tumor originates from epithelial components that undergo epithelial-to-mesenchymal transition.
Approximately half of patients are diagnosed at early stage and half at advanced stage.
More than one-third of women present with metastatic lymph nodes and approximately 10% have distant metastases.
ECS has the worst prognosis among endometrial cancers compared with other high-grade endometrial carcinomas.
Surgical resection with adjuvant therapy remains the standard of care in most cases.
Rarity of ECS limits prospective clinical trials and the development of specific management guidelines.
The review discusses molecular characteristics and new treatment regimens for primary (early and advanced) and recurrent ECS.

Limitations: This article is a review and presents no new primary data.; The rarity of ECS limits the ability to conduct prospective clinical trials and to establish optimal treatment regimens (stated in abstract).; No specific treatment guidelines exist for ECS, reflecting limited high-quality evidence (stated in abstract)..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Human trialTrialReported positiveStrong evidenceTier 4 · clinicaln = 381

Relacorilant and nab-paclitaxel in patients with platinum-resistant ovarian cancer (ROSELLA): an open-label, randomised, controlled, phase 3 trial

Lancet (London, England) · Jun 2025 · randomized, controlled, open-label phase 3 trial

Relacorilantplatinum-resistant ovarian cancerepithelial ovarian cancerprimary peritoneal cancerfallopian tube cancer

This phase 3 randomized trial tested whether adding relacorilant to nab-paclitaxel helped women with platinum-resistant ovarian cancer. The combination improved progression-free survival and also showed a longer overall survival at an interim analysis. Side effects were similar between groups after accounting for nab-paclitaxel exposure, and no new safety signals were seen.

Reported effects: progression-free survival hazard ratio 0.7 [0.54–0.91], p p=0.0076, n=381 · progression-free survival median 6.54 mo [5.55–7.43], n=188 · +3 more

Studied with: nab-paclitaxel.

Key findings

Progression-free survival was significantly longer with relacorilant plus nab-paclitaxel than with nab-paclitaxel alone.
An interim overall survival analysis also favored the combination.
Adverse events were similar across groups when adjusted for nab-paclitaxel exposure; no new safety signals were observed.

Limitations: Open-label design; Overall survival result was based on a planned interim analysis; Trial is ongoing; Funding from the drug manufacturer.

This study evaluated relacorilant as an added anticancer agent in platinum-resistant ovarian cancer.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Human · observationalMechanismReported positiveLimited evidenceTier 3 · early human

EPHB1 Protein Promoted the Progression of Prostate Adenocarcinoma Through Phosphorylating GSK3B and Activating EPHB1-GSK3B-SMAD3 Pathway

Human mutation · Jun 2025 · RNA-seq cohort analysis (GSVA, WGCNA, LASSO) and somatic mutation analysis combined with in vitro cell line functional experiments (CCK-8, EdU, Transwell, western blot, coculture, immunofluorescence)

prostate adenocarcinoma

The study combined RNA-seq analysis of prostate adenocarcinoma patients with cell-line experiments to investigate apoptosis-related features and identify drivers of high-risk disease. EPHB1 was identified as overexpressed in tumor cells and associated with poorer prognosis; in cell lines, EPHB1 interacted with GSK3B to increase p-SMAD3 and raise antiapoptotic and invasion markers, while knockdown of EPHB1 or GSK3B reduced p-SMAD3, promoted proapoptotic features, and decreased macrophage M2 polarization.

Key findings

Prostate adenocarcinoma samples had significantly lower apoptosis scores (by GSVA) and a RiskScore derived from WGCNA/LASSO stratified patient risk.
Somatic mutation analysis identified EPHB1 and KIF13A among top mutant genes and EPHB1 was overexpressed in 22RV1 and PC-3 tumor cell lines.
Low levels of EPHB1 indicated a better prognosis in Kaplan-Meier survival analysis.
Overexpression of EPHB1 increased cell viability, proliferation, and invasion in cell-line assays; knockdown reduced these phenotypes.
EPHB1 physically interacted with GSK3B and high EPHB1 expression promoted p-SMAD3 expression along with higher levels of antiapoptotic and invasion markers (BCL2, Snail, N-CAD) in 22RV1 cells.
Knockdown of GSK3B and EPHB1 inhibited p-SMAD3 activation, promoted proapoptotic features, and reduced macrophage M2 polarization in coculture assays.

Limitations: No sample size or cohort size for the RNA-seq/patient analyses reported in the abstract.; Mechanistic validation was performed in cell lines (22RV1, PC-3) without in vivo (animal) experiments.; The RiskScore and bioinformatic findings are observational and require external clinical validation.; No clinical intervention or patient-level experimental manipulation was performed..

This study implicates EPHB1 in promoting prostate adenocarcinoma progression via the EPHB1-GSK3B-SMAD3 signaling axis and links it to tumor cell invasion, apoptosis regulation, and macrophage M2 polarization.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Human · observationalMixed resultsLimited evidenceTier 3 · early humann = 26

Real-world experience and prognostic factors in ovarian carcinosarcoma: a single-center retrospective study from China

Frontiers in oncology · Jun 2025 · single-center retrospective study

ovarian carcinosarcoma

This single-center retrospective study reviewed 26 patients with ovarian carcinosarcoma treated between March 2012 and October 2023 and recorded baseline features, treatments, and survival. Median progression-free survival (PFS) for the cohort was 17.53 months. Several clinical/pathologic features (ascites ≥500 ml, age ≥58, tumor diameter <10 cm, Ki-67 ≥70%) showed trends toward longer PFS but the reported comparisons were not statistically significant. Four homologous recombination deficiency (HRD)-positive patients who received a PARP inhibitor had a median PFS of 22.68 months.

Reported effects: median PFS (all patients) 17.53 mo, n=26 · PFS, ascites ≥500 ml vs <500 ml 27.83 mo, p p=0.12 · +8 more

Key findings

Twenty-six patients met inclusion criteria; the median PFS of all enrolled patients was 17.53 months.
Patients with ascites ≥500 ml had PFS 27.83 months vs. 13.7 months (p=0.12, HR 0.72), showing a trend toward better prognosis.
Patients age ≥58 years had PFS 22.93 months vs. 13.53 months (p=0.354, HR 0.62), showing a trend toward better prognosis.
Patients with tumor diameter <10 cm had PFS 27.83 months vs. 12.80 months (p=0.095, HR 0.36), showing a trend toward better prognosis.
Patients with Ki-67 ≥70% had PFS 22.93 months vs. 13.53 months (p=0.093, HR 0.39), showing a trend toward better prognosis.
Five patients underwent genetic testing; 4 were HRD-positive and treated with a PARP inhibitor. The median PFS of those 4 patients was 22.68 months.

Limitations: Small overall sample size (n=26); Single-center, retrospective design with potential for selection and information bias; Very small genetic-testing subgroup (5 tested; 4 HRD-positive) limits conclusions about PARP inhibitor outcomes; Reported subgroup comparisons showed p-values > 0.05 (described as trends) and thus were not statistically significant; No randomized or controlled comparison reported in the abstract; No details on PARP inhibitor dosing, duration, or toxicity provided in the abstract.

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Human · observationalMixed resultsLimited evidenceTier 3 · early humann = 6

Ovarian Rhabdomyosarcoma in Children

Cureus · Jun 2025 · retrospective analysis

ovarian rhabdomyosarcoma

This retrospective case series reviewed six pediatric patients with ovarian rhabdomyosarcoma treated over a 25-year period at a national cancer center in Peru. Most tumors had embryonal histology, four patients presented with distant metastases (stage/group IV), none tested positive for fusion genes, and all received chemotherapy plus surgery with efforts to preserve fertility when appropriate. Three patients received abdominopelvic radiotherapy (2,400 cGy in 16 sessions); one low-risk patient survived up to 94 months and the authors report multimodal treatment produced survival exceeding 87 months in some cases.

Reported effects: number of patients 6, n=6 · abdominopelvic radiotherapy total dose 2400, n=3 · +3 more

Key findings

Six female patients aged between five months and 13 years were included.
Four patients were classified as clinical stage/group IV due to distant metastases; two were low-risk.
The majority had embryonal histology and none tested positive for fusion genes.
All patients underwent chemotherapy and surgery; surgical approaches emphasized fertility preservation and varied by disease extent.
Three patients received intensity-modulated abdominopelvic radiotherapy at a total dose of 2,400 cGy delivered in 16 sessions for peritoneal sarcomatosis (two for persistent disease after chemotherapy and surgery, one for high-risk histology).
One low-risk patient achieved a survival of up to 94 months.
Authors conclude ovarian rhabdomyosarcoma is rare, presents with nonspecific clinical/radiologic features, immunohistochemistry is essential for diagnosis, and multimodal treatment can achieve long-term survival, including in metastatic cases.

Limitations: Very small sample size (n=6).; Retrospective, single-center design increases risk of selection and reporting bias.; Heterogeneous disease stages and treatments among patients limit generalizability.; Limited outcome detail reported for individual patients (only one specific long-term survival reported).; No control or comparison group and no standardized prospective follow-up reported.; Molecular/genetic testing beyond fusion-gene negativity is not described in the cohort..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Lab · in vitroMechanismMixed resultsPreclinical onlyTier 1 · lab

Proteomic Analysis of ARID1A-Deficient Ovarian Clear Cell Carcinoma Cells Reveals Differential Mitochondria ETC Subunit Abundances and Targetable Mitochondrial Pathways

International journal of molecular sciences · Jun 2025

ovarian clear cell carcinoma

The authors performed biochemical and proteomic analyses on ARID1A-deficient ovarian clear cell carcinoma cells. They found marked upregulation of specific subunits of mitochondrial electron transport chain Complexes I, III, and IV. Despite this upregulation, the cells did not show increased sensitivity to broad-spectrum inhibitors of these complexes. The authors suggest that selectively inhibiting specific ETC subunits might better exploit metabolic vulnerabilities in ARID1A-deficient cells.

Key findings

ARID1A-deficient ovarian clear cell carcinoma cells depend heavily on mitochondrial respiration (as stated by the authors).
Proteomic and biochemical analyses revealed marked upregulation of specific subunits within mitochondrial ETC Complexes I, III, and IV in ARID1A knockout cells.
Upregulation of these ETC subunits did not translate into increased sensitivity to broad-spectrum inhibitors targeting the complexes.
Authors propose that selective inhibition of specific ETC subunits could be a more promising approach than broad-spectrum mitochondrial inhibitors.

Limitations: In vitro cell-line study only; no in vivo or clinical data reported in the abstract.; Abstract does not report sample sizes, quantitative metrics, or statistical results.; No specific inhibitors or compounds are named or characterized in the abstract.; Functional or therapeutic efficacy of selective ETC subunit inhibition is suggested but not demonstrated in this study..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewFormulationReported positiveLimited evidenceTier 4 · clinical

Promising biomedical applications using superparamagnetic nanoparticles

European journal of medical research · Jun 2025

tumors (general)brain tumors (drug delivery across the blood-brain barrier)

This review summarizes recent developments in magnetic (superparamagnetic) nanoparticles for biomedical use. It describes their physicochemical properties, surface functionalization, and applications including MRI contrast enhancement, targeted drug delivery (including across the blood-brain barrier), and hyperthermia-based cancer therapies that produce localized heat to kill malignant cells.

Key findings

Magnetic nanoparticles (MNPs) have high surface-area-to-volume ratio, adjustable size, magnetic sensitivity, and biological compatibility.
External magnetic fields enable precise control of MNPs for targeted therapeutic and diagnostic applications.
MNPs have been explored for MRI enhancement, selective drug transport, hyperthermia cancer therapy, and biomolecular separation.
In oncology MNPs can facilitate direct delivery of therapeutic compounds to tumors, potentially reducing systemic side effects and increasing treatment specificity.
MNPs can produce localized heat under alternating magnetic fields, which is useful for hyperthermia therapy to selectively eradicate malignant cells.
Surface functionalization with polymers, ligands, and stabilizers improves stability, minimizes immune responses, and optimizes in vivo performance.

Limitations: Review article with no original experimental data reported in this paper.; Abstract provides no quantitative results, clinical trial data, species, dosing, or sample-size information.; Potential translational gaps between preclinical/technical studies and clinical implementation are not addressed in detail in the abstract.; Broad summary without methodological details or critical appraisal provided in the abstract..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Animal studyMechanismReported positivePreclinical onlyTier 2 · animal

Drosha: a new tumor suppressor in pineoblastoma

Genes & development · Jun 2025 · genetically engineered mouse models

pineoblastoma

Researchers used genetically engineered mouse models that represent different molecular subtypes of pineoblastoma to examine the roles of miRNA-processing enzymes Drosha and Dicer1. They found that loss of either Drosha or Dicer1 partially mimicked the tumorigenic effects of Rb1 deletion by promoting cell cycle progression via derepression of Plagl2 and cyclin D2. The study reports a novel mechanism in which disrupted miRNA processing can drive pineoblastoma development and notes that targeting downstream proliferative drivers could be a potential therapeutic strategy.

Key findings

Multiple genetically engineered mouse models representing distinct molecular subtypes of pineoblastoma were developed.
Loss of either Drosha or Dicer1 partially mimicked the tumorigenic effects of Rb1 deletion.
Loss of Drosha or Dicer1 promoted cell cycle progression through derepression of Plagl2 and cyclin D2.
Disrupted miRNA processing is reported as a novel mechanism driving pineoblastoma development.
Authors highlight a potential therapeutic strategy of targeting downstream proliferative drivers.

Limitations: Study was performed in mouse models only (no human interventional data reported).; Abstract provides no sample size, statistical details, or quantitative results.; Therapeutic strategy is suggested but not tested in this report..

Direct investigation of molecular drivers of pineoblastoma using mouse models; mechanistic relevance to tumorigenesis.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Animal studyMechanismReported positivePreclinical onlyTier 2 · animal

An imbalance between proliferation and differentiation underlies the development of microRNA-defective pineoblastoma

Genes & development · Jun 2025

pineoblastomapineal tumor

The authors deleted Drosha or Dicer1 in the developing mouse pineal gland to model microRNA-defective pineoblastoma. These mice developed pineal tumors with loss of microRNAs (notably let-7/miR-98-5p), derepression of microRNA target genes, and upregulation of S-phase genes and developmental homeobox transcription factors. Blocking tumor proliferation promoted expression of pinealocyte maturation markers and reduced some embryonic markers, and inhibiting signaling downstream of the oncofetal transcription factor Plagl2 impaired tumor growth. The study suggests that targeting downstream proliferation drivers may limit growth of tumors caused by loss of microRNA processing.

Key findings

Ablation of Drosha or Dicer1 in the developing pineal gland of mice produces pineal tumors characterized by loss of microRNAs, particularly the let-7/miR-98-5p family, and derepression of microRNA target genes.
Pineal tumors driven by Drosha or Dicer1 loss show upregulation of S-phase genes and homeobox transcription factors and phenocopy tumors driven by Rb1 loss.
Blocking proliferation in these tumors facilitates expression of pinealocyte maturation markers and reduces some embryonic markers, although select embryonic markers remain elevated due to continued absence of the repressing microRNAs.
Plagl2 is identified as a microRNA target and an oncofetal transcription factor that regulates progrowth genes; inhibiting Plagl2-related signaling impairs tumor growth.

Limitations: Animal (mouse) genetic-ablation model only — findings not demonstrated in human patients.; Study models genetic loss of microRNA processing (Drosha/Dicer1 ablation), which may not fully recapitulate the diversity of human tumor genetics.; No clinical or human data reported to support translational efficacy or safety of targeting the identified pathways..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewInconclusiveModerate evidenceTier 4 · clinical

AGO Recommendations for the Diagnosis and Treatment of Patients with Early Breast Cancer: Update 2025

Breast care (Basel, Switzerland) · Jun 2025 · guideline update

early breast cancer

This paper presents the AGO (German Gynecological Oncology Group) Breast Committee's 2025 update of evidence-based recommendations for diagnosis and treatment of patients with early breast cancer. The abstract does not provide details of specific recommendations, methods, or results.

Key findings

The article presents the 2025 update of evidence-based recommendations for the diagnosis and treatment of patients with early breast cancer.
The abstract does not report specific recommendations, levels of evidence, or details of changes from prior guidelines.

Limitations: Abstract contains only a brief statement and provides no detail on methods, literature search, or recommendation content.; No specific recommendations, evidence grades, or actionable clinical details are reported in the abstract.; This is a guideline/review document and not a primary study of any compound or intervention..

Guideline update relevant to clinical management of early breast cancer.

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewSupportive careReported positiveModerate evidenceTier 4 · clinicaln = 11

Physical activity guidelines in oncology: A systematic review of the current recommendations

Critical reviews in oncology/hematology · Jun 2025 · systematic review of guidelines

Supportive care

This systematic review summarized 11 society-endorsed guidelines on physical activity for patients with cancer published in the past 15 years. Most guidelines recommend combining aerobic and resistance training, typically suggesting about 150 minutes per week of moderate activity plus resistance training twice weekly; several guidelines also addressed prescription details, medical clearance, precautions, referral specialists, and motivational aspects.

Reported effects: number_of_guidelines_included 11 · high_quality_guidelines_AGREE_II_>=60% 7 · +8 more

Key findings

A total of 11 guidelines met the inclusion criteria.
Seven were considered high quality, scoring 60% in the AGREE II tool.
All the guidelines recommended to include aerobic and resistance training as types of activities.
Regarding the physical activity dosage, most suggested a generic 150minutes/week of moderate-intensity activity plus resistance training twice a week.
Three guidelines reported instructions for exercise prescription, including frequency, intensity, and duration of training sessions.
Six guidelines reported exercise testing/medical clearance instructions, 9 provided considerations regarding adaptation/precautions, and 7 detailed the specialists for referral.
Four guidelines considered motivational aspects related to physical activity and cancer.
Authors conclude more high-quality research is needed to develop more tailored guidelines.

Limitations: Review included only guidelines published in the last 15 years (may omit older guidance).; Qualitative synthesis only; no quantitative/meta-analytic pooling reported.; Relatively small number of guidelines (11) and variable detail across guidelines (only 3 provided full exercise prescription specifics).; Abstract does not report details on guideline heterogeneity or patient populations covered by each guideline..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed

Meta-analysisReported positiveStrong evidenceTier 4 · clinicaln = 60

Association between red and processed meat consumption and colorectal cancer risk: a comprehensive meta-analysis of prospective studies

GeroScience · Jun 2025 · meta-analysis of prospective studies

colorectal cancercolon cancerrectal cancer

This meta-analysis pooled 60 prospective studies to evaluate associations between red, processed, and total meat consumption and colorectal, colon, and rectal cancer risk. Higher intake of red, processed, and total meat was each associated with modestly increased hazard ratios for colorectal, colon, and rectal cancer in the pooled analyses.

Reported effects: Red meat - colon cancer HR 1.22 [1.15–1.3] · Red meat - colorectal cancer HR 1.15 [1.1–1.21] · +7 more

Key findings

Red meat consumption was associated with increased risk of colon cancer (HR = 1.22, 95% CI 1.15-1.30), colorectal cancer (HR = 1.15, 95% CI 1.10-1.21), and rectal cancer (HR = 1.22, 95% CI 1.07-1.39).
Processed meat consumption was associated with increased risk of colon cancer (HR = 1.13, 95% CI 1.07-1.20), colorectal cancer (HR = 1.21, 95% CI 1.14-1.28), and rectal cancer (HR = 1.17, 95% CI 1.05-1.30).
Total meat consumption was associated with increased risk of colon cancer (HR = 1.22, 95% CI 1.11-1.35), colorectal cancer (HR = 1.17, 95% CI 1.12-1.22), and rectal cancer (HR = 1.28, 95% CI 1.10-1.48).

Limitations: Observational prospective studies cannot establish causation; associations may reflect residual confounding.; Potential heterogeneity across included studies (populations, exposure assessment, covariate adjustment) may affect pooled estimates.; Dietary measurement error and misclassification in the original studies may bias results.; Abstract does not report dose-response specifics or uniform exposure definitions across studies..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMechanismInconclusiveLimited evidenceTier 4 · clinical

Emerging, Uncommon, and Aggressive Pediatric Kidney Tumors: An Update and Diagnostic Pitfalls

Surgical pathology clinics · Jun 2025 · narrative review

Wilms tumordiffuse anaplastic Wilms tumorblastemal Wilms tumoranaplastic sarcoma of kidneyclear cell sarcoma of kidneypediatric renal tumor

This narrative review summarizes the clinical, histopathological, and molecular features of several uncommon and aggressive pediatric kidney tumors (including diffuse anaplastic Wilms tumor, blastemal Wilms tumor, anaplastic sarcoma of the kidney, and clear cell sarcoma of the kidney). The authors note these tumors are rare and can pose diagnostic challenges for pathologists, and they emphasize that accurate diagnosis is essential to ensure appropriate management.

Key findings

Favorable-histology Wilms tumors are the most prevalent pediatric renal tumor, while the remainder comprises a small but diverse group of malignant neoplasms.
Uncommon pediatric renal tumors discussed include diffuse anaplastic Wilms tumor, blastemal Wilms tumor, anaplastic sarcoma of kidney, and clear cell sarcoma of kidney.
Because of their rarity, these tumors may pose diagnostic challenges for pathologists.
Accurate diagnosis is essential to ensuring these aggressive tumors are managed appropriately.
The article summarizes salient clinical, histopathological, and molecular features of these uncommon tumors.

Limitations: Narrative review rather than primary experimental or clinical research; no new patient-level data reported in the abstract.; Abstract does not report methods (e.g., systematic search strategy), so potential selection bias in included literature cannot be assessed from the abstract.; Rarity of the tumors discussed implies limited published data and possible incomplete characterization..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Human · observationalMixed resultsLimited evidenceTier 3 · early humann = 11310

Epidemiology and clinical course of large cell neuroendocrine carcinoma of the lung: The Japanese lung cancer registry study

Lung cancer (Amsterdam, Netherlands) · Jun 2025 · prospective registry study (Japanese Joint Committee of Lung Cancer Registry)

large cell neuroendocrine carcinomasmall cell lung cancersquamous cell carcinomaadenocarcinoma

This prospective registry study analyzed 11,310 Japanese lung cancer patients (80 with LCNEC) from January 2012 to April 2016 to compare clinical characteristics, chemotherapy response, and survival across histologies. LCNEC patients were mostly older male smokers and had lower overall response and disease control rates to first-line cisplatin- or carboplatin-based chemotherapy in stage IV disease compared with SCLC. Three-year survival was similar between LCNEC (14.2%) and SCLC (15.9%), and Cox analysis showed no statistically significant difference in overall survival (HR 0.818, 95% CI 0.611-1.096, p = 0.178).

Reported effects: cohort_size 11310, n=11310 · LCNEC_count 80, n=80 · +9 more

Key findings

Total cohort: 11,310 patients from the JJCLCR database.
In total, 80 patients (0.7%) were diagnosed with LCNEC.
LCNEC patients had median age 68 years, 93.8% men, and 97.5% smokers.
In stage IV patients, best overall response and disease control rates for first-line cisplatin-based chemotherapy were 34.8% and 43.5% for LCNEC but 60.6% and 69.7% for SCLC.
For first-line carboplatin-based chemotherapy in stage IV patients, overall response and disease control rates were 29.4% and 41.2% for LCNEC, but 56.1% and 68.4% for SCLC.
The 3-year survival rates were 14.2% for LCNEC, 15.9% for SCLC, 17.8% for squamous cell carcinoma, and 27.1% for adenocarcinoma.
Cox hazard analysis comparing overall survival between LCNEC and SCLC showed hazard ratio 0.818 (95% CI 0.611-1.096, p = 0.178), not statistically significant.

Limitations: Small number of LCNEC cases (80) relative to the full registry cohort.; Observational registry design without randomized treatment assignment.; Potential heterogeneity in treatments and management across registry sites.; Follow-up limited to registry period (opened Jan 2012; completed Apr 2016) with no median follow-up duration reported in the abstract..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Animal studyReported positivePreclinical onlyTier 2 · animaln = 72

TROP2 expression and therapeutic targeting in uterine carcinosarcoma

Gynecologic oncology · Jun 2025 · archival tissue analysis plus patient-derived organoid and xenograft preclinical study

Sacituzumab-govitecanuterine carcinosarcomaendometrial carcinoma

This study looked at TROP2 levels in uterine carcinosarcoma samples and tested the TROP2-targeting antibody-drug conjugate sacituzumab govitecan in patient-derived organoid and xenograft models. Most tumors had detectable TROP2, and the organoid models responded to the drug in a dose-dependent way. In two xenograft models, tumor volume was lower with sacituzumab govitecan than without it.

Reported effects: TROP2 expression in primary UCSs 90%, n=72 · Higher TROP2 expression by histologic subtype, p p < 0.001 and p = 0.022, n=72 · +2 more

Key findings

TROP2 protein and mRNA were detected in at least 90% of primary uterine carcinosarcomas.
Tumors with a predominant carcinomatous component or homologous differentiation had higher TROP2 expression than those with predominant sarcomatous component or heterologous differentiation.
All 9 uterine carcinosarcoma organoid models responded in a dose-dependent manner to sacituzumab govitecan.
Both xenograft models showed significant reduction in tumor volume with sacituzumab govitecan.

Limitations: Preclinical study; findings are from archival tissues, organoids, and mouse xenografts, not patients.; Only 2 xenograft models were tested.; No clinical outcomes, safety data, or survival data in humans were reported.; The abstract does not provide dosing details or treatment duration..

Supports preclinical exploration of TROP2-targeted therapy in uterine carcinosarcoma.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMechanismReported positiveModerate evidenceTier 4 · clinical

Folate Receptor Alpha in Advanced Epithelial Ovarian Cancer: Diagnostic Role and Therapeutic Implications of a Clinically Validated Biomarker

International journal of molecular sciences · May 2025 · review

Mirvetuximab-soravtansineepithelial ovarian cancerhigh-grade serous ovarian carcinomaplatinum-resistant epithelial ovarian cancerovarian neoplasms

This review summarizes the role of folate receptor alpha (FRα) in ovarian cancer, noting that FRα is frequently overexpressed in high-grade serous ovarian carcinoma. It describes that a VENTANA IHC assay is approved as a companion diagnostic to select patients (≥75% tumor cells with moderate to strong membrane staining) for the FRα-targeted antibody-drug conjugate mirvetuximab soravtansine, and discusses biological significance, IHC technical issues, and heterogeneity of expression across subtypes and tissue samples.

Key findings

FRα is frequently overexpressed in several epithelial malignancies, particularly in high-grade serous ovarian carcinoma.
The VENTANA FOLR1 (FOLR1-2.1) RxDx Assay (IHC) is now approved as a companion diagnostic for selecting patients eligible for mirvetuximab soravtansine.
Clinical trials (SORAYA and MIRASOL) demonstrated significant clinical benefit in platinum-resistant epithelial ovarian cancer patients with high FRα expression (≥75% of tumor cells with moderate to strong membrane staining).
The review summarizes biological significance of FRα in ovarian cancer progression and its predictive value for targeted therapy.
Technical aspects of IHC assessment, including scoring interpretation and pre-analytical variables, are discussed.
Heterogeneity in FRα expression across histological subtypes and tumor sites, and differences between archival versus fresh tissue, are important considerations.

Limitations: This is a review article and does not present new, individual patient-level data.; FRα expression heterogeneity across histologic subtypes and tumor sites may limit generalizability of biomarker-based selection.; IHC technical factors and pre-analytical variables can affect assessment of FRα and thus patient selection.; The companion diagnostic and demonstrated benefit apply specifically to patients with high FRα expression (≥75%), so findings may not extend to lower expressors..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewInconclusiveLimited evidenceTier 4 · clinical

Mucinous Ovarian Carcinoma: Integrating Molecular Stratification into Surgical and Therapeutic Management

Biomedicines · May 2025 · narrative review

mucinous ovarian carcinomaepithelial ovarian cancer

This review summarizes what is known about mucinous ovarian carcinoma, a rare subtype of ovarian cancer with distinct molecular features such as KRAS mutations and HER2 amplifications. It discusses surgery, fertility-sparing approaches, and adjuvant therapy, and notes that targeted strategies like MEK inhibitors and HER2-directed therapies are being investigated for selected molecular subgroups. The abstract does not report new patient data or trial results.

Key findings

MOC has frequent KRAS mutations and HER2 amplifications.
Expansile and infiltrative histologic subtypes may guide lymphadenectomy decisions.
Fertility-sparing surgery appears safe in FIGO stage IA expansile MOC.
The role of adjuvant therapy in early-stage disease remains debated because of chemoresistance.
MEK inhibitors and HER2-directed therapies are under investigation for selected molecular subgroups.

Limitations: Narrative review rather than original study.; No new experimental or clinical outcome data reported in the abstract.; No quantitative effect estimates or trial results provided.; Conclusions depend on heterogeneous retrospective cohorts, molecular studies, and guidelines..

Provides a review of molecularly informed management options for mucinous ovarian carcinoma, including discussion of targeted therapies.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMechanismInconclusiveModerate evidenceTier 4 · clinical

How to differentiate primary mucinous ovarian tumors from ovarian metastases originating from primary appendiceal mucinous neoplasms: a review

Pathology oncology research : POR · May 2025 · review

mucinous ovarian neoplasmappendiceal mucinous neoplasmappendiceal mucinous carcinoma

This review examines how to distinguish primary mucinous ovarian tumors from ovarian metastases that originate from appendiceal mucinous neoplasms. It summarizes differences in preoperative symptoms, imaging, microscopic features, and immunophenotype, and notes that definitive origin is confirmed only by postoperative pathological examination. The authors suggest that antigen values and imaging may hint at the source preoperatively and that better immunohistochemical markers and molecular features could improve diagnosis in the future.

Key findings

Mucinous ovarian metastases of appendiceal origin can mimic primary ovarian mucinous neoplasms and occur in up to half of women with primary appendiceal mucinous carcinomas (as emphasized in the review).
Differences useful for differentiation include preoperative symptoms, radiological findings, a spectrum of microscopic features, and the immunophenotype of the tumors.
Treatment options including surgical management and adjuvant chemotherapy protocols are briefly overviewed but diagnostic confirmation relies on postoperative pathology.
Investigating more accurate immunohistochemical markers and novel molecular features may improve diagnostic accuracy in future research.

Limitations: Narrative review only—no new primary data generated in this article.; Abstract indicates definitive tumor origin can be confirmed only after postoperative pathological examination, limiting preoperative diagnostic certainty.; Pathological similarity between appendiceal metastases and primary ovarian mucinous neoplasms complicates differentiation.; Review does not provide quantitative synthesis or validated new diagnostic markers (per abstract)..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMechanismInconclusiveLimited evidenceTier 4 · clinical

Mesenchymal Nonmeningothelial Tumors of the CNS: Evolving Molecular Landscape and Implications for Neuroradiologists

AJNR. American journal of neuroradiology · May 2025 · narrative review

mesenchymal nonmeningothelial tumors of the central nervous systemFET::CREB fusion-positive tumorsCIC-rearranged sarcomaprimary intracranial sarcoma, DICER1-mutantdural angioleiomyomaspindle cell neoplasm with NTRK rearrangement

This narrative review summarizes the WHO CNS5 updates to the classification and diagnostic criteria for mesenchymal nonmeningothelial CNS tumors and aligns CNS entities with soft-tissue tumor taxonomy. It highlights newly defined histomolecular entities (FET::CREB fusion-positive, CIC-rearranged sarcoma, and DICER1-mutant primary intracranial sarcoma), discusses emerging entities such as dural angioleiomyomas and NTRK-rearranged spindle cell tumors, and emphasizes that molecular techniques are essential for accurate diagnosis because histology and immunophenotype are often nonspecific.

Key findings

WHO CNS5 substantially revised terminology and diagnostic criteria for mesenchymal nonmeningothelial CNS tumors to better align with soft-tissue tumor classification.
The CNS chapter includes entities that occur exclusively or primarily in the CNS, most arising from the meninges and mainly located in the supratentorial compartment.
These tumors are grouped into soft tissue, chondro-osseous, and notochordal categories; soft tissue tumors are subdivided into fibroblastic, vascular, and skeletal muscle subtypes.
A new subcategory 'tumors of uncertain differentiation' includes three histomolecular entities: FET::CREB fusion-positive, CIC-rearranged sarcoma, and primary intracranial sarcoma, DICER1-mutant.
Emerging entities such as dural angioleiomyomas and spindle cell neoplasms with NTRK rearrangements are discussed though not included in WHO CNS5.
Because histology and immunophenotype are often nonspecific for tumors of uncertain differentiation, molecular techniques have become indispensable for accurate diagnosis.

Limitations: Narrative review without original, patient-level data reported in this article.; Not a primary research study; no new experimental results or pooled quantitative synthesis provided.; Scope and methods of literature selection are not detailed in the abstract (potential for incomplete coverage)..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMechanismInconclusiveLimited evidenceTier 4 · clinical

Cellular origins of mucinous ovarian carcinoma

The Journal of pathology · May 2025 · narrative review

mucinous ovarian carcinoma

This narrative review summarizes pathological, epidemiological and molecular evidence about the cellular origins of mucinous ovarian carcinoma (MOC). The authors propose a model distinguishing Müllerian-type from gastrointestinal-type mucinous differentiation and outline possible origins including teratoma-derived tumours, lesions associated with Brenner tumours/Walthard nests, mucinous metaplasia in Müllerian tumours, and gastrointestinal metaplasia of ovarian inclusions. The model is hypothetical and the authors state it requires validation and mechanistic study.

Key findings

MOC is a rare histotype of epithelial ovarian cancer and its cellular origin is not well established.
The review distinguishes Müllerian from gastrointestinal-type mucinous differentiation.
A small proportion of gastrointestinal-type mucinous tumours arise from teratoma.
Some gastrointestinal mucinous tumours are associated with Brenner tumours and arise from associated benign lesions (Walthard nests).
Other mucinous tumours may develop through mucinous metaplasia in established Müllerian tumours or via gastrointestinal metaplasia of epithelial or mesothelial ovarian inclusions.
The proposed model remains to be validated and its mechanistic basis is not yet understood.

Limitations: Narrative review — no new primary experimental or clinical data presented.; Proposed model is hypothetical and unvalidated according to the authors.; Mechanistic pathways underlying the model are not established.; MOC is a rare tumour type, limiting the available direct evidence (as noted in the abstract)..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewReported positiveLimited evidenceTier 3 · early human

Primary dermal melanoma

Clinics in dermatology · May 2025 · review

primary dermal melanomamelanomaskin neoplasms

This review summarizes primary dermal melanoma (PDM), a rare (<1%) melanoma subtype that occurs entirely in the dermis or subcutis and lacks connection to the epidermis. It emphasizes that PDM can histologically mimic cutaneous melanoma metastasis, explains that careful history, exam, and imaging are needed to exclude other primaries, and notes that PDM is associated with an unexpectedly favorable prognosis.

Reported effect: estimated incidence

Key findings

Primary dermal melanoma (PDM) is a rare subtype of melanoma with an estimated incidence of <1%.
PDM manifests entirely in the dermis or subcutis and histopathologically mimics cutaneous melanoma metastasis due to its lack of connection to the overlying epidermis.
A thorough history and examination, including imaging evaluation for metastatic disease, reveals no prior history or concurrent primary cutaneous or metastatic melanoma lesion.
Despite its histopathologic similarities to melanoma metastasis, PDM is associated with an unexpectedly favorable prognosis.
The review discusses the clinical and histopathologic features of PDM as a distinct subtype of melanoma, as well as the current approach to clinical staging and management.

Limitations: Narrative review rather than a systematic review or meta-analysis (no primary data reported in abstract).; PDM is rare (<1%), so the evidence base is likely limited by small numbers and case series.; Histopathologic similarity to metastatic melanoma may complicate diagnosis and classification in published reports..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Meta-analysisMixed resultsLimited evidenceTier 4 · clinicaln = 1780

Head and Neck Squamous Cell Carcinoma of Unknown Primary-Who Can Be Offered Surgery as the Sole Treatment Modality? A Systematic Review

Clinical otolaryngology : official journal of ENT-UK ; official journal of Netherlands Society for Oto-Rhino-Laryngology & Cervico-Facial Surgery · May 2025 · Systematic review of observational cohort studies with qualitative synthesis

head and neck squamous cell carcinoma of unknown primary (HNSCCUP)

This systematic review synthesized observational cohort studies reporting outcomes for patients with head and neck squamous cell carcinoma of unknown primary (HNSCCUP) treated with surgery alone. Reported 3-year overall survival among surgery-only patients varied widely (43.9%–100%), and outcomes appeared more favorable in a subset with early-stage p16/HPV-positive, N1 disease without extracapsular spread. Data for p16/HPV-negative disease were limited.

Reported effects: number_of_studies 14 · total_patients 1780 · +8 more

Key findings

Fourteen eligible studies were identified, including 1780 patients, of whom 294 received surgery as their sole treatment.
Among patients receiving surgery alone (n=294 across seven studies), 3-year overall survival ranged from 43.9% to 100%.
Three-year disease-free survival was reported in four studies (n=62) and ranged from 42.8% to 67.0%.
Five-year overall survival in three studies (n=31) ranged from 36.6% to 75.0%; 5-year DFS ranged from 43.6% to 67.0%.
Primary emergence rates ranged from 11.1% to 33.3% (seven studies, n=157).
Regional relapse ranged from 0.0% to 50.0% (five studies, n=60).
Distant metastasis ranged from 0.0% to 3.3% (three studies, n=45).
Patients treated with surgery alone were predominantly p16/HPV positive, N1 (TNM7) and without extracapsular spread (ECS).

Limitations: All included studies were observational cohorts (no randomized trials) and synthesis was qualitative.; Outcomes reported across studies were heterogeneous with wide ranges.; Many outcome estimates derive from small numbers of patients/studies (e.g., 3-year DFS n=62; 5-year outcomes n=31).; Data are limited or lacking for p16/HPV-negative disease.; Potential for selection bias in which patients were chosen for surgery alone is not addressed in detail in the abstract..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 8

Clinicopathologic and Molecular Characterization of Gynecologic Carcinosarcomas With a Mesonephric-Like Carcinomatous Component

The American journal of surgical pathology · May 2025 · case series with clinicopathologic evaluation and next-generation sequencing

gynecologic carcinosarcomaendometrial carcinosarcomalower uterine segment carcinosarcomaovarian carcinosarcoma

The authors report a clinicopathologic and genomic analysis of eight gynecologic carcinosarcomas with a mesonephric-like carcinomatous component. Sequencing (done separately for carcinomatous and sarcomatous parts in some tumors) showed identical single-nucleotide variants between components, low tumor mutational burden (<10 mutations/Mb), microsatellite stability, and KRAS codon 12 mutations in all sequenced cases. Additional alterations (eg, PTEN, PIK3CA, ARID1A) were identified in several tumors. This is a small descriptive case series and does not include functional experiments or outcome correlations beyond staging.

Reported effects: n_cases 8, n=8 · mean_age 65.6 · +11 more

Key findings

Eight cases of gynecologic MLCS (endometrial, lower uterine segment, and ovarian) were identified and evaluated.
Genomic DNA extraction and NGS were performed separately on carcinomatous and sarcomatous components of 4 tumors and on combined components of 2 tumors.
The carcinomatous and sarcomatous components were observed to harbor the same single nucleotide variations when sequenced separately.
All cases had less than 10 mutations/Mb and were microsatellite stable.
All sequenced cases (6/6, 100%) harbored KRAS point mutations in codon 12 (p.G12D n=2; p.G12A n=2; p.G12V n=2).
Five cases showed additional alterations including ARID1A, PTEN, PIK3CA, SPOP, TET1, BUB1, LYN and PTPRD.
Authors suggest the combination of KRAS and PTEN/PIK3CA alterations is consistent with combined endometrioid and mesonephric differentiation in MLCS.

Limitations: Small sample size (8 cases) limits generalizability.; Only 6 tumors underwent NGS (4 separately by component, 2 combined), so not all cases had component-specific sequencing.; Descriptive molecular profiling without functional validation of mutations.; No survival or treatment-outcome correlations reported beyond FIGO stage..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 8

Clinicopathologic and Genomic Analysis of Uterine Serous Carcinomas Arising From Endometrial Hyperplasia

The American journal of surgical pathology · Apr 2025 · retrospective molecular cohort study

uterine serous carcinomaendometrial hyperplasia

Researchers identified 8 uterine serous carcinomas with concurrent endometrial hyperplasia and performed tumor-normal panel sequencing on the carcinoma and hyperplasia separately. In 7 of 8 paired cases the carcinoma and hyperplasia were clonally related and often shared TP53 mutations; one case was genetically unrelated and another shared only a single mutation. ARID1A mutations were more common in hyperplasia-associated USC than in atrophy-associated USC (43% vs 0%; P = 0.02).

Reported effects: cases_screened_with_sequencing_and_slides_available 267, n=267 · cases_with_sufficient_tissue_for_molecular_studies 8, n=8 · +5 more

Key findings

Of 267 USCs with available sequencing and slides, 8 cases with concurrent carcinoma and hyperplasia had sufficient tissue for molecular study.
In 7 of these 8 cases (87.5%), USC and hyperplasia were clonally related and shared multiple mutations.
TP53 hotspot mutations were shared between carcinoma and hyperplasia in 4 cases (57% of the clonally related cases).
In 1 case (USC4) the carcinoma and hyperplasia were genetically unrelated and the hyperplasia was TP53 wild-type.
In another case (USC5) the carcinoma and TP53 wild-type hyperplasia shared 1 of 11 mutations and were distinct at the copy number level.
ARID1A mutations were more prevalent in hyperplasia-associated USC than in atrophy-associated USC (43% vs. 0%; P = 0.02).

Limitations: Very small molecular cohort (only 8 cases with sufficient tissue) limits generalizability.; Retrospective selection of cases and requirement for sufficient tissue may introduce selection bias.; No functional experiments to demonstrate causality or biological consequences of shared mutations.; Clinical outcome data and broader validation cohorts are not reported in the abstract..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Human · observationalMechanismMixed resultsLimited evidenceTier 3 · early humann = 18

Exploring the Genetic and Clinical Landscape of Dedifferentiated Endometrioid Carcinoma

International journal of molecular sciences · Apr 2025

dedifferentiated endometrioid carcinomaendometrial cancer

This observational study analyzed 18 Japanese cases of dedifferentiated endometrioid carcinoma, with immunostaining on tumor components and whole-exome sequencing in three cases. The authors report that DDEC comprised 2.0% of endometrial cancers, had poor 5-year outcomes (PFS ≈40%, OS ≈30%), and that 66.7% of patients were mismatch repair deficient; they found differing mutation patterns between well-differentiated and undifferentiated components and suggest several targeted therapies could be relevant based on genetics.

Reported effects: incidence of DDEC among endometrial cancers 2% · 5-year progression-free survival 40% · +2 more

Key findings

Incidence of DDEC was 2.0% among endometrial cancers.
The 5-year progression-free survival for DDEC was approximately 40%.
The 5-year overall survival for DDEC was approximately 30%.
Immunohistochemistry indicated 66.7% of patients were mismatch repair deficient.
The rate of p53 mutations in this series was higher than reported previously, and p53 mutations in undifferentiated components were associated with poor prognosis.
Whole-exome sequencing (n = 3) showed different gene mutations and mutation signatures between well-differentiated and undifferentiated components.
New genetic mutations in undifferentiated regions were uncommon in the three sequenced cases.
Among the three sequenced cases: one showed homologous recombination deficiency, and the other two had MSI-high and hypermutator phenotypes.
Authors suggest that immune checkpoint inhibitors, PARP inhibitors, and drugs targeting the p53 pathway may be therapeutically relevant to DDEC based on the genetic findings.

Limitations: Small overall sample size (18 cases); Whole-exome sequencing performed in only 3 cases; Observational, descriptive design with no interventional testing of suggested therapies; Single-country (Japanese) cohort which may limit generalizability; No functional validation of suggested therapeutic targets reported in the abstract.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMechanismInconclusiveLimited evidenceTier 4 · clinical

Concurrent occurrence of adenocarcinoma and urothelial carcinoma of the prostate: Coexistence mechanisms from multiple perspectives

World journal of clinical cases · Apr 2025

prostate adenocarcinomaprostate urothelial carcinoma

This editorial/review examines the concurrent occurrence of prostate adenocarcinoma and prostate urothelial carcinoma by synthesizing existing literature. It summarizes proposed mechanisms for their coexistence and for a possible transformation between histologies — including androgen receptor involvement, gene mutations, altered cell signaling, tumor multipotent stem cell differentiation, epithelial-mesenchymal transition, and mesenchymal-epithelial transition. The authors aim to improve diagnostic accuracy and support more personalized clinical approaches, but the article discusses hypotheses and literature rather than reporting new experimental trial data.

Key findings

The article explores potential mechanisms underlying coexistence of prostate adenocarcinoma and prostate urothelial carcinoma, including androgen receptor roles, gene mutations, and complex interactions in cell signaling pathways.
The authors discuss hypotheses that prostate adenocarcinoma may transform into urothelial carcinoma via processes such as tumor multipotent stem cell differentiation, epithelial-mesenchymal transition, and mesenchymal-epithelial transition.
The stated goal is to inform more accurate diagnoses and more personalized clinical treatments and to lay groundwork for improving patient prognoses.

Limitations: Editorial/narrative review rather than original experimental study.; Mechanisms and transformation hypotheses are speculative and based on literature synthesis, not on new experimental validation within this article.; No methods, sample sizes, or systematic review/meta-analysis methodology are reported in the abstract..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMechanismMixed resultsLimited evidenceTier 4 · clinicaln = 95

Molecular Prognostic Factors in Uterine Serous Carcinomas: A Systematic Review

Current oncology (Toronto, Ont.) · Apr 2025 · systematic review

uterine serous carcinoma

This systematic review searched PubMed/Medline and Cochrane through February 2025 and included 95 studies of uterine serous carcinomas. The authors report that these tumors are characterized by TP53 mutations and extensive copy number alterations and are commonly classified in the copy number-high/p53abn molecular group. The review identified 66 distinct molecular characteristics and new cancer signatures that may have prognostic significance and could inform tailored treatment strategies, though these findings require further validation.

Reported effects: included_studies 95 · distinct_molecular_characteristics 66

Key findings

Uterine serous carcinomas are an aggressive minority of endometrial cancers.
These tumors are characterized by mutations in TP53 and extensive copy number alterations and are primarily classified in the copy number-high/p53abn molecular prognostic group.
The systematic review searched PubMed/Medline and Cochrane databases through February 2025 and included 95 studies.
A total of 66 distinct molecular characteristics and new cancer signatures with potential prognostic impact were identified across the included studies.
Authors suggest these molecular findings may inform clinical practice and aid development of tailored treatment strategies for patients with uterine serous carcinoma.

Limitations: Review limited to English-language articles (English-only search was performed).; Systematic review format reported; no pooled meta-analytic effect sizes or patient-level pooled estimates are presented in the abstract.; Prognostic markers and new signatures identified across multiple studies may be heterogeneous and require independent validation before clinical application.; Abstract does not report the quality assessment of included studies or patient-level sample sizes..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewInconclusiveLimited evidenceTier 4 · clinical

Current Treatment of Uveal Melanoma

Cancers · Apr 2025

uveal melanoma

This is a review article titled "Current Treatment of Uveal Melanoma" that discusses treatments for uveal melanoma. The provided abstract text is incomplete and does not report specific interventions, results, or conclusions.

Limitations: Provided abstract is incomplete/truncated and contains no detailed results.; Review article — no original experimental or clinical trial data reported in the abstract.; No specific treatments, doses, outcomes, or quantitative results are stated in the provided text.; Unable to assess study design, population, or funding from the abstract..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewInconclusiveLimited evidenceTier 4 · clinical

ESMO Clinical Practice Guideline Express Update on the management of metastatic pancreatic cancer

ESMO open · Apr 2025 · ESMO Clinical Practice Guideline Express Update

metastatic pancreatic cancer

This is an ESMO clinical practice guideline express update addressing recent developments in managing metastatic pancreatic cancer. The update was issued following the approval of first-line nanoliposomal irinotecan (NALIRIFOX) and provides updated first- and second-line treatment recommendations and an updated management algorithm.

Key findings

This ESMO Clinical Practice Guideline Express Update addresses developments in the management of metastatic pancreatic cancer.
It has been issued following the approval of first-line nanoliposomal irinotecan (NALIRIFOX regimen).
Updated first- and second-line treatment recommendations are provided.
An updated management algorithm for metastatic pancreatic cancer is also included.

Limitations: Abstract-only summary of a guideline; no methodological details or evidence tables are provided in the abstract.; No primary patient-level data, sample sizes, or outcome measures are reported in the abstract.; No information on funding, conflicts of interest, or the strength/grade of specific recommendations is provided in the abstract..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewReported negativeLimited evidenceTier 3 · early human

Addressing Alcohol Use and Cancer Risk

Nursing for women's health · Apr 2025

This editorial states that alcohol consumption is a leading cause of preventable cancer. It also notes that cancer risk may increase even with small amounts of alcohol.

Key findings

Alcohol consumption is a leading cause of preventable cancer.
Risk may increase with small amounts of alcohol.

Limitations: Editorial with no original data or methods reported.; No quantitative results, effect sizes, or study design described in the abstract.; Not an empirical study; conclusions are presented without new supporting data in this article abstract..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed

Human · observationalMechanismMixed resultsLimited evidenceTier 3 · early humann = 39

Primary ovarian leiomyosarcoma: results from an analysis by the French Sarcoma Group (Ovarian SArcoma MAnagement - OSAMA Study)

International journal of gynecological cancer : official journal of the International Gynecological Cancer Society · Apr 2025 · retrospective multicenter study using the national NetSarc database

primary ovarian leiomyosarcomaovarian neoplasmsleiomyosarcoma

This retrospective multicenter study analyzed 39 patients with primary ovarian leiomyosarcoma from the French Sarcoma Group database to describe clinical, surgical, pathological features and outcomes. Median tumor size was large (134 mm); 15 patients (44%) died of disease. Certain pathologic features (high mitotic counts, progesterone receptor negativity) were associated with worse survival. The authors conclude surgery is the mainstay for early-stage disease and the role of adjuvant therapy remains unclear.

Reported effects: total patients included 39 · localized disease - n 35 · +14 more

Key findings

39 patients were included (35 localized, 4 metastatic).
Median tumor size was 134 mm.
Radical surgery was performed in 21 patients (62%) and wide surgery in 13 patients (38%).
Tumor grade 3 reported in 17 of 34 patients (50%); necrosis in 29 of 34 (85%); mitoses ≥20/HPF in 17 of 34 (50%); Ki-67 >30% in 17 of 27 patients (63%).
Estrogen receptor positive in 14 of 27 patients (52%); progesterone receptor positive in 10 of 27 patients (37%).
Adjuvant chemotherapy given in 12 of 34 patients (35%); pelvic adjuvant radiotherapy in 8 of 34 (23%).
Among early-stage cases, 9 had isolated pelvic recurrence and 18 had parenchymal distant metastases.
Fifteen patients (44%) died of disease.
High mitotic counts and progesterone receptor negativity were associated with worse survival in early-stage disease.

Limitations: Retrospective study design.; Small sample size (n=39) for subgroup and prognostic analyses.; Heterogeneous and incompletely reported treatment approaches (adjuvant therapies given in subsets).; Some pathological and biomarker data were available only in subsets (denominators vary: data reported for 34 or 27 patients), indicating missing data.; No control group or prospective follow-up protocol reported..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Human trialTrialMixed resultsStrong evidenceTier 4 · clinicaln = 558

Tumor Treating Fields therapy in platinum-resistant ovarian cancer: Results of the ENGOT-ov50/GOG-3029/INNOVATE-3 pivotal phase 3 randomized study

European journal of cancer (Oxford, England : 1990) · Mar 2025 · Phase 3 randomized controlled trial

Paclitaxelplatinum-resistant ovarian cancer

This randomized phase 3 study compared Tumor Treating Fields (TTFields) plus weekly paclitaxel versus paclitaxel alone in 558 patients with platinum-resistant ovarian cancer. Overall survival was similar between groups (median 12.2 vs 11.9 months; HR 1.01, p=0.89). Grade 65 3 adverse events were similar, while grade 1/2 device-related skin events occurred in 83.6% of patients receiving TTFields. An exploratory post-hoc analysis in PLD-naive patients reported longer median OS with TTFields+PTX (16 vs 11.7 months; nominal HR 0.67, p=0.03).

Reported effects: median OS (intent-to-treat) 12.2 mo · HR for OS (intent-to-treat) 1.01 [0.83–1.24], p=0.89 · +3 more

Studied with: paclitaxel.

Key findings

558 patients were randomized to TTFields+PTX (n=280) or PTX (n=278).
Primary endpoint overall survival: median OS 12.2 months with TTFields+PTX vs 11.9 months with PTX (HR 1.01; 95% CI 0.83-1.24; p=0.89).
Grade 65 adverse events were similar between treatment groups.
Grade 1/2 device-related skin adverse events occurred in 83.6% of patients receiving TTFields.
Exploratory post-hoc in PLD-naive patients: median OS 16 months with TTFields+PTX (n=113) vs 11.7 months with PTX (n=88); nominal HR 0.67 (95% CI 0.49-0.94); p=0.03.

Limitations: Primary endpoint (OS) was not improved in the intent-to-treat population.; The favorable finding in PLD-naive patients is from an exploratory post-hoc subgroup analysis and may not be definitive.; Potential for multiple comparisons and subgroup selection bias in post-hoc analyses.; Device-related skin adverse events were frequent (grade 1/2 in 83.6% of TTFields patients).; Abstract does not report longer-term follow-up details or quality-of-life data..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed

Case reportMixed resultsLimited evidenceTier 3 · early humann = 1

Extrapulmonary small cell carcinoma of the liver treated with chemotherapy and durvalumab

Radiology case reports · Mar 2025 · case report

Etoposide Durvalumab Carboplatinextrapulmonary small cell carcinoma of the liver

This is a single-patient case report of extrapulmonary small cell carcinoma of the liver in a 52-year-old woman. The patient received systemic chemotherapy with carboplatin and etoposide combined with durvalumab, had clinical improvement of symptoms, but died 10 months after starting chemoimmunotherapy. The authors note that optimal treatment for EPSCC is generally extrapolated from small cell lung cancer and that there is insufficient evidence to routinely recommend immunotherapy in this group.

Reported effects: tumor_dimensions, n=1 · time_to_death_after_starting_chemoimmunotherapy 10 mo, n=1

Studied with: carboplatin, etoposide, carboplatin + etoposide.

Key findings

Diagnosis of EPSCC of the liver was made after biopsy and immunohistochemistry (positive for CKA1/A3, chromogranin, synaptophysin, CD56 and TTF-1).
Abdominal MRI showed an enlarged liver secondary to a mass affecting segments IV, V, VI, VII and VIII of 16.9 × 9.4 cm.
Systemic chemotherapy with carboplatin and etoposide plus durvalumab was started.
There was clinical improvement of the symptoms after starting treatment.
The patient died 10 months after starting chemoimmunotherapy treatment.
Authors state that optimal treatment of EPSCC is generally extrapolated from small cell lung cancer and there is insufficient evidence to routinely recommend immunotherapy for EPSCC.

Limitations: Single-patient case report (n=1), so findings are not generalizable.; No control or comparator group to assess treatment effect.; No dosing, schedule, or detailed treatment toxicity information provided.; Cannot establish causality or efficacy from a single observational case.; EPSCC is rare and treatment recommendations are extrapolated from small cell lung cancer, limiting direct applicability..

This report describes use of carboplatin + etoposide chemotherapy combined with durvalumab in a patient with extrapulmonary small cell carcinoma of the liver.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMixed resultsLimited evidenceTier 4 · clinical

Pancreatic ductal adenocarcinoma (PDAC): clinical progress in the last five years

Expert opinion on investigational drugs · Mar 2025

pancreatic ductal adenocarcinomapancreatic neoplasmsPDAC

This is a narrative review summarizing recent clinical and translational advances for pancreatic ductal adenocarcinoma (PDAC) over the last five years. It describes progress in genomic profiling, targeted therapies, and immunotherapy approaches and highlights strategies aimed at the tumor microenvironment such as IL-6 and CD137 inhibitors, CAR-T, therapeutic vaccines, KRAS-targeted drugs beyond G12C, and tumor treating fields. The authors note that dense stroma and an immunosuppressive microenvironment remain major challenges. The review highlights ongoing clinical trials but does not report new primary data.

Key findings

Advances in genomic profiling have revealed complex molecular and cellular heterogeneity of PDAC, creating new avenues for therapy.
Emerging therapeutic strategies target dysregulated molecular pathways and the tumor microenvironment to try to overcome drug resistance.
Novel immunotherapy strategies, including immune checkpoint inhibitors and CAR T-cell therapies, are being explored to modulate the immunosuppressive microenvironment of PDAC.
IL-6 and CD137 inhibitors, CAR-T, and therapeutic cancer vaccines are described as promising approaches despite the challenges posed by dense stroma and immune suppression.
KRAS-targeted therapies are expanding beyond G12C inhibitors, and tumor treating fields (TTF) are under investigation (PANOVA-3 trial mentioned).

Limitations: This is a narrative review; no original experimental or clinical trial data are presented in the article itself.; No quantitative synthesis (meta-analysis) or new pooled estimates are provided.; Conclusions are necessarily broad and based on heterogeneous studies with variable stages of development and evidence levels.; Many of the highlighted strategies are described as investigational and their clinical efficacy in PDAC is not established in this review..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed

ReviewInconclusivePreclinical onlyTier 1 · lab

Sono-Piezo Dynamic Therapy: Utilizing Piezoelectric Materials as Sonosensitizer for Sonodynamic Therapy

Advanced science (Weinheim, Baden-Wurttemberg, Germany) · Mar 2025 · review

cancer

This review defines the concept of Sono-Piezo Dynamic Therapy (SPDT) and summarizes research on using piezoelectric materials as sonosensitizers in sonodynamic therapy for cancer. It explains that ultrasound induces electron-hole separation in piezoelectric materials, which can produce redox potentials enabling generation of reactive oxygen species (e.g., superoxide). The article discusses various piezoelectric materials, their feasibility, advantages and disadvantages, and highlights challenges such as low water solubility and poor tumor specificity of many sonosensitizers.

Studied with: ultrasound.

Key findings

Introduces SPDT: piezoelectric materials can serve as sonosensitizers when activated by ultrasound.
Mechanistic point: ultrasound causes separation of electron-hole (e--h+) pairs; improving crystal structure or adding nanoparticles can reduce recombination, allowing charge accumulation and redox potential reaching O2/·O2-.
Reviews multiple piezoelectric materials and discusses their feasibility, advantages, and disadvantages as sonosensitizers.
Highlights practical limitations for current sonosensitizers including low water solubility, poor tumor specificity, and metabolic susceptibility.

Limitations: Review article; no new original experimental data are presented in this paper.; Focus is on preclinical mechanisms and materials; the abstract does not report human clinical data.; No quantitative efficacy metrics or outcome data are provided in the abstract.; Potential conflicts of interest or funding sources are not reported in the abstract..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewInconclusiveLimited evidenceTier 4 · clinical

Melanoma in pregnancy

Seminars in perinatology · Mar 2025

cutaneous melanomamelanoma

This narrative review summarizes published literature on cutaneous melanoma diagnosed during pregnancy. The authors report that pregnancy does not appear to worsen maternal melanoma outcomes and, except for rare placental or fetal metastases, melanoma usually does not cause major obstetric or fetal complications. They note that localized melanoma is managed according to general population guidelines, while advanced melanoma in pregnancy is challenging because of limited research and lack of unified management recommendations.

Key findings

Cutaneous melanoma is the most common malignancy in women of childbearing age and accounts for nearly one-third of malignancies diagnosed during gestation.
Based on available literature, pregnancy does not seem to worsen maternal outcomes from melanoma.
Aside from placental and fetal metastases, melanoma does not seem to cause serious obstetric or fetal complications.
Treatment of localized melanoma during pregnancy follows guidelines for the general population.
Advanced melanoma in pregnancy poses unique challenges due to lack of unifying research and management recommendations.
The review highlights diagnostic clinical pearls and multidisciplinary management considerations for melanoma in the child-bearing population.

Limitations: Narrative review with no primary data reported in this article.; Abstract states pathophysiology during pregnancy is not well understood, indicating knowledge gaps.; Authors note a lack of unifying research and management recommendations for advanced melanoma in pregnancy, implying limited high-quality evidence..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

ReviewMixed resultsLimited evidenceTier 4 · clinical

Controversies in the management of mucinous ovarian tumors

International journal of gynecological cancer : official journal of the International Gynecological Cancer Society · Mar 2025

mucinous ovarian carcinoma (MOC)epithelial ovarian cancer

This narrative review summarizes controversies in diagnosis, surgery, and systemic therapy for mucinous ovarian carcinoma (MOC), a rare subtype of epithelial ovarian cancer. The authors emphasize difficulties distinguishing primary from metastatic mucinous tumors, debate fertility-sparing surgery and lymphadenectomy approaches, and note poor response to standard ovarian chemotherapy with several unvalidated alternative strategies (gastrointestinal regimens, HER2-targeted ADCs, immune checkpoint inhibitors for MSI, and combinations targeting RAS/WEE1). They recommend histologic subtyping, molecular profiling, multidisciplinary care, and international collaboration to enable larger studies and improve management.

Studied with: RAS pathway inhibitors + WEE1 inhibitors.

Key findings

MOC is rare (<5% of epithelial ovarian cancers) and has distinct molecular, histologic, and clinical features leading to controversies in diagnosis and treatment.
Distinguishing primary MOC from metastatic mucinous tumors (eg, gastrointestinal primaries) is challenging and misclassification can impair management, emphasizing the need for high-quality pathologic review.
Surgical management is controversial: fertility-sparing surgery should be considered in young patients with early-stage disease, but feasibility requires careful selection; systematic lymphadenectomy has been de-escalated for expansile MOC but is recommended for early-stage infiltrative MOC.
Advanced-stage MOC tumors are often bulky and chemoresistant; the benefit of extensive cytoreduction must be weighed against surgical morbidity.
Systemic therapy responses to standard ovarian cancer regimens are poor; alternative approaches discussed include gastrointestinal-based chemotherapy regimens, HER2-targeted antibody-drug conjugates (eg, trastuzumab deruxtecan), immune checkpoint inhibitors for microsatellite unstable MOC, and preclinical/early-phase combination strategies targeting RAS and WEE1.

Limitations: MOC rarity limits the size of studies and clinical trial evidence available.; Diagnostic overlap with gastrointestinal primaries can lead to misclassification in clinical series.; Many alternative therapeutic strategies cited lack robust clinical validation (reliance on pre-clinical and early-phase data).; This is a narrative review and does not present new primary patient-level data or a systematic meta-analysis..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

ReviewInconclusiveLimited evidenceTier 4 · clinical

Mesenchymal Neoplasms of the Kidney and Perinephric Soft Tissue

Surgical pathology clinics · Mar 2025

kidney mesenchymal neoplasmsperinephric soft tissue neoplasmsmetanephric stromal tumorcongenital mesoblastic nephroma (classic)congenital mesoblastic nephroma (cellular)anaplastic sarcoma of the kidneyclear cell sarcoma of the kidneymalignant rhabdoid tumorPEComa/angiomyolipomaanastomosing hemangiomaperinephric myxoid pseudotumor of fatwell-differentiated/dedifferentiated liposarcomasarcomatoid carcinoma

This is a narrative review that summarizes mesenchymal tumors of the kidney and tumors of the perinephric soft tissue. The author reviews specific entities (for example, metanephric stromal tumor, congenital mesoblastic nephroma, anaplastic and clear cell sarcomas, malignant rhabdoid tumor, PEComa/angiomyolipoma, and anastomosing hemangioma), discusses perinephric myxoid pseudotumor of fat, and highlights diagnostic pitfalls such as well-differentiated/dedifferentiated liposarcoma and sarcomatoid carcinoma.

Key findings

Perinephric soft tissue biopsies are sometimes submitted as 'kidney' masses, which can cause diagnostic confusion.
The review covers a range of renal mesenchymal neoplasms including metanephric stromal tumor, classic and cellular congenital mesoblastic nephroma, anaplastic sarcoma, clear cell sarcoma of the kidney, malignant rhabdoid tumor, PEComa/angiomyolipoma, and anastomosing hemangioma.
Perinephric myxoid pseudotumor of fat is discussed as a distinct entity.
The author discusses diagnostic pitfalls presented by well-differentiated/dedifferentiated liposarcoma and sarcomatoid carcinoma.

Limitations: Narrative review only; no original patient-level data or new experimental results are presented in the abstract.; Abstract does not state systematic review methods, so comprehensiveness and selection criteria are unclear.; No quantitative data, outcomes, or diagnostic performance metrics are reported in the abstract.; Focus is diagnostic/pathologic; therapeutic implications or clinical outcomes are not addressed in the abstract..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

ReviewMechanismMixed resultsModerate evidenceTier 4 · clinical

Updates and controversies in the management of uterine serous carcinoma and uterine carcinosarcoma

International journal of gynecological cancer : official journal of the International Gynecological Cancer Society · Mar 2025 · Review

uterine serous carcinomauterine carcinosarcoma

This is a narrative review summarizing recent evidence on molecular classification, biomarkers, and new treatment approaches for uterine serous carcinoma and uterine carcinosarcoma. The authors highlight biomarkers such as HER2, TP53, and mismatch repair deficiency/microsatellite instability, discuss circulating tumor DNA and precision-based treatment options, and note survival disparities for non-Hispanic Black and other underserved minority patients. They conclude that continuing to prioritize biomarker-driven therapies and developing novel treatments through clinical trials — integrated with surgery and cytotoxic chemotherapy — is necessary.

Reported effects: proportion_of_cases 15% · proportion_of_deaths 50%

Key findings

Uterine serous carcinoma and uterine carcinosarcoma are rare but account for a disproportionate share of endometrial cancer deaths.
These subtypes have a high likelihood of metastasis and multisite recurrence and are biologically distinct from other endometrial cancers.
The review analyzes the role of biomarkers including HER2, TP53, and mismatch repair deficiency/microsatellite instability and their influence on treatment strategies and surveillance.
Circulating tumor DNA (ctDNA) is discussed as a potential tool.
Novel precision-based treatment options are described and the authors call for continued development of biomarker-driven therapies through clinical trials.
Disparate survival outcomes for non-Hispanic Black and other underserved minority patients are identified, and strategies to improve their outcomes are discussed.

Limitations: Narrative review rather than primary research; no new experimental or trial data presented in the abstract.; Abstract provides no methods, search strategy, or inclusion criteria (potential selection bias).; Rare tumor subtypes mean available evidence is likely limited and heterogeneous (implicit limitation).; No quantitative synthesis (meta-analysis) or new clinical outcome data reported in the abstract..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMechanismReported positiveLimited evidenceTier 3 · early human

The regulatory role of ZFAS1/miRNAs/mRNAs axis in cancer: a systematic review

Oncology research · Feb 2025 · Systematic review with bioinformatic analyses (PRISMA-guided literature search and database analyses)

ovarian cancersarcomapancreatic cancer

This systematic review and bioinformatic analysis examined the relationships among the long noncoding RNA ZFAS1, microRNAs, and mRNAs in cancer. The authors report that ZFAS1 often acts as a sponge for multiple miRNAs, highlight a strong negative correlation with miR-150-5p, and find that higher ZFAS1 expression is associated with poorer overall survival in ovarian, sarcoma, and pancreatic cancers. They also identify involvement of signaling pathways including STAT3 and Wnt/β-catenin and roles in RNA binding and ribonucleoprotein formation.

Reported effect: correlation miR-150-5p vs ZFAS1 -0.346, p=3.27e-16

Key findings

ZFAS1 serves as a sponge for numerous miRNAs (ceRNA activity).
miR-150-5p is significantly correlated with ZFAS1 across multiple databases (p-value = 3.27e-16, R-value = -0.346).
Kaplan-Meier survival analysis indicated an association between ZFAS1 expression levels and worse overall prognosis in ovarian, sarcoma, and pancreatic cancers.
ZFAS1/miRNAs/mRNAs axis involves signaling pathways including STAT3, SKA1, LPAR1, and Wnt/β-catenin.
ZFAS1 is implicated in molecular processes such as RNA binding and ribonucleoprotein formation.

Limitations: This paper is a systematic review and bioinformatic analysis rather than primary experimental or clinical data.; Findings are largely observational and correlative; causality is not established.; No sample sizes or patient-level details are reported in the abstract for the survival analyses.; Potential heterogeneity and publication bias across the included studies are not detailed in the abstract.; No experimental validation of the bioinformatic predictions is reported in the abstract..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Case reportReported positiveLimited evidenceTier 3 · early humann = 1

Primary Low-Grade Endometrial Stromal Sarcoma of the Ovary Arising From Endometriosis: A Case Report

Cureus · Feb 2025 · case report

ovarian low-grade endometrial stromal sarcoma (LGESS)

This case report describes a 52-year-old woman diagnosed with primary low-grade endometrial stromal sarcoma of the ovary arising adjacent to endometriosis who underwent optimal cytoreductive surgery followed by medroxyprogesterone acetate (MPA). The patient received MPA 600 mg/day reduced to 400 mg/day for side effects and remained recurrence-free three years after treatment. Imaging and pathology (ER/PgR/CD10 positive) supported the diagnosis of endocrine-dependent LGESS. The authors suggest that surgery plus hormonal therapy contributed to durable remission in this single case.

Reported effects: left ovarian mass size_length 100, n=1 · left ovarian mass size_width 50, n=1 · +6 more

Studied with: optimal cytoreductive surgery (total hysterectomy, bilateral salpingo-oophorectomy, subtotal omentectomy, rectal resection).

Key findings

Transvaginal ultrasound revealed a 100×50 mm left ovarian mass with a 30 mm thick cystic component.
PET-CT showed mild FDG uptake with SUVmax of 3.05 and no distant metastases.
Intraoperatively the left ovary was enlarged (10 cm) with peritoneal dissemination; frozen section suggested granulosa cell tumor.
Definitive histopathology and immunohistochemistry (ER+, PgR+, CD10+) confirmed LGESS; final FIGO stage IIIB (pT3bNxM0).
Patient underwent total hysterectomy, bilateral salpingo-oophorectomy, subtotal omentectomy, and high anterior rectal resection.
Postoperative hormonal therapy with medroxyprogesterone acetate at 600 mg/day (reduced to 400 mg/day for weight gain) was given.
The patient remained recurrence-free three years post-treatment.

Limitations: Single-patient case report (n=1) — cannot generalize efficacy or safety of MPA for ovarian LGESS.; No control or comparator group to attribute recurrence-free status to MPA versus surgery or natural history.; Observational, retrospective description without standardized outcome measures.; Initial intraoperative frozen section misdiagnosed tumor (granulosa cell), illustrating diagnostic uncertainty.; Long-term safety beyond reported weight gain is not reported; follow-up limited to three years in this report..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMechanismReported positiveLimited evidenceTier 4 · clinical

Recent Advances in Pineoblastoma Research: Molecular Classification, Modelling and Targetable Vulnerabilities

Cancers · Feb 2025

pineoblastoma

This review summarizes recent advances in pineoblastoma research, describing major molecular subtypes driven by DICER/DROSHA loss, RB1 loss, or cMYC activation and noting differing prognoses between them. It reports that mouse models have been developed for RB1-, DICER1- and DROSHA-driven subtypes (a MYC-driven model is not yet established) and discusses tumor cell of origin, progression, autophagy, and potential targetable vulnerabilities while highlighting that metastatic disease is incurable and standard treatments can impair neurocognitive function.

Key findings

Pineoblastoma comprises several major molecular subtypes: (i) loss of microRNA processing factors DICER and DROSHA, (ii) loss of RB1, and (iii) amplification/induction of cMYC.
The DICER/DROSHA subtype is characterized by a relatively good prognosis whereas RB1- and MYC-driven subtypes exhibit exceedingly poor prognosis.
Mouse models have recently been established for RB1-, DICER1- and DROSHA-driven pineoblastoma subtypes; a MYC-driven mouse model has not yet been established.
The review discusses disease biology including cell of origin, tumor progression, the role of autophagy, and describes targetable vulnerabilities that could inform future precision therapies.
Standard treatment (surgery, radiation, systemic chemotherapy) improves survival but compromises neurocognitive function; metastatic pineoblastoma is described as incurable.

Limitations: This article is a review and does not present new primary experimental or clinical data.; Many conclusions discussed are based on recent preclinical models and not yet validated in humans.; A MYC-driven pineoblastoma mouse model has not been established, limiting preclinical study of that high-risk subtype.; Pineoblastoma is a rare disease, which limits available clinical data and may hinder generalizability of findings..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewInconclusiveLimited evidenceTier 3 · early human

Atypical Pelvic Tumors in Children

Cancers · Feb 2025 · literature review and case series (selected cases presented)

sacrococcygeal teratomaovarian teratomarhabdomyosarcomaEwing sarcomacervical cancersmall cell neuroendocrine carcinoma of the ovaryEwing sarcoma/primitive neuroectodermal tumor (ES/PNET) of the ovarydiffuse large B-cell lymphoma of the ovariesovarian Sertoli-Leydig cell tumor (SLCT)neuroblastomaplexiform neurofibromaRosai-Dorfman disease

The authors review selected atypical pelvic tumors seen in children and present their own cases, focusing on imaging (MRI) characteristics. They describe a variety of reproductive-system and nervous-system tumors (including rare ovarian and testicular neoplasms, lymphomas, neuroblastoma, plexiform neurofibroma, and Rosai-Dorfman disease). The study sought radiological features that could help radiologists reach correct diagnoses but emphasizes that MRI cannot be interpreted alone and must be combined with clinical, syndromic and laboratory information.

Key findings

Selected atypical pelvic tumors in children are presented, many arising in the reproductive system (examples listed include cervical cancer, ovarian small cell neuroendocrine carcinoma, ES/PNET of the ovary, ovarian DLBCL, and ovarian SLCT associated with DICER1 syndrome).
Tumors originating from the nervous system discussed include neuroblastoma and plexiform neurofibroma (both NF1-associated and not associated with NF1).
Rosai-Dorfman disease involving pelvic and inguinal lymph nodes is presented as an additional differential diagnosis.
The authors aimed to identify radiological (MRI) features to guide radiologists toward correct diagnosis, but state that MR images must be interpreted alongside clinical picture, comorbidities/syndromes, and laboratory results.

Limitations: Study presents selected cases and a literature review rather than a systematic or comprehensive series; potential selection bias.; No sample size, quantitative diagnostic accuracy, or outcome data are reported in the abstract.; Imaging findings are descriptive and the abstract does not report validation of MRI features against definitive diagnoses or standardized criteria..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Human · observationalMechanismReported positiveLimited evidenceTier 3 · early human

The Evolutionary Forest of Pancreatic Cancer

Cancer discovery · Feb 2025

pancreatic ductal adenocarcinoma

The authors examined the genomes of pancreatic ductal adenocarcinoma and quantified genomic features using evolutionary metrics. They report identifying a novel prognostic biomarker for PDAC. The abstract does not provide sample sizes, methods, numeric results, or details about validation or clinical utility.

Key findings

Described and quantified the genomic features of PDAC in the context of evolutionary metrics.
Identified a novel prognostic biomarker.

Limitations: Abstract does not report sample size, cohorts, methods, or statistical details.; No quantitative results or validation data are provided in the abstract.; Clinical utility or prospective validation of the reported biomarker is not described.; Observational genomic analysis — does not establish causality or therapeutic effect..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewReported positiveModerate evidenceTier 4 · clinical

Recent advances in Tumor Treating Fields (TTFields) therapy for glioblastoma

The oncologist · Feb 2025 · narrative review

glioblastomagrade 4 gliomapediatric central nervous system tumorsbrain metastaseslung cancerovarian cancerpancreatic cancergastric cancerhepatic cancer

This review summarizes Tumor Treating Fields (TTFields), a noninvasive device that delivers alternating electric fields to tumors. It reports mechanisms of action (mitotic disruption, DNA replication/DNA damage response effects, reduced motility, and immune enhancement), notes FDA approval for newly diagnosed and recurrent glioblastoma, and describes clinical data showing efficacy across patient groups, a tolerable safety profile, and correlations between higher device usage/dose and longer survival. The review also highlights promising pilot studies combining TTFields with immunotherapy and radiotherapy and ongoing studies in pediatric patients and other solid tumors.

Studied with: immunotherapy, radiotherapy.

Key findings

TTFields is a locoregional, noninvasive, portable device that delivers alternating electric fields to tumors through arrays placed on the skin.
Based on global pivotal randomized phase III clinical studies, TTFields therapy (Optune Gio) is FDA-approved for newly diagnosed and recurrent glioblastoma and CE-marked for grade 4 glioma.
Multimodal mechanisms include disruption of cancer cell mitosis, inhibition of DNA replication and damage response, interference with cell motility, and enhancement of systemic adaptive immunity.
Clinical data show efficacy in a broad range of patients with a tolerable safety profile, including high-risk subpopulations.
New analyses confirmed that overall and progression-free survival positively correlated with increased device usage and dose of TTFields at the tumor site.
Pilot/early phase clinical studies of TTFields with immunotherapy and with radiotherapy in newly diagnosed GBM have shown promise; new pivotal studies are planned.
Recent and ongoing studies are evaluating TTFields in pediatric care, other CNS tumors, brain metastases, and several advanced-stage solid tumors (lung, ovarian, pancreatic, gastric, hepatic).

Limitations: This article is a narrative review rather than original research; the abstract does not present new primary numeric results.; Abstract provides no numeric effect sizes, confidence intervals, p-values, or sample sizes for the studies discussed.; Claims about broader tumor types, pediatric use, and combinations are based on pilot/early-phase studies and ongoing research and thus remain preliminary.; Potential for selection or publication bias in the reviewed literature is not addressed in the abstract.; Funding sources and potential conflicts of interest are not reported in the abstract..

The review focuses on TTFields therapy's mechanisms, clinical efficacy/safety data in glioblastoma, and exploratory uses in other CNS and solid tumors.

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Case reportMechanismInconclusiveLimited evidenceTier 3 · early humann = 2

High-grade corded and hyalinized endometrioid carcinoma of "no specific molecular profile": report of two cases

Pathologica · Feb 2025 · case report (two cases)

corded and hyalinized endometrioid carcinomaendometrioid carcinomaendometrial carcinoma

This paper reports two human cases of high-grade corded and hyalinized endometrioid carcinoma (CHEC) that showed a "no specific molecular profile" (NSMP). Both tumors had a markedly atypical, mitotically active corded component merging with FIGO G3 endometrioid carcinoma and squamous/morular differentiation, and both showed nuclear β-catenin accumulation, retained mismatch repair protein expression, wild-type p53 pattern, and no POLE mutations. The authors note heterogeneity in age and presentation (patients aged 25 and 81) and suggest these tumors be considered a variant of FIGO G3 endometrioid carcinoma.

Reported effects: number_of_cases 2 · tumor_size_case1 6 · +2 more

Key findings

Both cases demonstrated a markedly atypical and mitotically active corded component merging with a FIGO G3 endometrioid component and accompanied by squamous/morular differentiation.
Both tumors showed nuclear β-catenin accumulation, retained MMR protein expression, wild-type p53 pattern, and no POLE mutations.
Case #1 was a 6-cm endometrial mass in a 25-year-old woman, infiltrating the deep myometrium and cervical stroma, with diffuse lymphovascular space invasion.
Case #2 was an advanced, unresectable endometrial carcinoma involving the lower third of the vagina in an 81-year-old woman.
The corded component was absent in the hysterectomy specimen of case #1 and in the vaginal biopsy specimen of case #2.
Authors conclude these cases expand the clinical and molecular heterogeneity of high-grade CHEC and suggest considering them as a variant of FIGO G3 endometrioid carcinoma.

Limitations: Very small sample size (two cases) — case report-level evidence.; Descriptive pathology series without systematic follow-up or outcome data reported in the abstract.; No control or comparison group.; Methods for molecular testing (e.g., POLE testing) and detailed molecular data are not provided in the abstract.; Findings may not be generalizable..

Pathology case report that expands the morphological and molecular spectrum of high-grade corded and hyalinized endometrioid carcinoma (CHEC) by describing two human cases with NSMP.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Animal studyReported positivePreclinical onlyTier 2 · animal

Characterizing and targeting glioblastoma neuron-tumor networks with retrograde tracing

Cell · Jan 2025 · preclinical experimental study using retrograde tracing and genetic ablation in glioblastoma models

glioblastomabrain neoplasms

This study used rabies-virus-based retrograde tracing to map neurons connected to glioblastoma in experimental models. The authors found that glioblastoma formed widespread connections with neurons, and that cholinergic neurons promoted invasion. They also reported that radiotherapy increased neuron-tumor connectivity, while blocking neuronal activity together with radiotherapy had greater effects, and that genetic ablation of tumor-connected neurons halted glioblastoma progression in their models.

Studied with: radiotherapy.

Key findings

Glioblastoma integrated into neural circuits across the brain and showed widespread functional communication.
Cholinergic neurons were reported to drive glioblastoma invasion.
Radiotherapy increased neuron-tumor connectivity by increasing neuronal activity.
Simultaneous neuronal activity inhibition and radiotherapy showed increased therapeutic effects in the models.
Rabies-mediated genetic ablation of tumor-connected neurons halted glioblastoma progression in the study models.

Limitations: Preclinical animal/model-system study; no human clinical outcomes reported.; The abstract does not provide sample size, effect sizes, or statistical details.; Use of rabies-virus-based tracing and genetic ablation is experimental and not a standard clinical intervention.; Findings are based on glioblastoma models, so generalizability to patients is uncertain..

The study focuses on glioblastoma biology and experimental targeting of neuron-tumor networks, not on a repurposed drug or natural compound.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

ReviewMechanismInconclusiveLimited evidenceTier 1 · lab

Advances in MiRNAs Involved in Endometrial Carcinoma

Combinatorial chemistry & high throughput screening · Jan 2025 · Review

endometrial carcinoma

This is a review article summarizing recent studies on microRNAs (miRNAs) in endometrial carcinoma. The authors report that evidence supports miRNAs as important regulators of gene expression via binding to 3'-UTR regions. The review aims to clarify the association between miRNAs and endometrial carcinoma and to serve as a reference for further research into miRNA-related therapies.

Key findings

Endometrial carcinoma may be associated with abnormal gene expression.
Evidence supports that miRNAs act as critical regulators of gene expression through binding to the 3'-untranslated region (3'-UTR).
The review summarizes recent studies focusing on miRNAs that influence endometrial carcinoma.
The authors intend the review to provide a reference for further studies on miRNA-related drugs in endometrial carcinoma.

Limitations: This is a review article and presents no new experimental data.; Abstract does not describe review methods, selection criteria, or whether the review was systematic.; Abstract does not specify which findings are from human clinical studies versus preclinical (in vitro/animal) studies.; The review does not establish clinical efficacy or safety of miRNA-related therapies in patients..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Case reportMechanismInconclusiveLimited evidenceTier 3 · early humann = 2

POLE-mutated Endometrial "Carcinosarcoma"

International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists · Jan 2025 · Case report (2 cases)

Endometrial carcinomaCarcinosarcomaEndometrioid carcinoma

The authors report two cases that were morphologically suspicious for endometrial carcinosarcoma but did not meet essential diagnostic criteria. Molecular testing identified pathogenic POLE mutations in both cases, and the tumors were described as low-grade endometrioid carcinomas with a homologous sarcoma component. The report questions the existence of a true POLE-mutated carcinosarcoma entity.

Key findings

Two cases had morphologic suspicion for endometrial carcinosarcoma but lacked essential criteria for that diagnosis.
Pathogenic POLE mutations were detected on molecular testing in both cases.
A descriptive diagnosis rendered was endometrial endometrioid carcinomas, low-grade, with a homologous sarcoma component.
These observations challenge the existence of POLE-mutated 'carcinosarcoma.'

Limitations: Very small sample size (2 cases).; Case report design without a systematic series or controls.; No clinical follow-up, treatment, or outcome data reported in the abstract.; Abstract provides limited pathological and methodological detail..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

ReviewMechanismInconclusiveLimited evidenceTier 3 · early human

Metabolic dysfunction-associated steatotic liver disease and urinary system cancers: Mere coincidence or reason for concern?

Metabolism: clinical and experimental · Jan 2025 · narrative review

renal cell carcinomaurothelial carcinomaprostate adenocarcinoma

This narrative review summarizes and interprets conflicting evidence about whether metabolic dysfunction-associated steatotic liver disease (MASLD) is associated with urinary system cancers (renal cell carcinoma, urothelial carcinoma, and prostate adenocarcinoma). It discusses possible linking mechanisms such as insulin resistance and lipotoxicity but does not present new primary data.

Key findings

MASLD is described as a systemic disease characterized by insulin resistance and lipotoxicity.
Associations between MASLD and type 2 diabetes, cardiovascular disease, liver cirrhosis, and hepatocellular carcinoma are well described.
The association between MASLD and extra-hepatic cancers, specifically urinary system cancers, has received significantly less attention and the existing evidence is conflicting.
The review explores potential mechanisms (including insulin resistance and lipotoxicity) that could explain a higher risk of urinary system cancers in patients with MASLD.
The article is a narrative synthesis intended to help readers interpret the available literature rather than reporting new experimental or clinical data.

Limitations: Narrative review design (not a systematic review or meta-analysis) which may be prone to selection bias in included evidence.; No new primary data are presented in this article.; Abstract indicates the underlying evidence is conflicting, limiting firm conclusions.; Does not provide quantitative pooled estimates of association between MASLD and urinary system cancers..

Review examines potential links and mechanisms between MASLD and urinary system cancers.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 58

Immunohistochemical GATA3 expression in prostate adenocarcinoma: pitfalls

Journal of immunoassay & immunochemistry · Jan 2025 · retrospective study

prostate adenocarcinoma

This retrospective pathology study examined GATA3 immunohistochemical expression in 58 primary prostate adenocarcinomas collected 2019–2024. Nuclear GATA3 staining was observed in 4 of 58 cases (6.9%), all in higher-grade (Gleason 4 components of Gleason 7 [4+3]) tumors; benign glands and seminal vesicles showed rare positivity. The authors highlight that GATA3 can be expressed in prostate cancer and may cause a diagnostic pitfall when distinguishing from urothelial carcinoma.

Reported effects: mean age 67.8, n=58 · GATA3 nuclear expression prevalence 6.9%, n=58 · +4 more

Key findings

Fifty-eight cases have been included in the study with a mean age of 67.8 years-old.
GATA3 nuclear expression was observed in 6.9% (4/58) of cases, all classified as Gleason 7 (4 + 3) and ISUP grade 3.
Only the Gleason 4 or 5 components showed staining, while Gleason 3 components were negative.
Additionally, benign prostate glands and seminal vesicles showed rare GATA3 expression (4/58 and 1/58 cases, respectively).

Limitations: Retrospective, single-center design; Small sample size (58 cases); No clinical outcome or prognostic correlation provided; Immunohistochemistry performed with a single antibody clone/assay (Leica, L50-823) — potential method-dependent variability; No statistical analysis of associations or significance reported in the abstract.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Human · observationalMechanismMixed resultsLimited evidenceTier 3 · early humann = 425

Analysis of real world FRα testing in ovarian, fallopian tube, and primary peritoneal cancers

Gynecologic oncology · Jan 2025 · retrospective study

Mirvetuximab-soravtansineovarian cancerfallopian tube neoplasmsprimary peritoneal neoplasms

This retrospective study looked at 425 tumor samples from people with ovarian, fallopian tube, or primary peritoneal cancers to see how often folate receptor alpha (FRα) was present. FRα was found in 36.3% of cases and was more common in high-grade serous ovarian tumors and in samples from the ovary, fallopian tube, adnexa, or dominant pelvic masses than in metastatic sites. The study also found that some patients had different FRα results in different specimens, suggesting variability in testing results across samples.

Reported effect: positive rates 44.4%, p=0.02

Key findings

FRα was highly expressed in 36.3% of cases.
FRα positivity was significantly associated with high-grade serous ovarian histology.
Samples from the ovary, fallopian tube, adnexa, and dominant pelvic masses had higher FRα positivity than metastatic sites (44.4% vs 32.5%, p = 0.02).
Time between collection and testing did not impact FRα expression.
Among 8 patients with more than one specimen tested, 3 (37.5%) had discordant results.

Limitations: Retrospective single-study biomarker analysis.; No treatment outcomes or patient survival endpoints were reported.; Biomarker testing only; does not test mirvetuximab soravtansine efficacy.; Potential sampling and site-related heterogeneity.; Small subgroup with repeated specimens (n=8)..

Useful for understanding FRα testing patterns relevant to selecting patients for FRα-targeted therapy, but it does not evaluate anticancer efficacy.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Human · observationalReported positiveLimited evidenceTier 3 · early humann = 3

Neoadjuvant chemoimmunotherapy for small cell carcinoma of the esophagus: Clinical efficacy and biomarker exploration

Human vaccines & immunotherapeutics · Dec 2024 · case series (3 patients)

small cell carcinoma of the esophagus (SCCE)

This case series reports three patients with small cell carcinoma of the esophagus treated with chemoimmunotherapy. Two limited-stage patients received neoadjuvant chemoimmunotherapy followed by surgery and experienced notable, durable positive responses. The authors performed immunohistochemistry and whole exome sequencing and found that tumor CD8+ T-cell infiltration and PD-L1 expression were associated with favorable responses. This is described as the first reported use of neoadjuvant chemoimmunotherapy in limited-stage SCCE.

Studied with: chemotherapy, immunotherapy.

Key findings

Three SCCE patients (one extensive-stage, two limited-stage) were treated with chemoimmunotherapy.
The two limited-stage patients underwent surgery after neoadjuvant chemoimmunotherapy and experienced notable and enduring positive responses.
Comprehensive immunohistochemical analysis and whole exome sequencing indicated that infiltration of CD8+ T cells and PD-L1 expression in the tumor were key factors associated with favorable responses to chemoimmunotherapy.

Limitations: Very small sample size (three patients) from a case series; No control or comparison group; Treatment regimen details (drug names, doses, schedules) are not reported in the abstract; Follow-up duration and objective outcome measures are not described in the abstract; Observational case reports cannot establish causality; biomarker associations are exploratory.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Human · observationalReported negativeLimited evidenceTier 3 · early humann = 91

The Clinical Characteristics and Treatment Outcomes of Mesonephric Tumours of the Uterine Cervix: A Systematic Review and Proposal of Embryologically-Oriented Surgical Resection

Journal of clinical medicine · Dec 2024 · systematic review of case reports and case series

mesonephric adenocarcinoma of the uterine cervixcervical mesonephric adenocarcinoma (MNAC)

This systematic review pooled 49 publications describing 91 cases of cervical mesonephric adenocarcinoma. Most reported cases were stage I and hysterectomy was the most common surgical procedure; median follow-up was 29 months. Disease recurrence occurred in about one-third of cases (35.2%) with a median disease-free survival of 24 months; at follow-up 64.8% were in remission and 27.4% died of disease progression. The authors propose an embryologically oriented surgical approach based on their appraisal of existing surgical and adjuvant therapies.

Reported effects: included_publications 49, n=49 · cases_included 91, n=91 · +7 more

Key findings

49 publications were included in the analysis, describing 91 MNAC cases.
Most patients had stage I disease (70.8%) (n = 51).
Hysterectomy was performed in 77 patients.
The median follow-up was 29 months (range 1-199 months).
Disease recurrence was observed in 35.2% (n = 25) of the cases.
Median disease-free survival (DFS) was 24 months (range 1-199).
At follow-up, 64.8% (n = 46) of patients remained in remission irrespective of the treatment modality.
27.4% (n = 20) died due to disease progression.

Limitations: Evidence derives from case reports and case series rather than controlled trials.; Relatively small total number of cases (91) for pooled inference.; Heterogeneous and retrospectively reported treatments and outcomes across included publications.; Potential publication and selection bias inherent to systematic reviews of case reports/series.; Follow-up duration was variable (range 1–199 months) which may affect comparability of outcomes.; No randomized or controlled data available to support the proposed surgical approach..

Systematic review of clinical characteristics, management, and outcomes of cervical mesonephric neoplasms; proposes an embryology-informed surgical resection strategy.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMixed resultsLimited evidenceTier 4 · clinical

Current status of treatment for malignant ovarian sex cord-stromal tumors

Discover oncology · Dec 2024 · narrative review

malignant ovarian sex cord-stromal tumors

This narrative review summarizes current treatment approaches for malignant ovarian sex cord-stromal tumors. The authors state these tumors are often low-grade with generally good prognosis but have a tendency for long-term recurrence with high mortality after recurrence. Surgery is presented as the preferred primary treatment; recurrent or metastatic cases usually receive systemic adjuvant chemotherapy, and hormonal or targeted therapies may be tried individually when chemotherapy fails.

Key findings

Malignant ovarian sex cord-stromal tumors are generally low-grade malignant and have a good prognosis.
These tumors tend to recur in the long term, and mortality after recurrence is high.
Surgery is the preferred primary treatment, often combined with chemotherapy and other comprehensive treatments.
Recurrent and metastatic tumors usually require systemic adjuvant chemotherapy.
Hormonal or targeted therapy may be attempted on an individualized basis when chemotherapy fails.

Limitations: This is a narrative review and presents no new primary data in the abstract.; The abstract provides no quantitative efficacy, survival, or recurrence data.; No methods, selection criteria, or quality assessment of included studies are described in the abstract.; Recommendations appear generalized; the abstract indicates individualized use of hormonal/targeted therapy, implying limited definitive evidence..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Human · observationalReported positiveLimited evidenceTier 3 · early humann = 108

A systematic review of adult pineoblastoma

Frontiers in oncology · Dec 2024 · systematic review

pineoblastoma

This systematic review pooled 108 adult pineoblastoma cases from 32 articles and analyzed survival outcomes. The reported 5-year survival rate was 49.5% and the 10-year survival rate was 33.9%. Gross total resection was associated with better survival than subtotal resection or no surgery (P=0.018), and radiotherapy and chemotherapy were associated with improved survival (P<0.001; P=0.020); radiotherapy was an independent favorable factor in multivariate analysis (P<0.001).

Reported effects: total cases included 108, n=108 · median age at diagnosis 30, n=108 · +7 more

Key findings

Total of 108 adult cases from 32 articles; median age at diagnosis was 30 years.
5-year survival rate was 49.5% (95% confidence interval: 0.378-0.602).
10-year survival rate was 33.9% (95% confidence interval: 0.207-0.476).
During 10-year follow-up, gross total resection was more beneficial than subtotal resection and no surgery (P=0.018).
Radiotherapy and chemotherapy were associated with improved survival (P<0.001; P=0.020).
Multivariate COX analysis identified radiotherapy as an independent factor for beneficial prognosis (P<0.001); gross total resection tended to improve 5-year survival (P=0.079).

Limitations: Small total case number (n=108) compiled from heterogeneous sources (case reports, single-institution series).; Retrospective and observational data; no randomized controlled trials included.; Potential selection and reporting bias across included studies.; Heterogeneity of treatments and follow-up across studies limits causal inference..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 80

Explainable machine learning for predicting recurrence-free survival in endometrial carcinosarcoma patients

Frontiers in artificial intelligence · Dec 2024

endometrial carcinosarcoma

The authors developed an explainable machine learning model to predict recurrence-free survival using clinical, histopathological, chemotherapy and surgical data from a cohort of 80 patients with endometrial carcinosarcoma. In this cohort 32.5% of patients experienced recurrence. The model achieved a concordance index (C-index) of 70.00% (95% CI, 59.38-84.74), and the authors state this approach could help discriminate low- versus high-risk patients. The study is presented as a preliminary, first attempt at this task.

Reported effects: recurrence_rate 32.5%, n=80 · C-index 70% [59.38–84.74], n=80

Key findings

Cohort of 80 endometrial carcinosarcoma patients was analyzed.
32.5% of patients experienced recurrence.
The machine learning model achieved a C-index of 70.00% (95% CI, 59.38-84.74) for ranking survival times.
Authors conclude ML methods could support clinicians in discriminating low-risk vs high-risk of recurrence.

Limitations: Small sample size (80 patients).; Preliminary approach and described as a first study addressing this task.; No external validation of the model is reported in the abstract.; Observational cohort data (potential for overfitting and limited generalizability)..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMixed resultsLimited evidenceTier 4 · clinical

HER2-Positive Serous Endometrial Cancer Treatment: Current Clinical Practice and Future Directions

Medicina (Kaunas, Lithuania) · Dec 2024 · literature review

uterine serous carcinoma (serous endometrial carcinoma)endometrial cancer

This literature review summarizes current HER2-directed therapies for HER2-positive uterine serous (serous endometrial) carcinoma. The authors note that about one-third of serous endometrial cancers overexpress HER2 or have ERBB2 amplification and that clinical trials combining chemotherapy with anti-HER2 agents (mainly trastuzumab, alone or with pertuzumab) have shown promising results and been incorporated into international guidelines. The review also describes ongoing research into antibody–drug conjugates and tyrosine kinase inhibitors and highlights that acquired resistance and other unmet needs remain.

Studied with: chemotherapy, pertuzumab.

Key findings

Approximately one-third of patients with serous endometrial carcinoma may overexpress HER2/neu protein and/or show c-erBb2 (ERBB2) gene amplification.
HER2-directed treatments, especially trastuzumab alone or combined with pertuzumab and chemotherapy, have shown promising results in clinical trials and have been incorporated into international guidelines.
Antibody-drug conjugates and tyrosine kinase inhibitors targeting HER2 are under active investigation in endometrial cancer.
Acquired resistance to HER2-targeted therapies is an important unresolved problem in endometrial cancer and its mechanisms are mostly unknown.
Research is exploring earlier use of HER2-directed therapy in this disease.

Limitations: This is a literature review and does not present new primary experimental or trial data.; The abstract does not state this is a systematic review, so selection and synthesis methods are not described in the abstract.; No quantitative effect sizes or detailed trial outcome data are presented in the abstract.; Mechanistic understanding of acquired resistance in endometrial cancer is reported as largely unknown..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMixed resultsLimited evidenceTier 4 · clinical

SNO-EANO-EURACAN consensus on management of pineal parenchymal tumors

Neuro-oncology · Dec 2024 · consensus review

pineal parenchymal tumorspineocytomapineal parenchymal tumor of intermediate differentiationpineoblastomapapillary tumor of the pineal region

This international consensus review summarizes diagnostic and treatment approaches for rare pineal parenchymal tumors and related intrinsic pineal masses. It highlights recent genomic findings that informed refinements in the WHO 5th edition molecular classification and offers pragmatic clinical management recommendations ranging from surgery alone to intensive multimodal antineoplastic therapy.

Key findings

Pineal parenchymal tumors are rare and lack robust evidence-based treatment recommendations.
These tumors vary in biology, clinical characteristics, and prognosis, necessitating a range of treatments from surgical resection alone to intensive multimodal antineoplastic therapy.
Recent international genomic studies have refined the molecular-based disease classification, incorporated in the WHO 5th edition.
The review summarizes literature on diagnostic and therapeutic approaches and suggests pragmatic recommendations for clinical management of intrinsic pineal region masses (pineocytoma, PPTID, pineoblastoma), pineal cyst, and papillary tumors of the pineal region.

Limitations: Tumors are rare and high-quality evidence is sparse, limiting strength of recommendations.; Recommendations are based on literature review and consensus rather than randomized controlled trials.; Heterogeneity of tumor biology and prognosis may limit generalizability of suggested management approaches.; No new primary quantitative data are reported in this review..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Human · observationalReported positiveLimited evidenceTier 3 · early humann = 10

Real-world evidence of Trastuzumab Deruxtecan (T-DXd) Efficacy in HER2-expressing gynecological malignancies

BMC cancer · Dec 2024 · retrospective cohort

Trastuzumab-deruxtecan-t-dxd Trastuzumab-deruxtecanendometrial neoplasmsovarian neoplasmscervical neoplasmsuterine carcinosarcomauterine leiomyosarcomauterine serous carcinomaovarian carcinosarcomahigh-grade serous ovarian carcinomamucinous ovarian carcinomasquamous cervical carcinoma

This retrospective single-center study identified 10 patients with HER2-expressing (IHC 2+/3+) recurrent or metastatic gynecological cancers who received trastuzumab deruxtecan (5.4 mg/kg IV every 3 weeks). The cohort had a median progression-free survival of 5.4 months (95% CI 0.8-9.8). Five patients had a partial response, one had stable disease at 12 weeks, and four had disease progression at initial assessment. Clinical benefit was observed mainly in tumors with HER2 IHC 3+.

Reported effects: median PFS 5.4 mo [0.8–9.8], n=10 · partial responses 5, n=10 · +2 more

Key findings

10 patients with recurrent/metastatic HER2-expressing gynecological malignancies were treated with T-DXd.
Histologies included uterine neoplasms (n=5), cervical squamous carcinoma (n=1) and ovarian cancers (n=4).
Median age was 65.4 years (25th-75th percentile, 58.1-75.2 years).
HER2 by IHC: 5 patients were 3+ and 5 patients were 2+.
Median number of prior therapy lines was 4 (range 2-6); 2 uterine serous carcinoma patients were pretreated with trastuzumab and 4 patients had prior immunotherapy.
Dose: T-DXd 5.4 mg/kg IV every 3 weeks until progression/toxicity.
Median progression-free survival (PFS) in the cohort was 5.4 months (95% CI 0.8-9.8 months).
Responses: 5 patients had partial response (including 2 previously treated with trastuzumab), 1 patient had stable disease at 12 weeks, 4 patients had disease progression at initial assessment.
Most patients who derived clinical benefit had HER2 IHC 3+ expression.

Limitations: Retrospective, single-center design; Very small sample size (n=10); No control or comparator arm; Heterogeneous mix of gynecologic histologies; Heavily pre-treated population limits generalizability; Limited/absent reporting of safety or adverse event data in the abstract; Potential selection and reporting bias inherent to retrospective series.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMechanismInconclusiveLimited evidenceTier 4 · clinical

Laparoscopic prediction of primary cytoreducibility of epithelial ovarian cancer

Minerva obstetrics and gynecology · Dec 2024 · literature review

epithelial ovarian carcinomaovarian cancer

This review examined published data on using laparoscopy and other minimally invasive methods to predict whether primary debulking surgery can achieve no residual tumor (RT=0) in advanced epithelial ovarian cancer. The authors report that accurate assessment of intra- and extra-abdominal disease using a combination of imaging (MRI, PET, CT), surgical approaches (laparoscopy, mini-laparotomy), and blood markers (CA-125, HE4) helps determine tumor extent and can aid in personalizing the therapeutic approach. The article is a review and does not present new primary quantitative data on predictive accuracy.

Studied with: magnetic resonance imaging, positron emission tomography, computed tomography, laparoscopy, mini-laparotomy, CA-125, HE4.

Key findings

Laparoscopy and other minimally invasive surgical methods have been analyzed as tools to predict the possibility of obtaining residual tumor of 0 (RT=0) in primary debulking surgery for advanced epithelial ovarian carcinoma.
Accurate assessment of intra- and extra-abdominal pathology is essential to guide the surgeon in therapeutic choice.
Combining radiological methods (MRI, PET, CT), surgical approaches (mini-laparotomy, laparoscopy), and serological markers (CA-125, HE4) provides a more complete picture for determining tumor extent and personalizing therapy.

Limitations: This publication is a literature review and presents no new primary patient-level data.; Abstract does not state whether the review was systematic or the methods used for study selection or quality assessment.; No quantitative accuracy metrics (sensitivity, specificity, predictive values) or pooled estimates are reported in the abstract..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed

Human trialTrialReported positiveStrong evidenceTier 4 · clinicaln = 415

Hyperthermic intraperitoneal chemotherapy for recurrent ovarian cancer (CHIPOR): a randomised, open-label, phase 3 trial

The Lancet. Oncology · Dec 2024 · randomised, open-label, phase 3, multicentre trial

Cisplatinepithelial ovarian cancerrecurrent ovarian cancerhigh-grade serous ovarian cancerhigh-grade endometrioid ovarian cancer

This multicentre, randomized phase 3 trial compared cytoreductive surgery with or without intraoperative hyperthermic intraperitoneal cisplatin (HIPEC) in 415 women with first relapse of epithelial ovarian cancer. At a median 6.2 years follow-up, HIPEC improved overall survival (stratified HR 0.73, p=0.024; median OS 54.3 vs 45.8 months) but was associated with higher rates of grade 3 or worse adverse events within 60 days (49% vs 27%).

Reported effects: stratified hazard ratio for overall survival 0.73 [0.56–0.96], p=0.024, n=415 · median overall survival 54.3 mo [41.9–61.7], n=415 · +7 more

Studied with: cytoreductive surgery, platinum-based chemotherapy, bevacizumab (optional), planned PARP inhibitor use (stratification).

Key findings

415 patients randomised: 207 to HIPEC and 208 to no HIPEC.
Overall survival was significantly improved with HIPEC (stratified hazard ratio 0⋅73, 95% CI 0⋅56-0⋅96; p=0⋅024).
Median overall survival was 54⋅3 months (95% CI 41⋅9-61⋅7) with HIPEC versus 45⋅8 months (38⋅9-54⋅2) without.
At primary analysis 268 (65%) patients had died (126 [61%] of 207 in the HIPEC group; 142 [68%] of 208 in the no-HIPEC group).
Grade 3 or worse adverse events within 60 days occurred in 102 (49%) of 207 receiving HIPEC versus 56 (27%) of 208 receiving no HIPEC; common events included anaemia (47 [23%] vs 30 [14%]), hepatotoxicity (23 [11%] vs 18 [9%]), electrolyte disturbance (28 [14%] vs two [1%]), and renal failure (20 [10%] vs three [1%]).
There were three deaths within 60 days of surgery, all in the no-HIPEC group.

Limitations: Open-label design (no blinding).; Increased perioperative grade 3+ toxicity with HIPEC compared with no HIPEC.; Eligibility limited to patients with a first relapse ≥6 months after platinum-based chemotherapy who were amenable to complete cytoreduction; results may not generalise to other patient groups.; Optional use of bevacizumab and later planned PARP inhibitor use introduce heterogeneity in systemic therapy.; Conducted at specialist centres; generalisability to non-specialist settings is uncertain..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 32

Molecular characteristics of tubo-ovarian carcinosarcoma at different anatomic locations

Virchows Archiv : an international journal of pathology · Dec 2024 · targeted next-generation sequencing of tumor specimens (molecular profiling)

tubo-ovarian carcinosarcoma

The authors performed targeted next-generation sequencing of 32 tubo-ovarian carcinosarcoma specimens (including 7 serous effusions) covering 50 genes. They found 31 mutations in 25 of 32 tumors, with TP53 alterations predominant (25 mutations in 24 tumors); other mutations (RB1, MET, KRAS, PTEN, KIT) were rare. Patient-matched specimens shared the same TP53 mutation, and specimens with no detected mutations were more frequent among serous effusions than surgical specimens. The authors conclude TP53 mutations dominate the molecular landscape and note it is uncertain whether effusion-derived cells differ from solid lesions.

Reported effects: specimens_n 32, n=32 · patients_n 25, n=25 · +11 more

Key findings

Specimens (n=32) consisted of 25 biopsies/surgical resection specimens and 7 serous effusions (6 peritoneal, 1 pleural) from 25 patients.
Targeted next-generation sequencing covered 50 unique genes.
A total of 31 mutations were found in 25 of the 32 tumors studied, of which 1 had 3 mutations, 4 had 2 different mutations, and 20 had a single mutation.
The most common mutations were in TP53 (n=25 in 24 tumors; 1 tumor with 2 different mutations).
Less common mutations were found in RB1 (n=2), MET (n=1), KRAS (n=1), PTEN (n=1), and KIT (n=1).
Patient-matched specimens harbored the same TP53 mutation.
Tumors with no detected mutations were more common in serous effusion specimens (3/7; 43%) compared with surgical specimens (4/25; 16%).

Limitations: Small sample size (32 specimens from 25 patients).; Use of a targeted 50-gene panel limits detection to predefined genes and may miss other relevant alterations.; Observational molecular profiling without functional validation of variants.; Unclear generalizability given limited anatomic sampling and small number of effusion specimens..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Human · observationalMixed resultsLimited evidenceTier 3 · early humann = 25

Increase of primary intracranial sarcoma in children: Clinical manifestations, diagnosis, and management

Surgical neurology international · Nov 2024 · retrospective case series

primary intracranial sarcoma

This retrospective case series reviewed 25 children with primary intracranial sarcoma seen at a tertiary hospital in Peru from 2020–2023. Most presented with intracranial hypertension and radiologic hemorrhage; emergency craniotomy was common and gross total resection was achieved in 72% at first surgery. An adjuvant CTX-RT-CTX regimen was given to 72% of cases; among patients followed >1 year, those who started this regimen 2 weeks after gross total resection had survival >1 year compared with those who began complementary treatment after 4 weeks. The authors report an apparent increase in pediatric PIS incidence in recent years at their center.

Reported effects: cases_identified 25, n=25 · median_age 5, n=25 · +7 more

Key findings

Twenty-five pediatric PIS cases identified (study period Jan 2020–Dec 2023).
Median age was 5 years; slight female predominance (56%).
68% presented with features of intracranial hypertension; radiologic cerebral hemorrhage was present in 80% of those with ICH and convulsion.
All but one case had a supratentorial tumor.
Emergency craniotomy was performed in 84% of cases; gross total resection (GTR) at first surgery achieved in 72% of cases.
An adjuvant chemoradiotherapy-chemotherapy (CTX-RT-CTX) regimen was used in 72% of cases; 12% started this regimen 2 weeks after surgical resection.
Cases followed >1 year that received CTX-RT-CTX after GTR had survival >1 year compared with cases that received complementary treatment after 4 weeks.
The authors state the incidence of pediatric PIS has increased in Peru in recent years.

Limitations: Retrospective, single-center case series.; Small sample size (n=25).; No randomized or contemporaneous control group for the timing of adjuvant therapy comparison.; Survival comparison by timing of adjuvant therapy is not quantified and may be confounded by selection and follow-up bias.; Follow-up duration is not fully reported for all cases.; No statistical testing or confidence intervals reported in the abstract..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Human · observationalMechanismMixed resultsLimited evidenceTier 3 · early humann = 47

SOX17 expression in ovarian clear cell carcinoma

Journal of ovarian research · Nov 2024 · Immunohistochemical analysis of 47 OCCC whole-tissue specimens combined with immunoblotting and cell-line experiments

ovarian clear cell carcinoma

The authors examined SOX17 protein expression by immunohistochemistry in 47 ovarian clear cell carcinoma (OCCC) tissue specimens and studied SOX17 expression and regulation in OCCC cell lines. SOX17 expression was heterogeneous across tumors and cell lines; high SOX17 immunoreactivity trended toward worse patient outcomes but this was not statistically significant. In cell lines, SOX17 was abundant in OVISE and RMG-V but low in OVTOKO, where polyubiquitinated SOX17 accumulated after proteasome inhibition. Knockdown of the deubiquitinase UCHL1 in OVISE increased SOX17 polyubiquitination and subsequent proteasome degradation, suggesting impaired ubiquitin-mediated degradation can stabilize SOX17 in some OCCC cells.

Key findings

SOX17-high immunoreactivity tended to be related to unfavorable patient outcomes, although not statistically significant.
Double immunofluorescence staining demonstrated that SOX17 immunoreactivity was not associated with ARID1A immunoreactivity.
Immunoblotting revealed that SOX17 was abundantly expressed in cultured OVISE and RMG-V OCCC cells, but not in OVTOKO OCCC cells.
Polyubiquitinated bands of SOX17 were observed in MG132 treated OVTOKO, but not in OVISE or RMG-V OCCC cells.
si-RNA-mediated knockdown of a deubiquitinase enzyme, ubiquitin C-terminal hydrolase L1, increased polyubiquitination followed by proteasome degradation of SOX17 in OVISE.

Limitations: Observational, descriptive study of human tumor specimens without functional in vivo validation.; Prognostic association (SOX17-high vs outcomes) was not statistically significant.; Relatively small specimen cohort (n=47) limits generalizability and statistical power.; Cell-line findings (three lines) may not represent tumor heterogeneity in patients..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Human trialTrialReported positiveLimited evidenceTier 4 · clinicaln = 36

A randomized trial of pharmacological ascorbate, gemcitabine, and nab-paclitaxel for metastatic pancreatic cancer

Redox biology · Nov 2024 · randomized 1:1 controlled trial

Gemcitabine Sodium-butyratepancreatic ductal adenocarcinoma (metastatic)

This randomized trial compared standard gemcitabine plus nab-paclitaxel chemotherapy with or without high-dose intravenous vitamin C (75 g three times weekly) in patients with metastatic pancreatic cancer. Adding pharmacological ascorbate increased median overall survival (16 vs 8.3 months) and median progression-free survival (6.2 vs 3.9 months) and did not increase adverse events or worsen quality of life. The trial randomized 36 patients (34 received assigned treatment).

Reported effects: median overall survival 16 mo · HR overall survival 0.46 [0.23–0.92], p=0.03 · +3 more

Studied with: gemcitabine + nab-paclitaxel.

Key findings

Intravenous P-AscH- increased serum ascorbate levels from micromolar to millimolar levels.
P-AscH- added to gemcitabine + nab-paclitaxel (ASC) increased overall survival to 16 months compared to 8.3 months with gemcitabine + nab-paclitaxel (SOC) (HR = 0.46; 90 % CI 0.23, 0.92; p = 0.030).
Median progression free survival was 6.2 (ASC) vs. 3.9 months (SOC) (HR = 0.43; 90 % CI 0.20, 0.92; p = 0.029).
Adding P-AscH- did not negatively impact quality of life or increase the frequency or severity of adverse events.

Limitations: Small randomized sample (36 randomized, 34 treated) limits precision and generalizability.; Abstract reports 90% confidence intervals rather than the more conventional 95% CIs.; Trial phase and longer-term follow-up details are not reported in the abstract.; Single randomized trial; results require confirmation in larger studies..

Randomized clinical trial testing high-dose intravenous vitamin C added to first-line chemotherapy in metastatic pancreatic cancer with overall and progression-free survival endpoints.

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMechanismInconclusiveLimited evidenceTier 3 · early human

Advance of Circulating Tumor Cells in the Prognosis and Management of Endometrial Cancer

Cancer investigation · Nov 2024

endometrial cancer

This narrative review summarizes published evidence about circulating tumor cells (CTCs) and disseminated tumor cells (DTCs) in endometrial cancer. The authors report that a growing body of evidence suggests CTCs may provide a more complete tumor profile, help understand molecular mechanisms, and assist individual patient management. The review emphasizes the presence and clinical applications of CTCs/DTCs for prognosis and management and highlights the diagnostic value of tumor cells detected in urine.

Key findings

Endometrial cancer mortality has been increasing over the last twenty years (statement of clinical context).
A growing body of evidence suggests that circulating tumor cells (CTCs) may provide a more complete tumor profile and facilitate understanding of molecular mechanisms and individual management of endometrial cancer patients.
The review presents the presence and clinical applications of CTCs and disseminated tumor cells (DTCs) in endometrial cancer, with particular emphasis on prognosis and management.
The authors highlight the diagnostic value of tumor cells found in the urine of endometrial cancer patients.

Limitations: Narrative review only—no original primary data reported in this article.; Abstract does not specify search methods or criteria, so potential for selection bias or incomplete coverage of the literature.; No quantitative synthesis (meta-analysis) or new numerical results presented in the abstract..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 169

Progesterone receptor isoform B in the stroma of squamous cervical carcinoma: An independent favorable prognostic marker correlating with hematogenous metastasis

Taiwanese journal of obstetrics & gynecology · Nov 2024 · retrospective cohort study

squamous cervical carcinoma

This retrospective cohort study examined ERα, PR (A+B) and PRB expression in tumor and stromal compartments of 169 cervical carcinoma samples. Stromal PRB expression was associated with lower 5-year cancer mortality and with lower rates of hematogenous metastasis, and remained an independent predictor of lower 5-year mortality in multivariable analysis. Adding stromal PR or PRB to FIGO stage improved survival prediction accuracy.

Reported effects: stromal PRB association with 5-year mortality, p=0.011, n=169 · stromal ERα association with hematogenous distant metastasis rates, p=0.013, n=169 · +2 more

Key findings

ERα and PRs were predominantly expressed in the stromal compartment rather than within cervical cancer cells.
Stromal PRB expression significantly correlated with a lower 5-year mortality because of cervical cancer (p = 0.011).
Stromal ERα and PRB expressions correlated with lower hematogenous distant metastasis rates (p = 0.013 and p = 0.011, respectively).
In multivariable logistic regression analyses, stromal PRB independently conferred a lower risk of 5-year mortality (p = 0.022) regardless of age, histology, FIGO stage, tumor differentiation, lymphovascular space invasion, and lymphatic and hematogenous metastases.
Incorporation of stromal PR (A + B) and PRB expression into FIGO stage significantly enhanced the accuracy of survival prediction.

Limitations: Retrospective, observational single-center design; Correlative biomarker study that cannot establish causation; Potential subjectivity in immunohistochemical scoring by pathologists; No external validation cohort reported in the abstract; Abstract does not report effect sizes (HRs/ORs) or confidence intervals for the associations.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Human · observationalMechanismReported positiveModerate evidenceTier 3 · early humann = 122

STK11 (LKB1) immunohistochemistry is a sensitive and specific marker for STK11 adnexal tumours

Histopathology · Nov 2024 · immunohistochemical analysis of a cohort of human tumours (122 cases) including STK11 adnexal tumours and morphological mimics

STK11 adnexal tumourovarian neoplasmsovarian endometrioid carcinomatubo-ovarian high-grade serous carcinomaovarian mesonephric-like adenocarcinomaovarian carcinosarcomaperitoneal malignant mesotheliomapelvic plexiform leiomyomaovarian solid pseudopapillary tumourgranulosa cell tumourSertoli-Leydig cell tumourLeydig cell tumourSertoli cell tumoursteroid cell tumourfemale adnexal tumour of Wolffian originextra-ovarian sex cord-stromal tumour

Researchers performed STK11 (LKB1) immunohistochemistry on 122 human tumour samples, including 17 STK11 adnexal tumours and 105 morphological mimics. All 17 STK11 adnexal tumours showed complete loss of cytoplasmic STK11 staining. Nearly all other tumour types retained cytoplasmic STK11 staining, with the exception of one endometrioid carcinoma with mucinous differentiation showing complete loss and one high-grade serous carcinoma showing subclonal loss. The authors conclude STK11 IHC is a highly sensitive and specific marker for distinguishing STK11 adnexal tumour in the appropriate morphological context and could obviate confirmatory molecular testing.

Reported effects: total tumours tested 122, n=122 · STK11 adnexal tumours included 17, n=17 · +3 more

Key findings

IHC for STK11 was performed on 122 tumours, including 17 STK11 adnexal tumours and 105 morphological mimics (full list of mimics given in abstract).
All STK11 adnexal tumours showed complete loss of cytoplasmic staining for STK11.
All other tumour types showed retained cytoplasmic staining, except for one endometrioid carcinoma with mucinous differentiation which showed complete loss of STK11 expression and a high-grade serous carcinoma with subclonal loss.
Authors conclude STK11 IHC is a highly sensitive and specific immunohistochemical marker for distinguishing STK11 adnexal tumour from histological mimics and may obviate the need for confirmatory molecular studies in the appropriate morphological context.

Limitations: Small number of STK11 adnexal tumours (n=17), reflecting rarity of the entity.; Study reports a single cohort with no external validation cohort mentioned in the abstract.; Potential selection bias because tumour types were a selected set of morphological mimics.; Abstract does not report blinding, interobserver reproducibility, or diagnostic performance statistics (sensitivity/specificity values) beyond descriptive counts.; Two non-STK11 tumours showed loss/subclonal loss of STK11, indicating imperfect specificity in this cohort..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Human · observationalMechanismMixed resultsLimited evidenceTier 3 · early humann = 289

Molecular classification of ovarian high-grade serous/endometrioid carcinomas through multi-omics analysis: JGOG3025-TR2 study

British journal of cancer · Nov 2024 · multi-omics molecular profiling of tumor cohort (targeted DNA sequencing, RNA sequencing, DNA methylation array, SNP array) with unsupervised clustering

ovarian high-grade endometrioid carcinoma (HGEC)ovarian high-grade serous carcinoma (HGSC)endometrial high-grade carcinoma

The authors performed multi-omics profiling (DNA/RNA sequencing, methylation, SNP arrays) of ovarian high-grade endometrioid and serous carcinomas from the JGOG-TR2 cohort and analyzed public TCGA data. They identified four copy-number-based tumor groups (C1–C4); one group (C4, denoted 'HGEC-type') showed endometrium-like methylation, lack of BRCA1/2 alterations and CCNE1 amplification, low HRD scores, and more favorable prognosis.

Reported effects: JGOG-TR2 HGEC sample count 15 · JGOG-TR2 HGSC sample count 274 · +6 more

Key findings

Unsupervised clustering using copy number signatures identified four distinct tumor groups (C1, C2, C3 and C4).
C1 (n = 41) showed CCNE1 amplification and poor survival.
C2 (n = 160) and C3 (n = 59) showed high BRCA1/2 alteration frequency with low and moderate ploidy, respectively.
C4 (n = 22) was characterized by favorable outcome, higher HGEC proportion, no BRCA1/2 alteration or CCNE1 amplification, and low levels of HRD score, ploidy, intra-tumoral heterogeneity, cell proliferation rate, and WT1 gene expression.
C4 exhibited a normal endometrium-like DNA methylation profile and was defined as 'HGEC-type' tumors, which were also identified in TCGA-OV and TCGA-UCEC.

Limitations: Observational, cross-sectional molecular profiling without interventional or functional validation.; Relatively small number of HGEC samples in the primary cohort (15 HGEC samples) and small size of the C4 subgroup (n = 22).; Prognostic associations are reported but the abstract does not detail adjustment for potential clinical confounders or independent validation beyond TCGA re-analysis.; No therapeutic implications or prospective clinical validation provided in the abstract..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMechanismInconclusiveModerate evidenceTier 3 · early human

The "Other" Uterine Mesenchymal Neoplasms: Recent Developments and Emerging Entities

Advances in anatomic pathology · Nov 2024 · review

uterine mesenchymal neoplasmsinflammatory myofibroblastic tumorperivascular epithelioid cell tumoruterine tumor resembling ovarian sex cord tumorembryonal rhabdomyosarcomaNTRK-rearranged uterine sarcomaSMARCA4-deficient uterine sarcomaKAT6B/A::KANSL1 fusion uterine sarcomaMEIS1::NCOA2/1 fusion sarcoma

This narrative review summarizes recent developments in uncommon uterine mesenchymal tumors. It describes how increased molecular testing has improved understanding of their biology, led to recognition of new tumor entities (including NTRK-rearranged and SMARCA4-deficient sarcomas), and identified molecular alterations that may allow targeted therapy in some cases.

Key findings

Molecular testing has improved appreciation of the pathobiology of uterine mesenchymal neoplasms.
Identification of specific molecular alterations has permitted targeted therapy options in tumors that were typically unresponsive to conventional therapies.
Recognition that a subset of these tumors can have a hereditary basis.
Review discusses several uncommon tumors (inflammatory myofibroblastic tumor, perivascular epithelioid cell tumor, uterine tumor resembling ovarian sex cord tumor, embryonal rhabdomyosarcoma) and emerging entities (NTRK-rearranged, SMARCA4-deficient, KAT6B/A::KANSL1 fusion, MEIS1::NCOA2/1 fusion sarcomas).

Limitations: Narrative review with no new primary data reported in the abstract.; Abstract provides no methods, search strategy, inclusion/exclusion criteria, or sample sizes.; Findings are descriptive; no quantitative outcomes or systematic synthesis presented in the abstract.; Clinical implications (targeted therapy options) are described generally; efficacy or outcomes data are not provided in the abstract..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Case reportInconclusiveLimited evidenceTier 3 · early humann = 1

Case report: a rare case of duodenal metastasis of endometrial carcinosarcoma

Frontiers in oncology · Oct 2024 · case report

endometrial carcinosarcoma

This is a case report describing a rare instance of duodenal metastasis originating from endometrial carcinosarcoma. The abstract notes that endometrial carcinosarcoma contains both carcinoma and sarcoma elements, is aggressive with high recurrence and mortality, most commonly affects postmenopausal women, and typically metastasizes to lymph nodes, lungs, and the peritoneum.

Key findings

Reported a rare case of duodenal metastasis from endometrial carcinosarcoma.
Endometrial carcinosarcoma is described as a tumor with both carcinoma and sarcoma components and is typically aggressive with high recurrence and mortality.
Typical metastatic sites listed in the abstract are lymph nodes, lungs, and peritoneum.

Limitations: Single-patient case report (n=1), so findings are not generalizable.; Abstract provides no details about the patient’s clinical course, treatments, diagnostic imaging, or pathology findings.; No control group or systematic data collection; purely descriptive..

Descriptive clinical case report documenting an uncommon metastatic site for an aggressive endometrial tumor; not an interventional study.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Case reportInconclusiveLimited evidenceTier 3 · early humann = 1

Metastatic Small Cell Carcinoma of the Stomach

ACG case reports journal · Oct 2024 · case report

gastric small cell carcinomaGSCCsmall cell carcinoma of the stomach

This is a single-patient case report describing a 57-year-old man who presented with partial gastrointestinal obstruction and was found to have primary stage IV gastric small cell carcinoma with liver metastases. The authors note GSCC is a rare, aggressive neuroendocrine tumor with early widespread metastasis and historically poor overall survival (<12 months), and that treatment regimens often mirror those used for small cell lung carcinoma because of histopathologic similarity.

Key findings

Primary gastric small cell carcinoma (GSCC) is an extremely rare type of small cell carcinoma.
GSCC has an aggressive nature with early widespread metastasis and late detection, giving it a poor prognosis with overall survival of <12 months.
GSCC is a type of neuroendocrine tumor and, because of histopathological similarity to small cell lung carcinoma (SCLC), treatment regimens of GSCC include the same chemotherapy agents as SCLC.
Case reported: a 57-year-old man presented with signs of partial gastrointestinal obstruction and was found to have a primary stage IV GSCC with metastasis to the liver.

Limitations: Single-patient case report — findings are not generalizable.; No experimental intervention or comparative data reported.; No quantitative outcomes or follow-up data provided for this patient.; Prognostic statistic (<12 months overall survival) is presented as background rather than as a result from this case..

Clinical case description of a rare, aggressive gastric small cell carcinoma with metastatic disease.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Human · observationalMechanismReported negativeLimited evidenceTier 3 · early humann = 289

Race- associated molecular differences in uterine serous carcinoma

Frontiers in oncology · Oct 2024 · retrospective cohort genomic analysis

endometrial adenocarcinomauterine serous carcinoma

This single-institution retrospective study analyzed FoundationOne CDx genomic results from 289 patients with advanced or recurrent endometrial adenocarcinoma (January 2017–August 2022). Uterine serous carcinoma (USC) was more common among Black patients and CCNE1 amplification was more frequent in Black versus White patients; tumors with CCNE1 amplification had a high rate of progression within 12 months of first-line platinum and were associated with shorter median overall survival. PI3K/AKT/mTOR pathway mutations were reported less frequently in Black patients but that difference did not reach statistical significance in this report.

Reported effects: cohort size and racial composition, n=289 · USC proportion of tested tumors 26.3%, n=289 · +7 more

Key findings

Total cohort: 289 patients (29.4% Black, 52.6% White).
USC comprised 26.3% (76 of 289) of tested tumors; of USC tumors, 33 of 76 (44%) were Black.
USC occurred more frequently in Black patients (33 of 85 [38.8%] Black patients compared to 30 of 152 [19.7%] White patients, p<0.05).
Among USC, CCNE1 amplification occurred more frequently in Black patients than in White patients (12 of 33 [36.36%] vs 2 of 30 [6.67%], p<0.05).
PI3K/AKT/mTOR pathway mutations occurred less frequently among Black USC patients (16 of 33 [48.5%] vs 26 of 33 [86.7%], p=0.17).
Among patients with CCNE1 amplification, 73.3% (11 of 15) progressed on or within 12 months of first-line platinum-based therapy.
CCNE1 amplification was associated with shorter median overall survival (97.3 months vs 44.3; HR (95%CI): 7.1 (10.03, 59.4) p< 0.05).

Limitations: Single-institution, retrospective design which may introduce selection bias.; Small subgroup sizes for key comparisons (e.g., 15 patients with CCNE1 amplification), limiting precision.; Abstract does not report multivariable adjustment for potential confounders.; Some subgroup denominators and statistical reporting in the abstract appear inconsistent, which may affect interpretation..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMechanismReported positivePreclinical onlyTier 1 · lab

Component Composition and Features of Biological Activity of Viscum album (Viscaceae)

Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sections · Oct 2024

This is a review of the European mistletoe (Viscum album) summarizing its chemical composition and reported biological activities. The authors list main secondary metabolites (viscotoxins, lectins, carbohydrates, amino acids, flavonoids, triterpene acids, and nitrogenous compounds) and state that mistletoe extracts and components have antitumor, immunomodulatory, antidiabetic activities and may improve cognitive function.

Key findings

Major constituents listed include viscotoxins, lectins, carbohydrates, amino acids, flavonoids, triterpene acids, and nitrogenous compounds.
Mistletoe extracts and individual components are reported to exert antitumor, immunomodulatory, and antidiabetic activities, and to improve cognitive functions.

Limitations: This publication is a review and presents no new experimental data.; The abstract does not specify study types, models (in vitro, animal, human), doses, or quantitative results.; No specific cancer types, clinical trial data, or detailed mechanisms are provided in the abstract..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed

Lab · in vitroReported positivePreclinical onlyTier 1 · lab

Multifaceted Characterization and Therapeutic Evaluation of Co-precipitated Cobalt Ferrite Nanoparticles for Magnetic Hyperthermia Cancer Therapy

Journal of medical physics · Oct 2024

breast cancer (MCF-7 cell line)

Researchers synthesized cobalt ferrite (CoFe2O4) nanoparticles by chemical co-precipitation, characterized their structural and magnetic properties, and measured a zeta potential of -0.0048 V (4.8 mV). In vitro tests on MCF-7 breast cancer cells showed decreased cell viability with increasing nanoparticle concentrations; antimicrobial activity was also reported. The authors state the zeta potential was higher than that of MCF-7 cells and interpreted this as indicating effectiveness.

Reported effect: zeta potential -0.0048

Key findings

CoFe2O4 nanoparticles synthesized by chemical co-precipitation showed cubic structure, ferrite phase, and spherical magnetic nature.
The zeta potential was found to be - 0.0048V (4.8 mV).
Cytotoxicity analysis exhibited decreased cell viability with increasing concentrations of CoFe2O4 nanoparticles (in vitro, MCF-7 cells).
Antimicrobial studies displayed good inhibiting properties.
The authors state the zeta potential of the synthesized CoFe2O4 nanoparticles was higher than that of the breast cancer cells (MCF-7) and interpreted this as proof of effectiveness.

Limitations: In vitro study only (no animal or human data).; Abstract does not report quantitative cytotoxicity metrics (no percent viability values, no concentrations, no sample sizes, no statistical values).; No experiments described that apply magnetic hyperthermia (despite the stated aim).; No control or comparator details reported in the abstract.; Zeta potential value presentation is internally inconsistent (reported as "- 0.0048V (4.8 mV)") and lacks context for biological interpretation.; No mechanistic molecular data reported; conclusions about efficacy appear to be interpretive rather than demonstrated in vivo..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMixed resultsModerate evidenceTier 4 · clinical

NCCN Guidelines® Insights: Ovarian Cancer/Fallopian Tube Cancer/Primary Peritoneal Cancer, Version 3.2024

Journal of the National Comprehensive Cancer Network : JNCCN · Oct 2024 · Practice guideline / guideline insights

Ovarian CancerFallopian Tube CancerPrimary Peritoneal Cancer

These NCCN Guidelines Insights summarize multidisciplinary diagnostic workup, staging, and treatment recommendations for ovarian, fallopian tube, and primary peritoneal cancers. The report specifically describes how the evolving use of PARP inhibitors as maintenance and single-agent regimens informed the panel's recommendations.

Key findings

NCCN Guidelines provide multidisciplinary diagnostic workup, staging, and treatment recommendations for ovarian, fallopian tube, and primary peritoneal cancers.
The Insights detail how the evolution of the use of PARP inhibitors as maintenance and single-agent regimens informed panel recommendations in the guidelines.

Limitations: Abstract is a guideline summary and does not present original trial data or numerical results.; No specific recommendations, dosing, comparative efficacy, or level-of-evidence details are provided in the abstract.; Limited methodological detail in abstract about how evidence was reviewed or how recommendations were updated..

Guideline update addressing clinical management of ovarian/fallopian tube/primary peritoneal cancers with attention to PARP inhibitor use.

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed

Human · observationalInconclusiveLimited evidenceTier 3 · early human

Early-Life Factors and Early-Onset Endometrial Cancer Risk in the UK Biobank

JAMA network open · Oct 2024 · case-control

endometrial cancer

This is a case-control analysis of UK Biobank data that examined eight early-life factors in relation to risk of early-onset endometrial cancer among UK residents. The abstract states the study aim and design but does not report any results or effect estimates.

Key findings

The study investigated associations between 8 early-life factors and early-onset endometrial cancer risk using a case-control design in UK Biobank data.

Limitations: Abstract does not report any results, effect sizes, sample sizes, or statistical significance.; Observational case-control design is susceptible to confounding and bias.; Generalisability may be limited to UK Biobank participants/UK residents..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Case reportMechanismReported positiveLimited evidenceTier 3 · early humann = 2

Ever Expanding Morphologic Patterns of Mesonephric-like Adenocarcinomas of the Uterine Corpus: A Report of Two Tumors and a Brief Review of the Literature

International journal of surgical pathology · Oct 2024 · Report of two tumors (case reports) and brief literature review

mesonephric-like adenocarcinoma of the endometriumintestinal-type mucinous carcinoma (mimic)carcinosarcoma of the endometrium (mimic)

The authors report two cases of mesonephric-like adenocarcinoma (MLA) of the uterine corpus and provide a brief literature review. They describe two additional morphologic patterns for MLA: intestinal goblet cells that can mimic intestinal-type mucinous carcinoma, and squamous differentiation with spindle and epithelioid cells that can mimic carcinosarcoma. The abstract states that unique morphology, characteristic immunohistochemical staining patterns, molecular alterations, and pathologist awareness enable accurate identification of this tumor type.

Key findings

Mesonephric-like adenocarcinoma of the endometrium shows a variety of morphologic appearances (small glands, tubules with eosinophilic luminal material, papillary patterns, spindled cells, solid, corded and hyalinized patterns).
This report adds two additional morphologic patterns for MLA: (1) intestinal goblet cells mimicking intestinal-type mucinous carcinoma, and (2) squamous differentiation with spindle and epithelioid cells mimicking carcinosarcoma of the endometrium.
Accurate identification of MLA is possible through unique morphology, characteristic immunohistochemical staining patterns, molecular alterations, and awareness by pathologists.

Limitations: Very small sample size (two tumors / case reports).; No clinical outcome, treatment, or follow-up data provided in the abstract.; Brief review only; details of immunohistochemical or molecular findings are not provided in the abstract..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Human · observationalMechanismReported positiveLimited evidenceTier 3 · early human

Mesothelin promotes the migration of endometrioid carcinoma and is associated with the MELF pattern

Pathology, research and practice · Oct 2024 · Laser microdissection and RNA sequencing comparing EC with the MELF pattern; generation of MSLN-knockout and -knockdown endometrioid carcinoma cell lines for functional assays; immunohistochemical analysis of clinical tumor samples and comparison of blood CA125 levels.

endometrioid carcinomaendometrial neoplasms

The authors found mesothelin (MSLN) expression was predominant in endometrioid carcinoma cases with the MELF pattern. In cell-line experiments, MSLN promoted cell migration and epithelial–mesenchymal transition and regulated cadherin-6 (CDH6); CA125 was shown to regulate CDH6 via MSLN. Immunohistochemistry and blood measurements showed higher MSLN, CA125, and CDH6 in tumors with the MELF pattern.

Key findings

MSLN was predominantly expressed in endometrioid carcinoma cases with the MELF pattern identified by laser microdissection and RNA sequencing.
MSLN promoted migration and epithelial-mesenchymal transition (EMT) in MSLN-knockout and -knockdown endometrioid carcinoma cell lines.
Cadherin-6 (CDH6) expression was regulated by MSLN.
CA125 can regulate CDH6 expression via MSLN.
Immunohistochemical analyses showed MSLN, CA125, and CDH6 expression levels were considerably elevated in endometrioid carcinoma with the MELF pattern.
CA125 expression in tumors paralleled MSLN in staining intensity and also matched blood CA125 level patterns reported.

Limitations: Abstract does not report sample sizes for the clinical/immunohistochemical analyses.; Mechanistic functional data derive from cell-line (in vitro) knockout/knockdown models, not from in vivo models.; Correlative immunohistochemical findings do not prove causation in human tumors.; No clinical outcomes or intervention trial data are reported to link MSLN expression to patient prognosis or therapy response..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Human · observationalMechanismReported positiveLimited evidenceTier 3 · early human

Extrachromosomal circular DNAs in prostate adenocarcinoma: global characterizations and a novel prediction model

Frontiers in pharmacology · Sep 2024 · Bioinformatic analysis of Circular_seq and TCGA-PRAD transcriptome data with Cox and Lasso regression to build a prognostic risk model; immune infiltration and drug sensitivity analysed using in silico immunological algorithms

prostate adenocarcinoma

The authors mapped extrachromosomal circular DNA (eccDNA) in prostate adenocarcinoma and adjacent normal prostate tissues and integrated these data with TCGA-PRAD transcriptomes. They identified eccDNA-amplified differentially expressed coding genes, selected ZNF330 and PITPNM3 as key genes, and built a two-gene risk model. The high-risk group had worse survival, showed altered immune infiltration and features suggesting less likelihood of response to anti-CTLA-4/PD-1 therapies, and drug-sensitivity analysis nominated 10 drugs for further consideration.

Reported effects: differentially_expressed_eccDNAs 4290 · coding_genes_amplified_by_eccDNA 1981 · +2 more

Key findings

No significant difference in eccDNA size, type, or chromosomal distribution between PRAD and para-cancerous normal prostate tissues.
4,290 differentially expressed eccDNAs were identified and 1,981 coding genes were amplified.
499 eccDNA-amplified differentially expressed coding genes (eDEGs) were tested with the TCGA-PRAD transcriptome dataset.
Cox and Lasso regression identified ZNF330 and PITPNM3 as eccDNA-amplified key differentially expressed genes (eKDEGs) in PRAD.
A two-gene risk model based on ZNF330 and PITPNM3 stratified patients: the high-risk group was associated with poorer prognosis and this was validated in external data.
High-risk group was associated with altered immune cell infiltration, negative association with anti-CTLA-4/anti-PD-1 response and lower mutational burden, and showed features suggestive of immune escape by TIDE analysis.
Drug sensitivity analyses identified 10 drugs potentially instructive for PRAD treatment.

Limitations: Observational, bioinformatic study without prospective clinical validation of the prognostic model.; No functional or experimental (wet-lab) validation of the identified eKDEGs (ZNF330, PITPNM3) reported in the abstract.; In silico immunotherapy response predictions and drug sensitivity results were not tested in treated patients and require clinical validation.; Abstract does not report sample size or detailed cohort composition for the sequencing experiments..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Meta-analysisMixed resultsModerate evidenceTier 4 · clinical

Efficacy and safety of rucaparib in patients with recurrent high-grade ovarian carcinoma: A systematic review and meta-analysis

Taiwanese journal of obstetrics & gynecology · Sep 2024 · systematic review and meta-analysis

Rucaparibrecurrent high-grade ovarian carcinomaovarian cancer

This systematic review and meta-analysis pooled seven studies of rucaparib in patients with recurrent high-grade ovarian carcinoma. The pooled objective response rate (ORR) was 0.331 (95% CI 0.221–0.449) with high between-study heterogeneity (I2 = 92.4%), and the authors report improvements in PFS and OS versus controls. Safety signals were substantial: 98.7% experienced any treatment-emergent adverse event and 61% had grade ≥3 events; common AEs and hematologic abnormalities were reported.

Reported effects: number_of_articles 7 · ORR 0.331 [0.221–0.449] · +10 more

Key findings

The meta-analysis of seven articles revealed a pooled objective response rate (ORR) of 0.331 (95% CI, 0.221-0.449; I2=92.4%), particularly evident in the BRCA-mutated cohort.
Rucaparib consistently outperformed controls in progression-free survival (PFS) and overall survival (OS).
Safety evaluations indicated that 98.7% of patients experienced treatment-emergent adverse events (TEAEs), with 61% being grade 65;3.
Notable TEAEs included nausea (69.0%), fatigue (66.8%), vomiting (37.3%), and constipation (32.1%).
Hematological concerns comprised anemia (47.9%), thrombocytopenia, elevated AST/ALT (37.3%), and serum creatinine levels (19.7%).
The authors note that the rucaparib group recorded higher event rates across various metrics than controls and recommend careful monitoring and dose adjustments.

Limitations: High between-study heterogeneity (I2 = 92.4%) reported for the pooled ORR.; Pooled estimate derived from seven articles only, which may limit generalizability.; Abstract reports no numeric effect sizes (HRs/CIs) for PFS or OS despite stating improvements versus controls.; High rates of treatment-emergent adverse events and grade 65;3 events raise tolerability concerns affecting applicability..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed

Human trialTrialReported positiveStrong evidenceTier 4 · clinicaln = 100

First-line bevacizumab plus chemotherapy in Chinese patients with stage III/IV epithelial ovarian cancer, fallopian tube cancer or primary peritoneal cancer: a phase III randomized controlled trial

Journal of gynecologic oncology · Sep 2024 · Phase III randomized controlled trial, randomized 1:1

Bevacizumabepithelial ovarian cancerfallopian tube cancerprimary peritoneal cancer

This randomized phase III trial assigned 100 Chinese patients with newly diagnosed stage III/IV epithelial ovarian, fallopian tube, or primary peritoneal cancer after surgery to carboplatin/paclitaxel with either bevacizumab or placebo. Median progression-free survival was 22.6 months with bevacizumab plus chemotherapy versus 12.3 months with placebo plus chemotherapy (stratified HR 0.30, 95% CI 0.17–0.53). Treatment-related grade 3/4 adverse events were more frequent in the bevacizumab arm.

Reported effects: median PFS 22.6 mo · stratified hazard ratio for PFS 0.3 [0.17–0.53] · +1 more

Studied with: carboplatin, paclitaxel.

Key findings

Of randomized patients, 51 received bevacizumab + CP and 49 received placebo + CP.
Median PFS was 22.6 months with bevacizumab + CP (95% confidence interval [CI]=18.6, not estimable) and 12.3 months (95% CI=9.5, 15.0) with placebo + CP (stratified hazard ratio=0.30; 95% CI=0.17, 0.53).
Treatment-related grade 3/4 adverse events occurred in 46 of 49 (94%) patients receiving bevacizumab + CP, and 34 of 50 (68%) receiving placebo + CP.

Limitations: Relatively small randomized sample (100 patients).; Primary endpoint was investigator-assessed PFS (no central review stated).; Overall survival and longer-term outcomes not reported in the abstract.; Single-country (China) population may limit generalizability to other populations.; Adverse-event denominators reported in the abstract are inconsistent with the randomized-arm counts, which complicates interpretation of safety rates..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewInconclusiveLimited evidenceTier 4 · clinical

Locally advanced and metastatic endometrial cancer: Current and emerging therapies

Cancer treatment reviews · Sep 2024

endometrial cancer

This is a narrative review summarizing historical, current, and emerging therapies for locally advanced and metastatic endometrial cancer. It describes how tumor sequencing and The Cancer Genome Atlas classification have informed clinical practice and clinical trials, and highlights targeted therapies, hormonal therapies, and immunotherapy, including combinatorial approaches to overcome resistance.

Studied with: targeted therapies, immune checkpoint inhibitors, hormonal therapies.

Key findings

Tumor sequencing and The Cancer Genome Atlas classification have been major advancements informing management.
Clinical trials are investigating targeted therapies against signaling pathways, immune checkpoints, DNA integrity, growth factors, hormonal signaling, and metabolism.
Numerous trials are testing combinations of targeted therapies to overcome tumoral resistance, compensatory mechanisms, and tumor polyclonality.
The review particularly highlights clinical research on targeted and hormonal therapies, and also immunotherapy, reflecting an evolving treatment landscape.

Limitations: Narrative review without primary patient-level data or new experimental results presented in this article.; No quantitative treatment outcomes or effect sizes reported in the abstract.; Not a systematic review or meta-analysis (methodology for study identification/selection not described in abstract)..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Case reportReported negativeLimited evidenceTier 3 · early humann = 1

Primary ovarian leiomyosarcoma: a case report

The Journal of international medical research · Sep 2024 · case report

Gemcitabineovarian leiomyosarcoma

This is a case report of a woman in her late 50s diagnosed with primary ovarian leiomyosarcoma who underwent surgery. One month after surgery she received gemcitabine plus docetaxel chemotherapy for six months. Recurrence in the pelvic cavity was detected eight months after surgery. The report aims to raise awareness of this rare disease.

Reported effects: chemotherapy_duration 6 mo, n=1 · time_to_recurrence 8 mo, n=1

Studied with: gemcitabine + docetaxel.

Key findings

A woman in her late 50s presented with a 6-month history of abdominal pain and imaging revealed a pelvic mass.
She underwent surgery and was diagnosed with primary ovarian leiomyosarcoma.
One month postoperatively she began gemcitabine and docetaxel chemotherapy and continued this treatment for 6 months.
Eight months postoperatively recurrence was detected in the pelvic cavity.

Limitations: Single-patient case report (n=1), limiting generalizability; No chemotherapy doses or detailed regimen parameters provided; Short follow-up reported (recurrence at 8 months) with no long-term outcome data; No control or comparator group.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMechanismInconclusiveLimited evidenceTier 4 · clinical

Neuroendocrine neoplasms of the thymus

Frontiers in immunology · Aug 2024 · review

neuroendocrine neoplasms of the thymustypical carcinoidatypical carcinoidlarge cell neuroendocrine carcinomasmall cell carcinomathymus neoplasms

This is a narrative review summarizing neuroendocrine neoplasms of the thymus (tNENs), including typical and atypical carcinoid, large cell neuroendocrine carcinoma, and small cell carcinoma. The authors note these tumors are rare, that clinical and pathological data are scarce, and that tNENs share features with neuroendocrine neoplasms in other organs (notably the lung) while also having some distinct clinical and pathological characteristics; the review focuses on pathologic diagnosis and differential diagnosis.

Key findings

tNENs include typical carcinoid, atypical carcinoid, large cell neuroendocrine carcinoma, and small cell carcinoma.
These tumors are rare and there are scarce clinical and pathological data available in the literature.
tNENs share many common features with neuroendocrine neoplasms in other organs (such as the lung) but also demonstrate some distinct clinical and pathological features.
The review primarily focuses on pathologic diagnosis and differential diagnosis of tNENs.

Limitations: Narrative review rather than original research; no new primary data are reported.; Abstract states clinical and pathological data on tNENs are scarce, limiting conclusions.; No quantitative results, methods, or systematic review/meta-analysis methodology are provided in the abstract..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 1

Single-cell transcriptomics reveals tumor landscape in ovarian carcinosarcoma

Journal of Zhejiang University. Science. B · Aug 2024 · single-cell RNA sequencing (scRNA-seq) analysis of resected primary tumor with comparison to published scRNA-seq datasets

ovarian carcinosarcomahigh-grade serous ovarian carcinoma

The authors performed single-cell RNA sequencing on a resected primary ovarian carcinosarcoma and compared the data with published high-grade serous ovarian carcinoma and other OCS datasets. They identified malignant epithelial and malignant mesenchymal cells, four epithelial subclusters (one with high BRCA1 and TOP2A expression linked to cell cycle and drug-resistance features), and a mesenchymal subcluster C14 with an OCS-specific expression pattern. They also report FGF and PTN signaling as major pathways mediating epithelial–mesenchymal communication. The study provides a single-cell transcriptomic resource for exploring OCS heterogeneity.

Key findings

Both malignant epithelial and malignant mesenchymal cells were observed in the OCS patient sample.
Four epithelial cell subclusters were identified; epithelial subcluster 4 had high BRCA1 and TOP2A expression and was related to drug resistance and cell cycle.
Intercellular interaction analysis indicated FGF and PTN signaling as main pathways contributing to communication between epithelial and mesenchymal cells.
A mesenchymal subcluster (C14) showed OCS-specific expression (elevated CYP24A1, COL23A1, CCK, BMP7, PTN, WIF1, and IGF2) and distinct characteristics compared with another published OCS tumor and normal ovarian tissue.

Limitations: Analysis appears to be from a single resected tumor/patient, limiting generalizability.; Observational transcriptomic profiling without functional validation of identified pathways or subclusters.; No clinical outcome, treatment response, or longitudinal data reported.; Comparisons rely on previously published datasets rather than additional contemporaneous samples..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 18

Single-cell transcriptome profiles the heterogeneity of tumor cells and microenvironments for different pathological endometrial cancer and identifies specific sensitive drugs

Cell death & disease · Aug 2024 · Single-cell RNA sequencing of 18 human endometrial cancer samples across multiple pathological types, with patient-derived organoid drug testing and in vitro validation experiments

endometrial canceruterine clear cell carcinomaendometrioid endometrial carcinomauterine serous carcinoma

The authors performed single-cell RNA sequencing on 18 endometrial cancer samples across different pathological subtypes to map tumor-cell and microenvironment heterogeneity. They report pathology-specific tumor cell programs (immune-, proliferation-, or metabolism-modulating) and distinct microenvironment compositions, identified candidate drugs for each pathological group and confirmed drug activity in patient-derived organoids, and validated oncogenic effects of SOD2+ inflammatory cancer-associated fibroblasts in vitro. These findings provide descriptive molecular and cellular maps that may guide future, but not yet clinical, personalized approaches.

Reported effect: n_samples 18, n=18

Key findings

scRNA-seq was performed on 18 endometrial cancer samples from multiple pathological types.
Cancer cells showed pathology-associated hallmarks: immune-modulating in uterine clear cell carcinoma (UCCC), proliferation-modulating in well-differentiated endometrioid endometrial carcinoma (EEC-I), and metabolism-modulating in uterine serous carcinoma (USC).
Cancer cells from UCCC exhibited the greatest heterogeneity among the groups studied.
Potential effective drugs were predicted for each pathological group and their effectiveness was confirmed using patient-derived endometrial cancer organoids.
Tumor microenvironment differences: normal endometrium had prognostically favorable CD8+ cytotoxic T cells and NK cells, whereas tumors were dominated by CD4+ regulatory T cells, CD4+ exhausted T cells, and CD8+ exhausted T cells.
CXCL3+ macrophages with an M2 signature and angiogenesis association were found exclusively in tumors.
Epithelium-specific CAFs (eCAFs) predominated in EEC-I while SOD2+ inflammatory CAFs (iCAFs) predominated in UCCC.
The oncogenic effects of SOD2+ iCAFs were validated in vitro.

Limitations: Relatively small sample size (18 samples) limits generalizability.; Observational single-cell profiling: no prospective clinical outcome data or in vivo validation reported.; Drug effectiveness was confirmed in patient-derived organoids (ex vivo) but not in patients or animal models.; In vitro validation of SOD2+ iCAFs does not establish causality in vivo or clinical relevance.; Abstract does not report specific drug names, doses, or safety data..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewReported positiveLimited evidenceTier 3 · early human

Cyclic fasting-mimicking diet in cancer treatment: Preclinical and clinical evidence

Cell metabolism · Aug 2024 · review

This is a review of preclinical and early clinical evidence about cyclic fasting and fasting-mimicking diets (FMDs) in cancer. The authors summarize that in preclinical tumor models FMDs show antitumor effects and synergize with standard anticancer treatments while protecting normal tissues, and that phase 1/2 trials report FMD is safe, feasible, and associated with favorable metabolic and immune changes in patients. The review discusses underlying tumor-cell-autonomous and immune-mediated mechanisms, possible metabolic interventions to boost activity, and considerations for future clinical trials.

Studied with: standard anticancer treatments.

Key findings

In preclinical tumor models, cyclic fasting and FMDs produce antitumor effects and become synergistic when combined with a wide range of standard anticancer treatments while protecting normal tissues from treatment-induced adverse events.
Phase 1/2 clinical trials showed that cyclic FMD is safe, feasible, and associated with positive metabolic and immunomodulatory effects in patients with different tumor types.
The review examines tumor-cell-autonomous and immune-system-mediated mechanisms of fasting/FMD antitumor effects.
The authors discuss new metabolic interventions that could synergize with nutrient starvation to boost anticancer activity and address tumor resistance while minimizing toxicity.
The review highlights potential future applications of FMD in combination with standard anticancer strategies and considerations for designing clinical trials.

Limitations: This article is a review rather than a report of primary new clinical trial results.; Preclinical evidence may not translate to clinical benefit in patients.; Clinical evidence cited is limited to phase 1/2 trials (early-phase), with no larger randomized trials reported in the abstract..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed

ReviewReported positiveLimited evidenceTier 3 · early human

Environmental asbestos exposure and lung cancer

Lung cancer (Amsterdam, Netherlands) · Aug 2024 · narrative review

lung cancer

This is a narrative review of evidence from Turkey (and other studies) on environmental asbestos exposure and lung cancer. The authors report that environmental asbestos exposure is associated with increased lung cancer risk, that cancers appear to be diagnosed at a younger age, and that risk for women is similar to men; they state the dose–risk relationship appears linear with no safe threshold and recommend smoking cessation and consideration of screening for people in high-exposure areas.

Key findings

Environmental asbestos exposure is associated with increased risk of lung cancer in Turkey and other studies.
Lung cancer associated with environmental asbestos exposure seems to be diagnosed at a younger age.
The risk for women is in the same range as that for men.
The authors state the relationship between exposure dose and risk is linear and that a safe threshold cannot be established.
The authors recommend that people living in areas with increased environmental asbestos exposure be encouraged to join smoking cessation programs and be considered for lung cancer screening programs.
There is a need for additional studies on this topic.

Limitations: Narrative review rather than a systematic review or meta-analysis; no pooled quantitative risk estimates provided in abstract.; Conclusions appear to be based on observational studies (potential for confounding, exposure misclassification) rather than randomized data.; Regional focus on Turkey may limit generalizability to other settings.; Abstract provides no primary quantitative data or sample sizes..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed

Case reportInconclusiveLimited evidenceTier 3 · early humann = 1

Isolated left axillary nodal metastasis from endometrial carcinosarcoma: A case report and literature review

International journal of surgery case reports · Aug 2024 · case report

endometrial carcinosarcomauterine carcinosarcoma

This case report describes a 73-year-old woman who presented with a palpable left breast-tail mass; imaging showed enlarged left axillary lymph nodes with no breast primary. Excisional biopsy of the node showed metastatic disease of gynecologic origin and subsequent pelvic imaging and D&C diagnosed endometrial carcinosarcoma. The authors state this may be the first reported instance of isolated axillary lymph node metastasis from uterine carcinosarcoma presenting without pelvic or abdominal nodal involvement.

Key findings

Patient: 73-year-old woman presented with a left breast tail palpable mass.
Breast imaging (sonomammography and MRI) revealed multiple enlarged left axillary lymph nodes with malignant criteria but no suspected malignancy in either breast on imaging.
Excisional biopsy of an axillary lymph node diagnosed axillary lymph node metastasis from a gynecologic origin.
Abdominopelvic CT and pelvic MRI identified a suspicious endometrial mass; D&C pathology revealed endometrial carcinosarcoma.
Authors note this could be the first reported case of isolated axillary lymph node metastasis from uterine carcinosarcoma presenting as the initial symptom without pelvic or abdominal lymph node involvement.

Limitations: Single-patient case report limits generalizability.; No long-term follow-up or outcome data are provided in the abstract.; No systematic comparison group or epidemiologic data.; No mechanistic or molecular analyses reported in the abstract..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMechanismInconclusiveLimited evidenceTier 4 · clinical

Molecular genetics and research progress of uterine leiomyosarcoma

Yi chuan = Hereditas · Aug 2024 · review

uterine leiomyosarcoma

This article is a review of the molecular pathology of uterine leiomyosarcoma (uLMS). The authors summarize molecular genetic features, epigenetic variants, experimental models, and clinical research progress, and note that understanding of uLMS pathogenesis is inadequate and disease models are limited, which hinders development of effective therapies.

Key findings

uLMS is an aggressive malignant soft-tissue tumor arising from the myometrium that is difficult to distinguish from benign leiomyoma in early stages and has a poor prognosis.
Current studies of uLMS pathogenesis and disease biology are inadequate.
uLMS disease models are very limited, which hinders development of effective therapeutics.
The review systematically summarizes molecular genetic features, epigenetic alterations, experimental models, and clinical research progress, and discusses directions including tumor evolution, the tumor microenvironment, and therapy development.

Limitations: This publication is a review and does not present new primary experimental or clinical data.; Abstract does not describe review methods in detail (e.g., search strategy, inclusion criteria).; Field-level limitations noted by the authors include inadequate pathogenesis studies and limited disease models, which constrain conclusions about therapeutic development..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Case reportInconclusiveLimited evidenceTier 3 · early humann = 1

Rare case of giant ischiorectal leiomyosarcoma

International journal of surgery case reports · Aug 2024 · case report

leiomyosarcomasoft tissue sarcomaischiorectal leiomyosarcoma

This is a single-patient case report of a 25-year-old woman who presented with a left buttock swelling. MRI showed a large ischiorectal mass measuring 9 by 9.5 by 18 cm; the tumor was completely excised and immunohistochemistry confirmed leiomyosarcoma. The authors discuss diagnostic and therapeutic challenges due to the tumor's rarity and size and recommend individualized, multidisciplinary management.

Reported effects: tumor_dimension_1 9, n=1 · tumor_dimension_2 9.5, n=1 · +1 more

Key findings

Single case of ischiorectal leiomyosarcoma in a 25-year-old female presenting with a left buttock swelling.
MRI measured the tumor as 9 by 9.5 by 18 cm.
Complete surgical excision of the tumor was performed.
Immunohistochemistry confirmed the diagnosis of leiomyosarcoma.
Authors highlight rarity, diagnostic/therapeutic challenges, and recommend a multidisciplinary, individualized approach.

Limitations: Single-patient case report limits generalizability.; No long-term follow-up or outcomes (recurrence, survival) reported.; No control or comparative data to inform management decisions.; No details on surgical margins, adjuvant therapy, or postoperative course in the abstract..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Human · observationalReported positiveLimited evidenceTier 3 · early humann = 47

Anaplastic sarcoma of the kidney (DICER1-sarcoma of the kidney): A report from the International Pleuropulmonary Blastoma/DICER1 Registry

Pediatric blood & cancer · Aug 2024 · Registry cohort (International Pleuropulmonary Blastoma/DICER1 Registry) combined with comprehensive review/aggregation of previously published cases (pooled case series)

anaplastic sarcoma of the kidneykidney neoplasmDICER1-related tumor

Researchers combined cases from an international DICER1 registry and the published literature to assemble 47 cases of anaplastic sarcoma of the kidney (ASK). They report stage distribution, two-year event-free and overall survival by stage, and that chemotherapy was associated with markedly lower hazards of events and death (HR 0.09 for EFS and HR 0.08 for OS). Staging and outcome data were incomplete for some cases and the analysis is retrospective.

Reported effects: 2-year EFS stage I-II 81.8% [67.2–99.6], p p = .07, n=40 · 2-year EFS stage III-IV 46.6% [24.7–87.8], p p = .07, n=40 · +11 more

Key findings

Ten cases of ASK were identified in the Registry and 37 previously published cases were aggregated, for a total of 47 cases.
Staging data (available for 40 patients) were: 13 stage I, 12 stage II, 10 stage III, and 5 stage IV.
Outcome data were available for 37 patients.
Most (38 of 46) patients received upfront chemotherapy; 14 patients received upfront radiation.
Two-year event-free survival (EFS) for stage I-II was 81.8% (95% CI: 67.2%-99.6%) versus 46.6% (95% CI: 24.7%-87.8%) for stage III-IV (p = .07).
Two-year overall survival (OS) for stage I-II was 88.9% (95% CI: 75.5%-100.0%) versus 70.0% (95% CI: 46.7%-100.0%) for stage III-IV (p = .20).
Chemotherapy was associated with improved outcomes: hazard ratio for EFS 0.09 (95% CI: 0.02-0.31) and for OS 0.08 (95% CI: 0.02-0.42).

Limitations: Retrospective registry and literature-aggregated case series with inherent selection and reporting biases.; Small overall sample size (47 cases) and incomplete data (staging data available for 40 patients; outcome data for 37 patients).; Heterogeneous and non-standardized treatments across cases; not a randomized comparison.; Short/limited follow-up reported (two-year EFS/OS emphasized).; Stage comparisons did not reach conventional statistical significance (p = .07 for EFS; p = .20 for OS)..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMechanismInconclusiveLimited evidenceTier 4 · clinical

The role of biomarkers in the early detection of pancreatic cancer

Familial cancer · Aug 2024 · review

pancreatic cancer

This narrative review discusses current pancreatic surveillance and the need for better biomarkers to expand early detection beyond high-risk groups. It notes that current surveillance uses annual endoscopic ultrasound and MRI/MRCP for people with familial/genetic risk, and that accurate, inexpensive, safe biomarkers remain elusive. The authors highlight newer approaches such as personalized gene tests and artificial intelligence to integrate complex biomarker data as promising directions.

Key findings

Pancreatic surveillance can detect early-stage pancreatic cancer and achieve long-term survival in some cases.
Current surveillance involves annual endoscopic ultrasound (EUS) and MRI/MRCP and is recommended only for individuals who meet familial/genetic risk criteria.
More accurate, inexpensive, and safe biomarkers are needed to improve early detection and expand access, but have so far been elusive.
Newer approaches — gene tests to personalize biomarker interpretation and artificial intelligence to integrate complex biomarker data — offer promise for future clinically useful biomarkers.

Limitations: This is a narrative review rather than original primary data from a clinical study.; No new validated biomarkers or quantitative diagnostic performance metrics are reported in the abstract.; Recommendations are general and do not provide prospectively validated protocols for broader population screening.; Abstract does not report study methods, search strategy, or systematic review/meta-analysis methods..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Case reportMixed resultsLimited evidenceTier 3 · early humann = 1

Tarlatamab for Large Cell Neuroendocrine Carcinoma in a Young Adult: A Case Report

JTO clinical and research reports · Jul 2024 · case report

large cell neuroendocrine carcinoma of the lung

A 20-year-old man with metastatic large cell neuroendocrine carcinoma of the lung received tarlatamab, a DLL3-targeting bispecific T-cell engager. Treatment was complicated by transient cytokine release syndrome and resulted in a partial response. The authors state that bispecific T-cell engagers may offer a novel treatment approach for this cancer.

Key findings

A 20-year-old man with metastatic large cell neuroendocrine carcinoma of the lung was treated with tarlatamab.
Treatment was complicated by transient cytokine release syndrome.
Treatment resulted in a partial response.
Authors suggest bispecific T-cell engagers may offer a novel treatment approach for large cell neuroendocrine carcinoma of the lung.

Limitations: Single-patient case report (n=1).; No control or comparator provided.; Dose, treatment schedule, and duration of follow-up are not reported in the abstract.; Findings cannot be generalized from one case.; Safety data limited to a single transient cytokine release syndrome event with no longer-term safety outcomes reported..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Animal studyReported positivePreclinical onlyTier 2 · animal

CDC7 inhibition impairs neuroendocrine transformation in lung and prostate tumors through MYC degradation

Signal transduction and targeted therapy · Jul 2024

lung adenocarcinomaprostate adenocarcinomasmall cell carcinoma (lung and prostate)neuroendocrine transformation

The study tested CDC7 inhibition with simurosertib in models of neuroendocrine (NE) transformation in lung and prostate tumors. In in vivo models, CDC7 inhibition suppressed NE transdifferentiation and extended responses to targeted therapy and to cytotoxic drugs by inducing proteasome-mediated degradation of the MYC oncoprotein; a degradation-resistant MYC isoform reversed this effect.

Studied with: targeted therapy (unspecified), cisplatin, irinotecan.

Key findings

CDC7 is upregulated during the initial steps of neuroendocrine transformation after TP53/RB1 co-inactivation.
CDC7 inhibition with simurosertib suppressed NE transdifferentiation and extended response to targeted therapy in in vivo models of NE transformation.
CDC7 inhibition induced proteasome-mediated degradation of MYC, implicated in stemness and histological transformation.
Ectopic overexpression of a degradation-resistant MYC isoform reestablished the NE transformation phenotype even in the presence of simurosertib.
CDC7 inhibition markedly extended response to standard cytotoxics (cisplatin, irinotecan) in lung and prostate small cell carcinoma models.
Authors propose CDC7 inhibition as a strategy to constrain lineage plasticity and to treat NE tumors; simurosertib clinical trials are ongoing (not reported in this study).

Limitations: All reported experiments are preclinical (in vivo models); no human trial data are presented in this abstract.; The abstract does not report sample sizes, doses, or detailed experimental parameters.; Species and detailed model descriptions are not specified in the abstract.; Safety, toxicity, and clinical efficacy in patients are not addressed in this study..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Case reportReported positiveLimited evidenceTier 3 · early humann = 1

Primary Sternal Leiomyosarcoma

Annals of thoracic surgery short reports · Jul 2024 · case report

primary sternal leiomyosarcoma

A 70-year-old man had an incidentally discovered sternal lesion on PET-CT performed for prostate cancer staging. Biopsy showed spindle cells suggesting probable leiomyosarcoma and contrast CT found no other primary site, suggesting a primary sternal tumor. The patient underwent sternotomy and reconstruction with methyl methacrylate and had an uneventful recovery. The authors note primary sternal leiomyosarcoma is very rare (<0.7% of primary malignant bone tumors).

Key findings

Lesion was incidentally found on PET-CT during prostate cancer staging.
Interventional radiology biopsy showed spindle cells indicating probable leiomyosarcoma.
Contrast CT found no other primary site, supporting the interpretation of a primary sternal tumor.
Patient underwent sternotomy and reconstruction with methyl methacrylate and recovered uneventfully.
Primary sternal leiomyosarcoma is rare, comprising less than 0.7% of primary malignant bone tumors.

Limitations: Single case report (n=1) limits generalizability.; Diagnosis described as 'probable' leiomyosarcoma from biopsy; the abstract does not state whether resection pathology confirmed the diagnosis.; No long-term follow-up or oncologic outcomes reported beyond an 'uneventful recovery.'; No information on margins, adjuvant therapy, or postoperative oncologic surveillance provided..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Case reportMechanismInconclusiveLimited evidenceTier 3 · early humann = 1

Primary intracranial sarcoma, DICER-1 mutant, with hemorrhagic presentation: A case report

Surgical neurology international · Jul 2024 · case report

primary intracranial sarcoma

This is a single-patient case report of a 26-year-old man with a high-grade primary intracranial sarcoma found to have a DICER1-associated genomic profile. The tumor showed unusual hypervascularity with refractory hemorrhage and subdural effusions. Management included endovascular embolization, multiple surgeries, intrathecal etoposide, oral pazopanib, and adjuvant radiation; the abstract does not provide quantitative outcomes of these treatments.

Studied with: endovascular embolization, multiple surgical interventions, adjuvant radiation therapy.

Key findings

Patient had a high-grade spindle-celled neoplasm with sarcomatous features, multinucleated giant cells, and rare eosinophilic spheroids.
Genomic analysis identified the tumor as DICER1-associated primary intracranial sarcoma.
The case demonstrated anomalous hypervascularity, refractory hemorrhage, and subdural effusions as part of the presentation.
Therapies used included endovascular embolization, multiple surgical interventions, intrathecal etoposide injections, oral pazopanib, and adjuvant radiation therapy.

Limitations: Single-patient case report — findings may not generalize.; No control group or comparative data.; Abstract does not report quantitative outcomes or measures of treatment effectiveness.; Short/unclear follow-up and limited clinical outcome details in the abstract..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMechanismMixed resultsLimited evidenceTier 4 · clinical

Cancer-associated adipocytes in the ovarian cancer microenvironment

American journal of cancer research · Jul 2024 · review

ovarian cancer

This narrative review summarizes how adipocytes in the ovarian tumor microenvironment become cancer-associated adipocytes (CAAs) through dedifferentiation and how CAAs supply nutrients, growth factors, cytokines and metabolites that can support tumor growth, metastasis and alter drug response. The authors outline the physiological functions of CAAs and discuss progress toward using CAAs as therapeutic targets in ovarian cancer.

Key findings

Adipocytes in the tumor microenvironment can transform into cancer-associated adipocytes (CAAs) via dedifferentiation through interactions with tumor cells.
CAAs provide nutrients, growth factors, cytokines and metabolites to the tumor.
CAAs can later transdifferentiate into other stromal cells at a later stage.
CAAs alter tumor growth, metastasis and the drug response and ultimately influence the treatment and prognosis of ovarian cancer.
The review discusses progress in the use of CAAs as therapeutic targets in ovarian cancer.

Limitations: Narrative review — no new primary experimental or clinical data reported in this article.; Abstract does not describe systematic review methods or quantitative synthesis (no meta-analysis).; Unclear from abstract whether discussed CAA-targeting approaches have clinical efficacy or are limited to preclinical data..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Meta-analysisSupportive careMixed resultsLimited evidenceTier 4 · clinical

Management of Fatigue in Adult Survivors of Cancer: ASCO-Society for Integrative Oncology Guideline Update

Journal of clinical oncology : official journal of the American Society of Clinical Oncology · Jul 2024 · Systematic review of randomized controlled trials (RCTs) published 2013-2023

Supportive careadult survivors of cancer

This ASCO-SIO guideline update reviewed 113 randomized controlled trials (2013–2023) on interventions for cancer-related fatigue in adults. The panel found that exercise, cognitive behavioral therapy, and mindfulness-based programs improved fatigue both during and after treatment; American ginseng showed benefit during treatment, and CBT and mindfulness were effective for moderate–severe fatigue after treatment. The guideline advises clinicians to recommend several nonpharmacologic approaches and to avoid L-carnitine, antidepressants, wakefulness agents, and routine psychostimulants for cancer-related fatigue; overall certainty of evidence was low to moderate.

Key findings

The evidence base consisted of 113 randomized controlled trials.
Exercise, cognitive behavioral therapy (CBT), and mindfulness-based programs led to improvements in cancer-related fatigue both during and after completion of cancer treatment.
Tai chi, qigong, and American ginseng showed benefits during treatment.
Yoga, acupressure, and moxibustion helped manage fatigue after completion of treatment.
Psychoeducation and American ginseng may be recommended in adults undergoing cancer treatment.
For survivors after treatment, clinicians should recommend exercise, CBT, and mindfulness-based programs; CBT and mindfulness have shown efficacy for moderate to severe fatigue after treatment.
Patients at the end of life may be offered CBT and corticosteroids.
Clinicians should not recommend L-carnitine, antidepressants, wakefulness agents, or routinely recommend psychostimulants to manage cancer-related fatigue.
Certainty and quality of evidence were low to moderate for the interventions evaluated.

Limitations: Certainty and quality of evidence were reported as low to moderate.; The guideline is based on RCTs published 2013–2023 (time-limited search window specified).; Abstract reports aggregated findings and recommendations but does not provide participant-level sample sizes or detailed intervention dose/duration information..

Guideline update summarizing RCT evidence for interventions to manage cancer-related fatigue in adults.

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMechanismInconclusiveLimited evidenceTier 4 · clinical

Neuroinflammation in Glioblastoma: Progress and Perspectives

Brain sciences · Jul 2024

glioblastoma

This is a narrative review about neuroinflammation in glioblastoma. The authors summarize components of the tumor microenvironment, emphasize roles of resident and infiltrating inflammatory cells in glioblastoma pathogenesis, aggressiveness, and treatment resistance, and discuss anti-tumor microenvironment interventions as potential therapeutic targets.

Key findings

Glioblastoma has high morbidity and mortality despite multimodal treatment.
The tumor microenvironment is dynamic and heterogeneous and contains resident and infiltrating inflammatory cells.
Inflammatory cells within the tumor microenvironment regulate tumor aggressiveness and treatment resistance.
Targeting the tumor microenvironment, particularly neuroinflammation, is increasingly recognized as a potential therapeutic approach.
The review discusses interactions among tumor microenvironment components and potential anti-tumor microenvironment interventions.

Limitations: Review article with no new primary experimental or clinical data reported in the abstract.; Abstract does not specify whether this is a systematic review or a narrative review (possible selection bias).; No quantitative results, specific interventions, or clinical evidence are reported in the abstract..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Lab · in vitroFormulationReported positivePreclinical onlyTier 1 · lab

Zwitterionic nanoparticles for thermally activated drug delivery in hyperthermia cancer treatment

Nanoscale · Jul 2024

Paclitaxelovarian carcinoma

The authors developed zwitterionic thermoresponsive nanoparticles with an upper critical solution temperature (UCST) tuned to 43 °C to deliver paclitaxel intracellularly and release it upon hyperthermia. In cell experiments, the nanoparticles released nearly all encapsulated drug after 1 hour at 43 °C while retaining more than 95% of the payload at 37 °C, and paclitaxel-loaded nanoparticles produced greater therapeutic effects on ovarian cancer cells than non-encapsulated paclitaxel.

Reported effects: payload release after 1 h at 43 °C · payload retained at 37 °C

Studied with: paclitaxel.

Key findings

Thermoresponsive nanoparticles (NPs) with UCST behavior were synthesized via RAFT emulsion polymerization combining polyzwitterionic stabilizers and an oligoester biodegradable core.
The cloud point (Tcp) of the NPs was tuned to match hyperthermia treatment needs at 43 °C and used to control paclitaxel delivery.
"The NPs released almost entirely the encapsulated drug only following 1 h incubation at 43 °C, whereas they retained more than 95% of the payload in the physiological environment (37 °C), thus demonstrating their efficacy as on-demand drug delivery systems."
Administration of drug-loaded NPs to ovarian cancer cells produced therapeutic effects that outperformed conventional administration of non-encapsulated paclitaxel.

Limitations: In vitro cell-based study only; no in vivo or human data reported in the abstract.; Abstract does not report quantitative cytotoxicity metrics, cell line identities, sample sizes, or statistical analysis details.; No pharmacokinetic, biodistribution, safety, or long-term efficacy data presented..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Case reportReported negativeLimited evidenceTier 3 · early humann = 1

Sigmoido-ovarian fistula complicating ovarian carcinosarcoma: a case report

Annals of medicine and surgery (2012) · Jul 2024 · case report

ovarian carcinosarcoma

This is a case report of a 67-year-old woman who presented with abdominal pain and was found at surgery to have an ovarian carcinosarcoma fistulized into the sigmoid colon with pelvic peritonitis. She underwent en-bloc resection with formation of a terminal stoma; postoperative imaging showed diffuse lymph node metastases and she was scheduled for chemotherapy. The authors state that fistulization into the large intestine is a rare complication that worsens prognosis and that surgery plus adjuvant therapy are generally required.

Key findings

Spontaneous fistulization of ovarian carcinosarcoma into the digestive tract is rare.
The patient presented with abdominal pain; CT suggested a perforated sigmoid tumor with peri-colonic abscess and pneumoperitoneum.
Intraoperative findings were an ovarian tumor fistulized to the sigmoid colon with peritonitis.
An en-bloc resection with terminal stoma was performed.
Postoperative radiology revealed diffuse lymph node metastasis; the patient was scheduled for chemotherapy.
Authors note fistulization can cause tumor superinfection and pelvic peritonitis and may prevent the use of neoadjuvant chemotherapy, worsening chances of complete cytoreduction.
Conclusion: fistulization to the large intestine worsens prognosis; surgery is mandatory and adjuvant therapy is mostly needed.

Limitations: Single-patient case report limits generalizability.; No control or comparison group.; No quantitative or long-term outcome data reported (e.g., survival, response to chemotherapy).; Limited detail on pathology, operative findings, and postoperative course in the abstract..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Animal studyReported positivePreclinical onlyTier 2 · animal

PAD4 Inhibitor-Functionalized Layered Double Hydroxide Nanosheets for Synergistic Sonodynamic Therapy/Immunotherapy Of Tumor Metastasis

Advanced science (Weinheim, Baden-Wurttemberg, Germany) · Jul 2024

breast cancer (4T1 murine model)

This preclinical mouse study tested layered double hydroxide nanosheets loaded with the PAD4 inhibitor YW3-56 combined with ultrasound (sonodynamic therapy). The nanoagent generated reactive oxygen species under ultrasound, induced immunogenic cell death, inhibited PAD4-mediated citrullinated histone H3 and NET release, boosted immune-activated cells and M1 macrophages, lowered PD-1 expression, reduced primary tumor growth (69.5% tumor inhibition rate) and decreased lung metastases in a 4T1 model. These results are from an animal model and not from human trials.

Reported effect: tumor inhibition rate 69.5%

Studied with: ultrasound (sonodynamic therapy), a-CoW-LDH nanosheets (nanostructure delivery).

Key findings

a-CoW-LDH nanosheets act as a sonosensitizer to generate abundant ROS under ultrasound irradiation.
Loading YW3-56 onto a-CoW-LDH (a-LDH@356) plus ultrasound induced ROS generation and immunogenic cell death.
YW3-56 inhibited elevation of citrullinated histone H3 (H3cit) and the release of neutrophil extracellular traps (NETs).
Combination therapy upregulated the proportion of immune-activated cells and induced M1 macrophage polarization.
Combination therapy downregulated PD-1 expression on immune cells under ultrasound irradiation.
In the 4T1 tumor model the combination arrested primary tumor progression with a tumor inhibition rate of 69.5%.
The combination also prevented tumor metastasis, producing the least number of lung metastatic nodules among groups tested.

Limitations: Study performed in a single animal tumor model (4T1 murine breast cancer); no human data.; Abstract does not report sample sizes, randomization, or blinding.; Dose, dosing schedule and detailed toxicity/safety data are not reported in the abstract.; Long-term outcomes and durability of anti-metastatic effect are not described.; Mechanistic and translational relevance to humans remains unproven..

Preclinical demonstration that PAD4 inhibition delivered via LDH nanosheets can augment sonodynamic therapy, reduce NETs, and enhance anti-tumor immune responses to limit primary tumor growth and metastasis in a murine breast cancer model.

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Animal studyMechanismReported positivePreclinical onlyTier 2 · animal

Generation of glioblastoma in mice engrafted with human cytomegalovirus-infected astrocytes

Cancer gene therapy · Jul 2024

glioblastoma

Researchers isolated HCMV strains from glioblastoma tissues and used them to infect human astrocytes, transforming these cells into CMV-elicited glioblastoma cells (CEGBCs) that formed spheroids. When CEGBC-derived spheroids were orthotopically xenografted into mice they produced glioblastoma-like tumors that were nestin-positive in invasive regions, surrounded by GFAP-positive reactive astrocytes, showed EGFR and cMet gene amplification, and contained HCMV IE and UL69 genes and proteins.

Key findings

Three clinical HCMV strains isolated from glioblastoma tissues transformed human astrocytes into CMV-Elicited Glioblastoma Cells (CEGBCs).
Spheroids generated from CEGBCs produced glioblastoma-like tumors in orthotopically xenografted mice.
Resulting tumors were nestin-positive in invasive regions and were surrounded by GFAP-positive reactive astrocytes.
Tumors showed EGFR and cMet gene amplification and detection of HCMV IE and UL69 genes and proteins.

Limitations: Preclinical study using transformed human cells and mouse xenografts; no clinical/human outcome data provided.; Abstract provides no sample sizes, quantitative incidence, or statistical analysis.; Only three clinical HCMV strains are reported to have been isolated and tested (limited strain sampling).; No mention of control groups or negative controls in the abstract..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Case reportInconclusiveLimited evidenceTier 3 · early humann = 1

Incidental Cutaneous Melanoma

Journal of Brown hospital medicine · Jul 2024

cutaneous melanoma

This single-patient case report describes a young man who was admitted with sepsis and cellulitis and was incidentally found to have invasive cutaneous melanoma. The authors emphasize that recognizing melanoma is important to ensure timely diagnosis and treatment.

Key findings

A young man admitted to the hospital with sepsis and cellulitis was incidentally found to have invasive cutaneous melanoma.
The authors state that recognition of melanoma is important to ensure timely diagnosis and treatment.

Limitations: Single case report (n=1) limits generalizability; Abstract provides no systematic data, outcomes, or follow-up information; No control or comparison group; No details on management, staging, or prognosis in the abstract.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Case reportInconclusiveLimited evidenceTier 3 · early humann = 1

Small cell carcinoma of uterine cervix: A case report

Caspian journal of internal medicine · Jul 2024 · case report

small cell carcinoma of the uterine cervixcervical cancer

This is a case report of a 47-year-old woman with a history of breast cancer who presented with abnormal vaginal bleeding and was diagnosed with small cell carcinoma of the cervix. She underwent radical hysterectomy with bilateral salpingo-oophorectomy and then received postoperative adjuvant chemoradiation. The authors state that small cell carcinoma of the cervix is aggressive with poor prognosis and that optimal treatment remains unsettled.

Key findings

Patient: 47-year-old woman with prior breast cancer presented with abnormal vaginal bleeding and was diagnosed with small cell carcinoma of the cervix.
Treatment reported: radical hysterectomy and bilateral salpingo-oophorectomy followed by adjuvant chemoradiation.
Authors' conclusion: small cell carcinoma of the cervix is aggressive and has poor prognosis; optimal treatment remains unsettled.

Limitations: Single-patient case report (n=1), so findings are not generalizable.; Abstract does not report clinical outcome, follow-up duration, or treatment response.; No control group or comparative data.; Limited clinical and pathological detail provided in the abstract..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMechanismInconclusiveLimited evidenceTier 4 · clinical

Uterine serous carcinoma and uterine carcinosarcoma: molecular features, clinical advances, and emerging therapies

Clinical advances in hematology & oncology : H&O · Jul 2024

endometrial canceruterine serous carcinomauterine carcinosarcoma

This is a narrative review summarizing genomic and molecular features of uterine serous carcinoma (USC) and uterine carcinosarcoma (UCS). The authors note that USC and UCS are a small but increasing fraction of endometrial cancers and contribute disproportionately to endometrial cancer mortality, and that both subtypes have poor prognoses. The review summarizes clinical advances in primary advanced and recurrent disease and discusses emerging molecularly driven treatment strategies.

Key findings

Endometrial cancer, including high-grade subtypes, has a rising incidence and mortality.
Uterine serous carcinoma (USC) and uterine carcinosarcoma (UCS) account for a small but increasing proportion of endometrial cancer cases and a significant portion of endometrial cancer mortality.
USC and UCS are molecularly and clinically distinct but both have a poor prognosis.
There have been few therapeutic strategies directed specifically at these endometrial cancer subtypes to date.
The review summarizes genomic/molecular features, clinical advances for primary advanced and recurrent disease, and novel molecularly driven treatment strategies.

Limitations: Review article only — does not present new, patient-level primary data.; Abstract does not indicate this is a systematic review or meta-analysis, so selection and synthesis methods are not described.; Does not report specific quantitative efficacy data or comparative clinical trial results in the abstract..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Human trialTrialInconclusiveModerate evidenceTier 4 · clinical

Clinical Trial Protocol for ROSELLA: a phase 3 study of relacorilant in combination with nab-paclitaxel versus nab-paclitaxel monotherapy in advanced platinum-resistant ovarian cancer

Journal of gynecologic oncology · Jul 2024 · phase 3, randomized, 2-arm, open-label, global multicenter study protocol

Relacorilantadvanced platinum-resistant ovarian cancerrecurrent platinum-resistant high-grade serous epithelial ovarian cancerprimary peritoneal cancerfallopian tube cancer

This paper describes the ROSELLA phase 3 trial, which is testing relacorilant plus nab-paclitaxel versus nab-paclitaxel alone in women with recurrent platinum-resistant ovarian and related cancers. The study is designed to see whether adding relacorilant improves progression-free survival and other outcomes, and it will also assess safety and patient-reported outcomes. The abstract does not report trial results, only the study plan.

Studied with: nab-paclitaxel.

Key findings

ROSELLA is a phase 3, randomized, 2-arm, open-label, global multicenter study.
Participants are assigned 1:1 to relacorilant plus nab-paclitaxel or nab-paclitaxel monotherapy.
Primary endpoint is progression-free survival assessed by blinded independent central review.
Secondary endpoints include overall survival, objective response rate, duration of response, clinical benefit rate at 24 weeks, and CA-125 response.
The abstract reports no efficacy or safety results because it is a trial protocol.

Limitations: Protocol only; no outcomes or results are reported in the abstract.; No sample size is provided in the abstract.; No quantitative effect estimates are available.; Open-label design may introduce bias in some endpoints..

This is a phase 3 protocol in platinum-resistant ovarian cancer evaluating an anticancer combination.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text