Animal studyReported positivePreclinical onlyTier 2 · animal
Molecular cancer therapeutics · Sep 2026
This preclinical study tested a novel CDK12 inhibitor (CTX-439) alone and combined with the PARP inhibitor olaparib in uterine serous carcinoma (USC) cell lines and patient-derived xenograft models. CTX-439 suppressed expression of HR-related genes (including BRCA1 and BRCA2), induced DNA damage and apoptosis, inhibited tumor growth in PDX models with high CDK12 expression, and enhanced tumor sensitivity to olaparib. Analysis of genomic datasets found CDK12 amplification more frequent in USC than in high-grade serous ovarian carcinoma, associated with higher CDK12 expression and poorer prognosis, but not with HRD scores.
Studied with: olaparib.
Key findings
- USC exhibited a higher HRD score than other histologic subtypes of uterine endometrial carcinoma but lower than HGSOC.
- CDK12 amplification occurred more frequently in USC than in HGSOC but was not associated with HRD scores.
- Tumors with CDK12 amplification demonstrated high CDK12 expression, which correlated with poor prognosis in USC.
- The CDK12 inhibitor CTX-439 suppressed HR-related gene expression, including BRCA1 and BRCA2.
- CTX-439 induced apoptosis and DNA damage in USC models.
- CTX-439 inhibited tumor growth in USC PDX models with high CDK12 expression.
- CDK12 inhibition enhanced tumor sensitivity to the PARP inhibitor olaparib in USC PDX models.
Limitations: Preclinical study limited to cell lines and patient-derived xenograft (PDX) models; no human clinical data presented.; Abstract does not report sample sizes, dosing regimens, or toxicity/safety data.; No long-term outcomes or survival data in patients.; Findings from PDX models may not translate to clinical efficacy in humans..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed
Human · observationalMechanismReported positiveModerate evidenceTier 3 · early humann = 114
Cell reports. Medicine · Aug 2026 · Genome-wide DNA methylation profiling with unsupervised clustering and development/validation of a three-step machine-learning classifier using internal and external cohorts
mucinous ovarian carcinomaextraovarian mucinous metastasismucinous borderline ovarian tumor
The authors performed genome-wide DNA methylation profiling on mucinous ovarian tumors and extraovarian mucinous metastases to define epigenetic groups. They identified two methylation-based subtypes of mucinous ovarian carcinoma and two groups of mucinous borderline tumors, and developed a three-step machine-learning classifier that distinguished MOC from EOM with 95.5% accuracy in their analyses and 91.11% accuracy on an external validation set of 21 MOCs and 24 EOMs. The study proposes an epigenetic framework and a potential clinical classification tool for mucinous ovarian tumors.
Reported effects: classifier accuracy (internal/development) 95.5% · classifier accuracy (external validation) 91.11%, n=45
Key findings
- Methylation analysis defines two mBOT groups, one epigenetically similar to normal ovary and one resembling MOC.
- Unsupervised clustering reveals two distinct MOC methylation subtypes with potential prognostic relevance in the internal cohort.
- A three-step machine-learning classifier developed using the study data together with 389 external profiles distinguishes MOC from EOM with 95.5% accuracy.
- External validation on 21 MOCs and 24 EOMs yielded an accuracy of 91.11% for differentiating MOC from EOM.
Limitations: Observational tissue-profiling study without prospective clinical testing of the classifier.; Prognostic relevance of MOC subtypes is suggested only in the internal cohort and not externally validated in the abstract.; External validation sample for the classifier reported in the abstract is modest (21 MOCs and 24 EOMs).; Details on classifier training/validation procedures, confidence intervals, and independent performance metrics beyond overall accuracy are not provided in the abstract..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 107
Science advances · Aug 2026 · Proteogenomic analysis of tumors and paired normal adjacent tissues from 107 patients; preclinical optimization and testing of recombinant IL-33 in mouse models and pharmacokinetics in cynomolgus monkeys
pulmonary large-cell neuroendocrine carcinomanon-small cell lung carcinoma
Researchers performed proteogenomic analysis on tumors and matched normal tissues from 107 patients with pulmonary large-cell neuroendocrine carcinoma and identified molecular features, mutational signatures, and three LCNEC subtypes. Interleukin-33 (IL-33) was identified as a biomarker associated with increased T cell infiltration and antitumor activity; the authors optimized recombinant IL-33 and developed a PEGylated form that showed prolonged circulation in cynomolgus monkeys and stronger immune agonist activity in mouse models.
Key findings
- Proteogenomic analysis was performed on tumors and paired normal adjacent tissues from 107 LCNEC patients (81 pure LCNEC and 26 combined LCNEC).
- APOBEC mutational signatures strongly correlate with processes of tumor initiation and immune suppression in LCNEC.
- KEAP1 mutations correlate with metabolic reprogramming in LCNEC combined with NSCLC.
- A conflicting relationship was observed between neuroendocrine and immune phenotypes.
- Three LCNEC subtypes were identified, each with distinct prognosis features, microenvironment dysregulation, genetic alterations, and potential therapeutic targets.
- Interleukin-33 (IL-33) emerged as a critical therapeutic biomarker associated with enhanced T cell infiltration and antitumor activity.
- Recombinant IL-33 was optimized via site-directed mutagenesis and PEGylation.
- PEGylated recombinant IL-33 demonstrated prolonged circulation time in cynomolgus monkeys and superior immune agonist activity in mouse models.
Limitations: Therapeutic optimization and activity of recombinant/PEGylated IL-33 were tested only in animal models (mice) and assessed for circulation in cynomolgus monkeys; no clinical (human interventional) data are reported.; Proteogenomic analyses are observational and associative; causality of identified correlations (e.g., APOBEC signatures, KEAP1 mutations) is not established in patients.; The human cohort, while sizable for a rare tumor, is limited to 107 patients and subgroup sizes (81 vs 26) may limit power for some subtype analyses.; The abstract does not report dosing, safety, or efficacy endpoints in humans, nor detailed statistical measures for the reported associations.; Translatability of mouse and nonhuman primate findings to human clinical benefit is not demonstrated in this study..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Case reportInconclusiveLimited evidenceTier 3 · early humann = 1
IJU case reports · Jul 2026 · case report
endometrial carcinomaupper tract urothelial carcinoma (differential)
This is a single-patient case report of a 64-year-old woman whose ureteral mass and malignant urine cytology were initially suspected to be upper tract urothelial carcinoma. After nephroureterectomy, histopathology and PAX8 immunohistochemistry indicated the ureteral lesion was metastatic endometrial adenocarcinoma, and the patient was staged as IVB endometrial carcinoma.
Key findings
- Contrast-enhanced CT showed hydronephrosis and a left ureteral mass suggestive of upper tract urothelial carcinoma (UTUC).
- Urine cytology showed malignant cells, but ureteroscopy was inconclusive.
- Simultaneous surgery including nephroureterectomy was performed because UTUC would affect management and prognosis.
- Histopathology revealed ureteral adenocarcinoma morphologically similar to endometrial carcinoma.
- Immunohistochemical staining was PAX8 positive, supporting the diagnosis of metastatic endometrial carcinoma.
- Final diagnosis was stage IVB endometrial carcinoma.
Limitations: Single case report (n=1) limits generalizability.; No preoperative tissue diagnosis of the ureteral lesion was obtained (ureteroscopy inconclusive).; No follow-up outcomes or treatments after diagnosis are reported in the abstract.; No quantitative data or comparative analysis..
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
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
Human · observationalInconclusiveLimited evidenceTier 3 · early human
JAMA network open · Jul 2026 · cross-sectional
This cross-sectional study analyzed data from the National Cancer Database to examine the association between tobacco smoking cessation and cancer stage among US adults. The abstract provides no results, effect sizes, or conclusions about the association.
Key findings
- Cross-sectional analysis using the National Cancer Database to study the association between tobacco smoking cessation and cancer stage in US adults.
- The abstract does not report the study's results, numerical findings, or conclusions.
Limitations: Cross-sectional design — cannot establish temporality or causality between smoking cessation and cancer stage.; Study uses registry data (National Cancer Database), which can have selection and reporting biases.; Abstract provides no sample size, effect estimates, or details of adjustment, limiting interpretability..
AI summary of the abstract, human-reviewed · Aug 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Meta-analysisTrialMixed resultsModerate evidenceTier 4 · clinical
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
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
Human · observationalMechanismMixed resultsLimited evidenceTier 3 · early humann = 1331
bioRxiv : the preprint server for biology · Jun 2026 · multi-institutional cohort of 1,331 prostate cancer samples (observational genomic study)
prostate cancercastration-resistant prostate cancer
The authors analyzed a multi-institutional cohort of 1,331 prostate cancer samples to identify genomic determinants of progression to lethal castration-resistant disease. They report that rare AR-regulated MYC fusions and haploinsufficient CDKN1B loss are associated with poor outcome, while AR alterations predict improved prognosis. They also developed CAPrisk, a multi-omic classifier that stratifies patient outcomes across androgen receptor pathway inhibitors, taxanes, PARP inhibitors, and radium-223.
Studied with: androgen receptor pathway inhibitors, taxanes, PARP inhibitors, radium-223.
Key findings
- Rare AR-regulated MYC fusions were identified as genomic determinants associated with progression to lethal castration-resistant disease.
- Haploinsufficient CDKN1B loss was identified as a driver of poor outcome.
- Androgen receptor (AR) alterations were highlighted as predictors of improved prognosis.
- A multi-omic classifier, CAPrisk, was developed to stratify patient outcomes across AR pathway inhibitors, taxanes, PARP inhibitors, and radium-223.
Limitations: Observational genomic cohort study—associations do not establish causation.; Abstract does not report prospective clinical trial data or interventional testing.; Abstract provides no numerical performance metrics or independent validation details for the CAPrisk classifier.; No information in the abstract on clinical covariates, follow-up duration, or potential confounders..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
ReviewMechanismInconclusiveLimited evidenceTier 3 · early human
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
Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 20
The American journal of surgical pathology · Jun 2026 · retrospective case series
endometrioid carcinoma (ovary)endometrioid carcinoma (fallopian tube)
The authors reviewed 20 adnexal endometrioid carcinomas with sex cord-like morphology to describe their histology, immunohistochemistry, and genomics. They found most tumors were PAX8-negative, universally SOX17-positive, frequently showed nuclear beta-catenin staining, and 9 of 10 sequenced cases had activating CTNNB1 variants. These findings suggest SOX17 immunostaining and awareness of CTNNB1/beta-catenin alterations may help avoid misclassification of these tumors.
Reported effects: tumors identified 20 · ovarian_tumors 17 · +15 more
Key findings
- Twenty tumors (17 ovarian, 3 fallopian tube) were identified.
- Sex cord-like patterns included cords/trabeculae (n=17), small tubular glands (n=16), and "granulosa-like" nests (n=12).
- All tumors had conspicuous fibromatous stroma; 11 tumors had background endometrioid adenofibromas.
- Six tumors had associated endometriosis.
- PAX8 was positive in only 2/20 (diffuse in both).
- SOX17 was positive in all cases (focal in 1, diffuse in 19).
- Beta-catenin showed aberrant nuclear staining in 17/20.
- Of the 10 sequenced tumors, 9 showed activating pathogenic variants in CTNNB1; each of these also showed nuclear beta-catenin staining.
- All tumors lacked alterations in mismatch repair genes, TP53, and POLE (as reported).
Limitations: Small sample size (20 tumors).; Retrospective case series design with potential selection bias.; Genomic sequencing performed on a subset (10) of tumors only.; No control group of non-sex-cord-like endometrioid carcinomas presented for direct comparison.; No clinical outcome data or prospective validation reported..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed
ReviewMechanismMixed resultsModerate evidenceTier 4 · clinical
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
Case reportInconclusiveLimited evidenceTier 3 · early humann = 1
Cureus · May 2026 · case report
endometrial serous carcinomauterine serous carcinoma
This paper is a case report of a postmenopausal woman diagnosed with endometrial (uterine) serous carcinoma that arose from adenomyosis. The authors describe diagnostic challenges, clinical management, and prognosis for this single patient and include a literature review to provide broader context.
Key findings
- Reported a single case of uterine/ endometrial serous carcinoma arising from adenomyosis.
- Highlights diagnostic challenges when serous carcinoma is associated with adenomyosis.
- Discusses clinical management and prognosis for the reported patient.
- Includes a comprehensive review of the literature on this uncommon association.
Limitations: Single-patient case report limits generalizability.; No quantitative outcomes or comparative data reported.; No mechanistic or pathological detail provided in the abstract.; Prognostic implications cannot be inferred from one case..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
ReviewReported positivePreclinical onlyTier 1 · lab
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
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
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
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
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
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
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
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
Human · observationalMechanismReported positivePreclinical onlyTier 3 · early human
Cancer cell · Apr 2026 · Single-cell transcriptomics of pineal parenchymal tumors, integrative computational analyses, lineage-specific perturbation to generate preclinical models, and multi-omic characterization of tumors and models
pineoblastomapineal parenchymal tumorsretinoblastomaGroup 3 medulloblastomacentral nervous system malignancies
The authors performed single-cell transcriptome and multi-omic analyses of pineal parenchymal tumors and generated lineage-perturbed preclinical models to trace cellular origins. They mapped pineoblastoma origins to transient, cycling pinealocyte progenitors and identified a tumor-associated photoreceptor signature (TAPS) that is shared by pineoblastoma, retinoblastoma, and Group 3 medulloblastoma. Components of this photoreceptor signature were found to be selective dependencies across these CNS malignancies. The work proposes a developmental basis for molecular similarities and motivates further studies of these developmentally encoded programs.
Key findings
- Single-cell transcriptomes from pineal parenchymal tumors map pineoblastoma origins to transient, cycling pinealocyte progenitors during development.
- Lineage-specific perturbation in the early pineal gland produced preclinical models representative of consensus molecular subgroups.
- Multi-omic characterization of patient tumors and models uncovered a tumor-associated photoreceptor signature (TAPS) common to pineoblastoma, retinoblastoma, and Group 3 medulloblastoma.
- Transcriptional activity of the TAPS within respective cellular origins provides a developmental explanation for molecular similarities between these entities.
- Constituents of the photoreceptor signature are reported as selective dependencies across these anatomically distinct CNS malignancies, motivating future evaluation of developmentally encoded programs as potential vulnerabilities.
Limitations: Abstract does not report sample sizes or detailed cohort information.; Findings are primarily molecular and preclinical; no clinical therapeutic testing or patient outcomes are reported.; Selective dependencies are described but not shown to be therapeutically validated in patients within this study.; The abstract summarizes complex multi-omic and model work but provides no quantitative results or statistical measures..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 31
Histopathology · Apr 2026 · molecular DNA methylation and copy-number profiling of a series of uterine tumours
GREB1-rearranged uterine tumourUTROSCT (uterine tumour resembling ovarian sex cord tumour)uterine smooth muscle tumours (leiomyoma, leiomyosarcoma)endometrial stromal sarcomaembryonal rhabdomyosarcomaSMARCA4-deficient uterine sarcoma
The authors performed global DNA methylation and copy-number analyses on 10 GREB1-rearranged uterine tumours and 21 classic UTROSCTs (including 7 with ESR1::NCOA2/3 fusions). GREB1-rearranged tumours shared a DNA methylation cluster with UTROSCTs and were distinct from other uterine sarcoma types, but showed greater genomic complexity (more copy-number alterations) and more often lacked overt sex cord morphology.
Reported effects: Number of GREB1-rearranged uterine tumours 10 · Number of classic UTROSCTs 21 · +2 more
Key findings
- GREB1-rearranged uterine tumours show overlap in global methylation profiles with UTROSCT, including ESR1::NCOA2/3 positive cases, forming a DNA methylation cluster separate from several other uterine sarcoma types.
- GREB1-rearranged tumours displayed a greater degree of genomic complexity with more extensive copy number alterations than conventional UTROSCTs, including those with ESR1::NCOA2/3.
- GREB1-rearranged tumours frequently lacked overt sex cord morphology: only 1 GREB1-rearranged tumour displayed a prominent trabecular pattern while the remaining cases had diffuse/solid growth.
- All 7 ESR1::NCOA2/3-positive UTROSCTs demonstrated corded, nested, trabecular and/or tubular/sertoliform patterns.
Limitations: Small case series (31 tumours total) limits generalisability.; Observational molecular profiling without clinical outcome or functional validation data.; Comparisons are limited to the tumour types included; methylation/copy-number differences may not generalise to all uterine tumours..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Human · observationalMechanismMixed resultsLimited evidenceTier 3 · early humann = 57
Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · Apr 2026 · retrospective case series
tubo-ovarian carcinosarcomaovarian carcinosarcomafallopian tube neoplasm
This single-institution study reviewed 57 tubo-ovarian carcinosarcomas with median follow-up of 32.3 months. Most tumors (51/57, 89%) were p53-abnormal; a small subset (5/57, 9%) were p53 wild-type and all five had canonical KRAS codon 12 mutations and distinct endometrioid histology. The authors report the first primary POLE-mutated OCS in a patient with Lynch syndrome. KRAS-mutated tumors occurred at younger ages and lower stage but recurred in 2 of 5 patients.
Reported effects: median_follow_up 32.3 mo, n=57 · 5-year survival stage I/II 71%, n=57 · +9 more
Key findings
- The overall median follow-up period was 32.3 months.
- Five-year survival rates were 71% (stage I/II), 42% (stage III), and 17% (stage IV).
- Fifty-one (89%) tumors were of the p53-abnormal molecular subtype.
- Five (9%) tumors were of no specific molecular subtype, and all 5 of these tumors harbored canonical mutations in KRAS (codon 12).
- The first reported primary POLE-mutated OCS was identified in a patient with Lynch syndrome (assigned as a double-classifier POLE-mutated/mismatch repair-deficient molecular subtype).
- Compared with the p53-abnormal tumors, KRAS-mutated tumors occurred in younger women at lower stages, but did recur in 2 out of 5 (40%) patients.
- KRAS-mutated tumors always showed endometrioid rather than high-grade serous morphology and were usually ER, PR, and WT1 negative.
- Three KRAS-mutated tumors also had at least focal mesonephric-like histology.
Limitations: Single-institution case series (limited generalizability).; Relatively small overall sample size (n=57) and very small KRAS-mutated subgroup (n=5), limiting statistical power and conclusions about that subset.; Retrospective, observational design without experimental/functional validation.; Follow-up median 32.3 months may limit long-term outcome assessment..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed
ReviewReported positivePreclinical onlyTier 1 · lab
Molecular imaging and biology · Apr 2026
triple-negative breast cancer
This review summarizes sonodynamic therapy (SDT) as an ultrasound-driven, reactive-oxygen-species-generating approach combined with immunotherapy for triple-negative breast cancer. It covers SDT physical principles (acoustic cavitation, sonoluminescence, piezocatalysis), cell-death modes (apoptosis, ferroptosis, pyroptosis, mitophagy), innate immune pathways (cGAS-STING), and nanoplatform strategies such as oxygen-generating catalysts and GSH-depleting constructs. The authors discuss durability of anti-tumor immunity with combination therapies and outline preclinical toxicology and pharmacodynamic biomarker needs for translating SDT as an immuno-nanomedicine.
Studied with: immunotherapy.
Key findings
- SDT generates reactive oxygen species (ROS) using ultrasound and can combine localized apoptosis with systemic immune activation.
- The review integrates biophysical SDT mechanisms (acoustic cavitation, sonoluminescence, piezocatalysis) with non-apoptotic cell-death modalities (ferroptosis, pyroptosis, mitophagy).
- Innate nucleic acid receptor-sensing pathways such as cGAS-STING are discussed as immune-activating mechanisms for SDT-enhanced immunotherapy.
- Nanotechnology strategies covered include oxygen-generating catalysts, glutathione (GSH)-depleting constructs, biomimetic and stimulus-responsive carriers, and theranostic probes to address hypoxia and redox suppression.
- The review assesses durability of anti-tumor immunity induced by combination therapies and outlines necessary preclinical toxicology and pharmacodynamic biomarker studies to advance clinical implementation.
Limitations: This is a review article and does not present new primary experimental or clinical trial data.; The discussion is largely mechanistic and preclinical; the abstract does not report human clinical results or quantitative efficacy data.; Recommendations for preclinical toxicology and pharmacodynamics are outlined but specific safety or translational outcomes are not provided in this article..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed
ReviewMechanismMixed resultsModerate evidenceTier 4 · clinical
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
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
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
ReviewReported positivePreclinical onlyTier 1 · lab
Theranostics · Mar 2026
deep-seated solid tumorsdrug-resistant solid tumors
This is a systematic review of strategies to sensitize sonodynamic therapy (SDT) for cancer. It summarizes advances in sonosensitizer design, approaches to overcome tumor-microenvironmental suppression, and combinations with other modalities to boost reactive oxygen species generation and antitumor immune responses, while noting translational challenges.
Studied with: chemodynamic therapy, phototherapy, immunotherapy, ferroptosis induction, cuproptosis induction, bacteria-mediated targeted delivery.
Key findings
- SDT faces challenges including suboptimal sonosensitizer efficiency, suppression by the tumor microenvironment, and insufficient induction of antitumor immune responses.
- Sonosensitizer engineering strategies such as defect engineering, heterostructure construction, and use of piezoelectric materials can markedly enhance ROS generation via band structure modulation and mechano-electro-chemical coupling.
- Tumor-microenvironment-targeting approaches (hypoxia alleviation, antioxidant depletion, metabolic reprogramming, bacteria-mediated delivery) have been developed to mitigate ROS scavenging and improve tumor selectivity.
- SDT has been combined with chemodynamic therapy, phototherapy, immunotherapy, and ferroptosis/cuproptosis induction to trigger immunogenic cell death and reverse tumor immunosuppression.
- Persistent translational challenges include nanodelivery, controllable ROS generation, and lack of clinical standardization; development of multimodal, responsive, and biohybrid platforms may aid progress toward clinical application.
Limitations: Review article; does not present new experimental or clinical trial data.; Focus is largely on preclinical strategies and mechanisms rather than demonstrated clinical outcomes.; No quantitative clinical efficacy or safety results reported in this paper.; Identified challenges (nanodelivery, controllable ROS, clinical standardization) indicate translational gaps remain..
AI summary of the abstract, human-reviewed · Aug 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 216
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
Case reportInconclusiveLimited evidenceTier 3 · early humann = 1
Journal of neurosurgery. Case lessons · Mar 2026 · illustrative case report
primary intracranial sarcoma
This is a single-patient case report of a 55-year-old man who presented repeatedly over about 5 months with recurrent right frontal intraparenchymal hemorrhage. Multiple imaging studies including MR spectroscopy initially failed to identify an underlying lesion; only on the most recent presentation did MRI show a hemorrhagic mass that was resected and diagnosed as a primary intracranial sarcoma (DICER-1-mutant). The authors emphasize caution interpreting negative MR spectroscopy in hemorrhagic neoplasms and note difficulty timing resection when the cause of spontaneous IPH is unclear.
Key findings
- A 55-year-old man had recurrent, symptomatic right frontal intraparenchymal hemorrhage over an approximately 5-month period.
- Multiple imaging modalities, including MR spectroscopy, initially failed to identify an underlying lesion.
- On the most recent presentation MRI demonstrated evidence of a hemorrhagic mass.
- The hemorrhagic mass was resected and found to be a primary intracranial sarcoma (DICER-1-mutant).
- The report highlights the need to interpret negative MR spectroscopy results with caution in hemorrhagic neoplasms and the difficulty of determining optimal resection timing when spontaneous IPH has no clear etiology.
Limitations: Single-patient case report (n=1); findings may not generalize.; Observational retrospective description without control or comparison.; No quantitative diagnostic performance data provided for MR spectroscopy or other modalities.; Limited follow-up and limited detail about molecular/therapeutic implications in the abstract..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Animal studyReported positivePreclinical onlyTier 2 · animal
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
Human · observationalMechanismMixed resultsLimited evidenceTier 3 · early humann = 923
The journal of pathology. Clinical research · Mar 2026 · immunohistochemical study on tissue microarrays using the VENTANA FOLR1 CDx assay with standardized scoring criteria
tubo-ovarian tumorsendometrial tumorshigh-grade serous carcinoma (HGSC)low-grade serous carcinoma (LGSC)endometrial serous carcinomaserous borderline tumorendometrioid ovarian carcinomaclear cell ovarian carcinomamucinous ovarian tumorssex cord-stromal tumorsendometrial endometrioid carcinomasundifferentiated carcinomadedifferentiated carcinomaendometrial clear cell carcinoma
The study examined folate receptor alpha (FRα) expression by immunohistochemistry on tissue microarrays of 923 tubo-ovarian and endometrial tumors using the VENTANA FOLR1 CDx assay and standardized scoring. They found FRα expression most commonly in serous carcinomas (45% of HGSC, 25% LGSC) and less commonly in some endometrial serous and serous borderline tumors, while many other ovarian and endometrial tumor types were negative or rarely positive. The work is descriptive and does not report clinical outcomes or functional testing.
Reported effects: HGSC positive cases 45% · Low-grade serous carcinoma positive cases 25% · +4 more
Key findings
- HGSC (high-grade serous carcinoma): 45% positive cases
- Low-grade serous carcinoma: 25% positive cases
- Endometrial serous carcinoma: 11% positive cases
- Serous borderline tumor: 10% positive cases
- Endometrioid ovarian carcinoma: 2% positive cases
- Clear cell ovarian carcinoma: 1% positive cases
- Mucinous ovarian tumors, sex cord-stromal tumors, endometrial endometrioid carcinomas, undifferentiated and dedifferentiated carcinomas, and endometrial clear cell carcinomas were reported as negative
Limitations: Descriptive immunohistochemistry only — no functional assays or correlation with clinical outcomes reported in the abstract; Use of tissue microarrays may under-represent intratumoral heterogeneity; Cross-sectional/tissue-based study without longitudinal or therapeutic response data.
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
OtherSupportive careReported positiveLimited evidenceTier 3 · early humann = 14
Advances in physiology education · Mar 2026 · educational experiential learning program (Exercise is Medicine® video-based challenge)
Supportive careunspecified cancer types
This report describes an experiential, video-based educational initiative in which undergraduate students produced evidence-based videos highlighting exercise in cancer prevention and supportive care. Fourteen students created 12 videos; finalist videos promoted online generated >1,000 views. The authors conclude the initiative increased awareness of exercise oncology and is a scalable model for integrating exercise physiology into oncology education.
Reported effects: students engaged 14, n=14 · videos produced 12, n=12 · +1 more
Key findings
- An interdisciplinary team implemented an Exercise is Medicine® video-based challenge for undergraduate students.
- The challenge engaged 14 students who produced 12 evidence-based videos combining exercise physiology and cancer prevention/supportive care.
- Submissions were evaluated and finalists were shared for public voting at a regional conference; finalist videos promoted via social media and professional networks generated >1,000 views.
- Awards and promotion encouraged student engagement, collaboration, and advocacy for exercise in supportive cancer care.
- Authors report the initiative demonstrated students could synthesize and communicate complex scientific concepts and that the model is scalable for education in exercise oncology.
Limitations: Small participant number (14 students); limited generalizability.; Educational intervention only — no clinical or patient-centered outcomes were measured.; No control or comparison group reported.; Outcome metrics reported (e.g., video views) are surrogate measures of awareness rather than validated behavior change or health endpoints.; No long-term follow-up or assessment of impact on clinical practice or patient care reported..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed
ReviewReported positiveLimited evidenceTier 3 · early human
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
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
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
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
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
ReviewTrialInconclusiveLimited evidenceTier 4 · clinical
The Cochrane database of systematic reviews · Feb 2026 · protocol for a Cochrane Review (intervention)
non-small cell lung cancer (NSCLC)
This publication is a protocol for a Cochrane systematic review. The planned review will assess the benefits and harms of KRAS G12C inhibitors compared with chemotherapy in adults with advanced or metastatic NSCLC harboring the KRAS G12C mutation who are receiving second-line or later therapy; no results are reported in this protocol.
Key findings
- This is a protocol to assess the benefits and harms of G12C-inhibitors compared to chemotherapy in second line and beyond in adults with advanced/metastatic NSCLC with a KRAS G12C mutation.
Limitations: This document is a review protocol and reports no study results or pooled data.; No sample size, outcomes, or trial data are presented in the abstract..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
OtherReported positiveModerate evidenceTier 4 · clinical
ESMO open · Feb 2026 · practice_guideline
Rucaparibepithelial ovarian cancerrecurrent high FRα ovarian cancer This is an Express Update to the ESMO clinical practice guideline prompted by approval of rucaparib and MIRV. The update adds rucaparib as a first-line PARP inhibitor maintenance option for epithelial ovarian cancer and recommends MIRV for recurrent, high FRα ovarian cancer after 1–3 prior therapies with a platinum-free interval under 6 months. Updated treatment algorithms to support personalised therapy are also noted.
Key findings
- This Express Update has been issued in response to the approval of rucaparib and MIRV.
- It includes rucaparib as a first-line PARPi maintenance option in EOC.
- MIRV is recommended for recurrent, high FRα ovarian cancer after 1-3 prior therapies and platinum-free interval of <6 months.
- Updated treatment algorithms support personalised therapy in newly diagnosed and recurrent EOC.
Limitations: Abstract is an Express Update and provides no primary data, numerical outcomes, or details of the evidence reviewed.; No dosing, safety, or comparative efficacy data are reported in the abstract.; Short abstract format limits assessment of the strength and scope of recommendations..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
ReviewMechanismReported positiveLimited evidenceTier 3 · early human
International journal of clinical oncology · Feb 2026 · review
non-small cell lung cancer
This narrative review summarizes studies linking the human microbiome (microflora) with non-small cell lung cancer (NSCLC). It reports that patients with NSCLC have distinct microbial communities in tumors, airways, and intestines and that characteristic microbes and circulating microbial DNA may assist diagnosis. The review states that microbiome alterations can influence the efficacy and adverse effects of immunotherapy, and that interventions such as antibiotics, inhaled or oral probiotics, prebiotics, and dietary changes are proposed to rebalance microflora and may enhance immunotherapy. It also discusses possible molecular mechanisms and the potential for microbe-specific testing and targeted microbial therapies in NSCLC.
Studied with: immunotherapy.
Key findings
- Patients with NSCLC have distinct microflora within the tumor, airways, and intestines compared with healthy or benign lung disease patients.
- Characteristic microflora and circulating microbial DNA may assist in the diagnosis of NSCLC.
- Microflora changes can affect the efficacy of immunotherapy and treatment-related adverse effects during lung cancer therapy.
- Modulating microflora imbalance through antibiotics/probiotics nebulization, oral probiotic, prebiotics, and dietary modifications is proposed to rebalance microflora and enhance the effectiveness of immunotherapy.
- Microbe-specific testing and targeted microbial therapy are presented as potential new approaches for diagnosis and treatment of NSCLC.
Limitations: This article is a review (narrative) and does not present primary experimental or clinical trial data.; The abstract does not report quantitative results, randomized trial evidence, or systematic review/meta-analysis methodology.; Clinical effectiveness and safety of the proposed microbiome interventions are not demonstrated in this abstract and appear to be proposed rather than proven..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed
Animal studyReported positivePreclinical onlyTier 2 · animal
Advanced materials (Deerfield Beach, Fla.) · Feb 2026
orthotopic breast cancer
The authors developed MeTTh-PAE nanoparticles that form hydrophobic aggregates in acidic environments and enhance cavitation-triggered sonoluminescence under ultrasound, while aggregated MeTTh promotes intersystem crossing to increase ROS generation. These nanoparticles produced enhanced sonodynamic antitumor effects in both cell-based experiments and in vivo orthotopic breast cancer models.
Key findings
- MeTTh-PAE NPs are released as hydrophobic aggregates with a rough surface in response to an acidic environment.
- The aggregated state allows for highly enhanced cavitation-triggered sonoluminescence (SL) under ultrasound.
- As an aggregation-induced emission molecule, MeTTh demonstrates a highly promoted intersystem crossing process at its aggregated state, facilitating efficient SL-to-ROS conversion.
- Combining enhanced cavitation-driven SL generation and efficient SL-to-ROS conversion in MeTTh-PAE NPs results in an excellent sonodynamic antitumor effect in both in vitro and in vivo.
Limitations: Preclinical study only: findings are limited to in vitro experiments and animal (in vivo) models, with no human data reported.; Abstract provides no sample sizes, dosing details, toxicity/safety data, or statistical measures.; Mechanistic interpretations are presented but causality and detailed pathway validation are not shown in the abstract..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed
Human trialTrialReported positiveModerate evidenceTier 4 · clinicaln = 298
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, published automatically under the strong-evidence tier · Jul 2026; an editor has not yet reviewed it. Describes what this study reported, not medical advice. View on PubMed
OtherFormulationMixed resultsPreclinical onlyTier 1 · lab
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 positiveLimited evidenceTier 3 · early human
Cancers · Jan 2026
endometrial mixed carcinomaendometrial mixed-feature carcinomaendometrial serous carcinomaendometrioid carcinoma
This small cohort study compared clinical, histologic, and molecular features of mixed and mixed-feature endometrial carcinomas to pure serous and pure endometrioid carcinomas. The mixed tumors occurred in older patients, had shorter median disease-free survival, were high-grade and commonly composed of serous and endometrioid components, and showed identical TP53 and PIK3CA mutations between components consistent with a clonal origin. Mixed tumors also had additional alterations (e.g., TERT, MAP2K1) in higher-grade components, and ERBB2 amplifications were more frequent in the mixed groups.
Reported effects: median age 73 · median disease-free survival 23 mo · +2 more
Key findings
- Patients with mixed and mixed-feature carcinomas were older (median age: 73 years) and had worse disease-free survival (median: 23 months) than those with pure endometrioid carcinoma (median: 48 months).
- Mixed and mixed-feature carcinomas were histologically high-grade, most commonly comprising serous and endometrioid components.
- Molecular profiling supported a clonal origin, with identical TP53 and PIK3CA mutations between the two histologic components in each case.
- Additional gene mutations (e.g., TERT and MAP2K1) were found in higher-grade components.
- ERBB2 amplifications were more frequent in the mixed carcinoma groups (33%) compared to pure serous (11%) and pure endometrioid carcinomas (0%).
- Some mixed and mixed-feature carcinomas showed FBXW7 mutations not seen in pure endometrioid or pure serous carcinomas.
Limitations: Small cohort (described as a small cohort in the title/abstract).; No sample size or detailed study design reported in the abstract.; Observational design limits causal inference regarding outcomes.; Abstract gives no statistical measures (p-values, confidence intervals) or method details for molecular testing.; Potential limited genomic scope implied by the authors' call for targeted sequencing and larger cohorts..
AI summary of the abstract, human-reviewed · Aug 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Human · observationalMechanismReported positiveModerate evidenceTier 3 · early human
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
Human · observationalReported positiveLimited evidenceTier 3 · early humann = 94
American journal of epidemiology · Jan 2026 · retrospective cohort study
uterine serous carcinoma
This retrospective single-institution study identified 94 patients with stage I–II uterine serous carcinoma treated from 2006–2019 and examined associations between adjuvant therapies and outcomes. Most patients received adjuvant therapy, commonly chemotherapy plus vaginal brachytherapy; at median follow-up 33.5 months, 81.9% had no evidence of disease. Patients receiving six cycles of adjuvant chemotherapy had statistically better overall survival (P = .004) and recurrence-free survival (P = .02) compared with those who did not receive adjuvant chemotherapy.
Reported effects: sample_size 94, n=94 · median_followup 33.5 mo, n=94 · +10 more
Studied with: radiation therapy, vaginal brachytherapy.
Key findings
- Ninety-four patients were identified.
- Median follow-up time was 33.5 months.
- Median age was 68 years (range, 49-87).
- Most patients (n = 79, 84.0%) received adjuvant therapy; a majority received a combination of systemic chemotherapy and radiation therapy (n = 55, 58.5%), with chemotherapy plus vaginal brachytherapy the most common combination (n = 42, 44.7%).
- Most patients (n = 77, 81.9%) remained without evidence of disease, while 17 patients (18.1%) recurred.
- Patients receiving 6 cycles of adjuvant chemotherapy experienced improved overall survival (P = .004) and improved recurrence-free survival (P = .02) compared to those receiving no adjuvant chemotherapy.
Limitations: Retrospective, non-randomized design; Single-institution cohort; Relatively small sample size (n = 94); Potential selection and treatment-allocation bias; Median follow-up of 33.5 months is modest and may limit assessment of long-term outcomes; No chemotherapy regimen details or toxicity data provided in the abstract.
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed
Animal studyMixed resultsPreclinical onlyTier 2 · animal
Journal of experimental & clinical cancer research : CR · Jan 2026 · High-throughput drug screening in organoid models performed in presence of cisplatin or eribulin, with validation of top combinations in OCS cell line, organoid and PDX models including in vivo PDX experiments.
Cisplatinovarian carcinosarcomahigh-grade serous ovarian cancer (HGSOC) The authors performed high-throughput drug screens in ovarian carcinosarcoma (OCS) organoid models and validated top combinations in a unique OCS cell line, organoid and PDX models. Eribulin combined with either an EGFR inhibitor (erlotinib) or a MEK inhibitor (mirdametinib/PD0325901) produced synergistic effects in some in vitro models, and modest survival improvements in vivo, but several PDX models exhibited resistance mechanisms (high ABCB1 expression or KRAS mutation) limiting efficacy.
Reported effects: models_with_synergy 2, n=4 · PDX_models_with_resistance 2, n=3
Studied with: erlotinib, mirdametinib, PD0325901, cisplatin.
Key findings
- High-throughput screens identified eribulin-based combinations as most effective in OCS organoid models, while cisplatin-based combinations were more effective in HGSOC models.
- Eribulin plus erlotinib or eribulin plus a MEK inhibitor (mirdametinib/PD0325901) were the most effective combinations in OCS models, with synergy seen in two out of four models for each combination.
- OCS models appear particularly reliant on EGFR and MAPK signalling in vitro, especially in tumours with TP53 mutation.
- In vivo (PDX) experiments showed only modest survival improvements for eribulin plus erlotinib, and two of three PDX models had resistance mechanisms (high ABCB1 or KRAS activating mutation).
- KRAS-mutant OCS cell lines and organoids were sensitive to dual EGFR/MAPK targeting, with greater synergy when eribulin was added as a third agent.
Limitations: Preclinical study using in vitro organoids, cell lines and PDX models; no human clinical data reported.; Only modest in vivo survival benefit reported.; Synergy was observed in a subset of models (e.g., two of four organoid models), indicating heterogeneity and limited generalizability.; A small number of PDX models were tested (three), and two showed resistance mechanisms limiting efficacy.; No doses, schedules, or safety/toxicity data in humans provided..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Lab · in vitroMechanismReported positivePreclinical onlyTier 1 · lab
Frontiers in immunology · Jan 2026 · Integrated single-cell and bulk transcriptomic analysis with in vitro knockdown experiments in DU145 prostate cancer cells
prostate adenocarcinoma
The authors combined single-cell and bulk RNA sequencing analyses with laboratory experiments in DU145 prostate cancer cells. They found GDPD3 was upregulated in malignant prostate tissues and that knocking down GDPD3 reduced cell proliferation, invasion, migration and EMT. Mechanistically, GDPD3 influenced lysophosphatidic acid (LPA) levels; LPA induced EMT via LPAR1 and activation of AKT, and blocking LPAR1 or AKT reversed EMT. The study proposes GDPD3 as a potential therapeutic target and biomarker in prostate adenocarcinoma.
Key findings
- A 21-gene prognostic model was established from integrated single-cell and bulk RNA-seq analyses.
- QPCR and immunohistochemistry showed GDPD3 expression was significantly elevated in malignant prostate tissues.
- Knockdown of GDPD3 in DU145 cells inhibited tumor cell proliferation, invasion, and migration.
- GDPD3 regulated levels of lysophosphatidic acid (LPA).
- Inhibition or knockdown of the LPA receptor LPAR1 suppressed EMT.
- LPA promoted EMT through activation of the AKT signaling pathway, and inhibition of AKT reversed LPA-induced EMT.
Limitations: Functional validation was performed only in vitro (DU145 cell line); no in vivo (animal) experiments reported.; Prognostic model details, validation cohort performance metrics, and sample sizes are not provided in the abstract.; No clinical intervention or patient-level functional validation was reported.; Causality in patients is not established; transcriptomic associations may not translate to clinical benefit..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 25
International journal of gynecological cancer : official journal of the International Gynecological Cancer Society · Jan 2026 · case series with centralized pathology review
endometrial carcinomaovarian endometrioid carcinoma
The authors reviewed 25 patients with synchronous endometrial and ovarian endometrioid carcinomas and compared staging under the FIGO 2009 versus FIGO 2023 classifications with centralized pathology review. Applying FIGO 2023 (and ESGO risk stratification) changed stage in 5 patients (20%), with 2 downstaged and 3 upstaged; among 11 patients with disease limited to uterus and ovaries, 5 met stage IA3 and none recurred, including 2 managed with surgery alone. The authors conclude FIGO 2023 IA3 can improve risk stratification, particularly for low-grade, ER-positive tumors with favorable molecular profiles, but note issues about adequate staging surgery and ovarian grading criteria.
Reported effects: stage_shifts 20%, n=25 · downstaged_count 2, n=25 · +4 more
Key findings
- Study cohort comprised 25 patients with concurrent endometrial and ovarian tumors.
- Applying FIGO 2023 classification and ESGO risk stratification led to stage shifts in 5 patients (20%): 2 were downstaged and 3 were upstaged.
- Among 11 patients whose disease was limited to the uterus and ovaries, 5 met criteria for stage IA3 and none experienced recurrence; this group included 2 patients managed with surgery alone.
- FIGO 2023 stage IA3 classification enables more precise risk stratification, particularly in low-grade, estrogen receptor-positive tumors with favorable molecular profiles (POLE-mutated or p53 wild-type / non-specific molecular profile).
- The new classification raises operational issues: the need for appropriate staging surgery and debate about the optimal grading system for ovarian endometrioid carcinoma.
Limitations: Small sample size (25 patients).; Observational case-series design with potential selection bias.; Follow-up duration and timing of recurrence assessment are not reported in the abstract.; Low event counts (no recurrences reported) limit strength of outcome conclusions.; Generalizability limited by small cohort and lack of multi-center data in the abstract..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed
Animal studyReported positivePreclinical onlyTier 2 · animal
Advanced materials (Deerfield Beach, Fla.) · Jan 2026
glioblastoma
The authors developed innate immune-stimulating nanoparticles (INSTNA) carrying an iridium-based mitochondrial-targeting complex (Ir-mito) and siRNA against MCJ to impair mitochondrial respiration in glioblastoma cells. In cell experiments and a postoperative GBM mouse model, INSTNA induced mitochondrial oxidative phosphorylation stress and mitochondrial matrix release, remodeled the immunosuppressive tumor microenvironment, and produced pronounced tumor regression when delivered in a hydrogel and combined with tumor-treating fields. The study reports enhanced innate and adaptive immune activation associated with these effects. No human data are reported in the abstract.
Studied with: tumor-treating fields, hydrogel-mediated delivery.
Key findings
- INSTNA encapsulating Ir-mito and si-MCJ disrupt mitochondrial function of GBM cells.
- The engineered charge-reversal INSTNA impair the mitochondrial electron transport chain, inducing OXPHOS stress and mitochondrial matrix release.
- Combination with tumor-treating fields enhanced the disruption of mitochondrial function.
- Hydrogel-mediated delivery of INSTNA in a postoperative GBM mouse model significantly remodeled the immunosuppressive microenvironment.
- Treatment resulted in pronounced tumor regression and potentiation of innate and adaptive immune responses in the mouse model.
Limitations: Preclinical study using in vitro experiments and a mouse (postoperative GBM) model only; no human data reported.; Abstract does not report sample sizes, randomization, or control group details.; Safety, toxicity, and long-term outcomes are not reported in the abstract.; Quantitative effect sizes, statistical values, and detailed methods are not provided in the abstract..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed
ReviewMechanismMixed resultsLimited evidenceTier 4 · clinical
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
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
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
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
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
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
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
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
Case reportInconclusiveLimited evidenceTier 3 · early humann = 1
Turkish archives of otorhinolaryngology · Dec 2025
prostate adenocarcinomalarynx
This is a case report of an 80-year-old man who presented with productive cough and hoarseness. Laryngoscopy showed submucosal fullness in the right hemilarynx with airway narrowing, and biopsy with histopathology and immunohistochemistry diagnosed the lesion as laryngeal metastasis from prostate adenocarcinoma. The authors present the case because laryngeal metastases from prostate adenocarcinoma are rare.
Key findings
- Patient: 80-year-old male presented with productive cough and hoarseness.
- Videolaryngoscopy showed submucosal fullness in the right hemilarynx, pushing the right band ventricle mucosa medially and causing evident narrowing of the airway.
- Histopathological evaluation and immunohistochemical staining of an endolaryngeal submucosal biopsy specimen from the right ventricular fold diagnosed laryngeal metastasis of prostate adenocarcinoma.
- The case is presented because laryngeal metastases from prostate adenocarcinoma are scarce in the literature.
Limitations: Single-patient case report limits generalizability.; No information provided on treatment, follow-up, or patient outcome.; No quantitative data or comparative analysis.; Imaging and staging details beyond the described laryngoscopic findings are not provided..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Human · observationalMechanismReported positiveLimited evidenceTier 3 · early human
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
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
ReviewMechanismMixed resultsLimited evidenceTier 4 · clinical
Cancers · Dec 2025
glioblastoma
This review summarizes current knowledge about circulating tumor cells (CTCs) in glioblastoma, describing their unique properties, detection technologies, and the challenges of rarity, lack of epithelial markers, and the blood-brain barrier. It discusses potential uses of CTC analysis for assessing tumor heterogeneity, monitoring treatment response, detecting minimal residual disease and early relapse, and reviews preclinical mouse models (cell-line xenografts, patient-derived xenografts, genetically engineered mouse models) and their limitations.
Key findings
- CTCs have been detected in glioblastoma, challenging the traditional view of GBM as non-metastatic.
- Glioblastoma CTCs are rare, lack epithelial markers, and are affected by the blood-brain barrier, requiring specialized enrichment approaches.
- CTC analysis in glioblastoma may provide information on tumor heterogeneity, treatment response, and minimal residual disease.
- Emerging clinical studies are using CTCs for early relapse detection and therapy monitoring.
- Preclinical mouse models for glioblastoma include cell-line xenografts, patient-derived xenografts (PDX), and genetically engineered mouse models (GEMMs), each with advantages and limitations.
- PDX models retain genetic and histological features of primary tumors but cannot fully recapitulate human antitumor immunity; GEMMs allow study of specific genetic alterations but may lack intratumoral heterogeneity.
Limitations: This is a review article and does not present new primary experimental data.; CTCs in glioblastoma are rare and lack epithelial markers, which complicates detection and analysis.; The blood-brain barrier presents a challenge for CTC detection and interpretation.; Preclinical models discussed have known limitations: PDX models do not reflect human antitumor immunity and GEMMs may not capture intratumoral heterogeneity.; Clinical evidence is described as emerging, implying early-stage or limited-size clinical studies rather than definitive clinical validation..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Human · observationalMechanismInconclusiveLimited evidenceTier 3 · early human
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
Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 49
BMC cancer · Dec 2025 · descriptive observational analysis with univariate and multivariate survival analysis and methylation profiling
pineal parenchymal tumorspineoblastomapapillary tumor of the pineal regionpineal parenchymal tumor of intermediate differentiation (PPTID)pineocytomatrilateral retinoblastomamedulloblastoma
This observational study analyzed 49 patients with pineal parenchymal tumors and performed DNA methylation profiling on 20 cases. In pineoblastoma patients, younger age was significantly associated with worse overall survival and event-free survival, and metastatic status was associated with worse event-free survival. Methylation profiling separated tumors into multiple molecular groups (for example PB-miRNA-1, PB-RB1, and several single-case entities), illustrating marked heterogeneity.
Reported effects: Age impact on overall survival (OS) — univariate p-value, p=0.003, n=39 · Age impact on event-free survival (EFS) — univariate p-value, p=0.021, n=39 · +11 more
Key findings
- Study cohort comprised 49 patients with pineal parenchymal tumors, including 39 pineoblastomas.
- Univariate analysis among pineoblastomas showed age significantly impacted overall survival (OS) (p = 0.003) and event-free survival (EFS) (p = 0.021).
- Metastatic status impacted EFS in univariate analysis (p = 0.032).
- In multivariate analysis, only age remained significant for OS (p = 0.028).
- Methylation classification (on 20 cases) identified groups: PB-miRNA-1 (n = 10), PB-RB1 (n = 1), retinoblastoma-MYCN activated (n = 1), PPTID KBTBD4-altered (n = 1), papillary tumor of the pineal region (n = 1), medulloblastoma WNT activated (n = 1), medulloblastoma non-WNT/SHH (n = 1), CNS embryonal tumor with BRD4-LEUTX fusion (n = 1), and unclassified (n = 3).
Limitations: Relatively small overall sample size (n = 49) and small numbers within subgroups, limiting statistical power.; DNA methylation profiling was performed on a subset (20 of 49) of cases, which may limit representativeness of molecular findings.; Observational/descriptive design without randomization or standardized treatment information reported, limiting causal inference and generalizability.; Several molecular subgroups had only single cases, restricting ability to draw robust subgroup-specific conclusions..
Study supports the use of DNA methylation-based molecular classification for accurate diagnosis and prognostic stratification of pineal parenchymal tumors.
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
ReviewInconclusiveLimited evidenceTier 4 · clinical
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
OtherMechanismReported negativePreclinical onlyTier 1 · lab
Cell metabolism · Dec 2025
pancreatic cancer
This study examined mechanisms linking obesity to pancreatic cancer progression. It reports that extracellular vesicles from visceral adipose tissue reprogram immune cells via a cathepsin A–pseudouridine–mast cell axis. The authors conclude this pathway promotes immune evasion and resistance to checkpoint blockade therapy in pancreatic cancer.
Key findings
- Extracellular vesicles from visceral adipose tissue reprogram immune cells.
- This reprogramming occurs through a cathepsin A–pseudouridine–mast cell axis.
- The described mechanism provides a way obesity can drive immune evasion and resistance to checkpoint blockade therapy in pancreatic cancer.
Limitations: Abstract does not state the experimental model(s) used (cells, animals, or human tissue) or sample sizes.; No quantitative data, statistical results, or numeric effect sizes are reported in the abstract.; Abstract provides mechanistic insight but does not present clinical trial or patient outcome data to demonstrate relevance in humans..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed
Meta-analysisMechanismMixed resultsModerate evidenceTier 4 · clinicaln = 1510
Annals of medicine · Dec 2025 · systematic review and meta-analysis
endometrioid ovarian cancer (ENOC)clear cell ovarian cancer (CCOC)
This systematic review and meta-analysis pooled data from studies of TCGA molecular subtypes in endometriosis-associated ovarian cancers (ENOC and CCOC). It included 6 studies with 1,133 ENOC patients and 4 studies with 377 CCOC patients. ENOC showed higher frequencies of the POLEmut and MMRd subtypes and lower frequencies of NSMP and p53abn compared with CCOC. The p53abn subtype was associated with worse disease-free and progression-free survival in ENOC and worse disease-free survival in CCOC.
Reported effects: POLEmut frequency (ENOC vs CCOC) 2.29 [1.03–5.11], p=0.043 · MMRd frequency (ENOC vs CCOC) 3.54 [2.05–6.11], p 0.000 · +5 more
Key findings
- Six studies (1,133 ENOC patients) and four studies (377 CCOC patients) were included.
- ENOC had a higher frequency of the POLEmut subtype compared with CCOC (OR = 2.29).
- ENOC had a higher frequency of the MMRd subtype compared with CCOC (OR = 3.54).
- ENOC had a lower frequency of the NSMP subtype compared with CCOC (OR = 0.55).
- The frequency of the p53abn subtype did not differ significantly between ENOC and CCOC (OR = 0.97).
- In ENOC, the p53abn subtype was associated with reduced DFS (HR = 3.25) and reduced PFS (HR = 4.11).
- In CCOC, the p53abn subtype was associated with reduced DFS (HR = 5.52).
Limitations: Only a small number of studies were included (6 for ENOC, 4 for CCOC).; Meta-analysis relies on published study-level data; individual patient data were not reported.; Potential heterogeneity across included studies (staging, methods for subtype assignment) is not detailed in the abstract.; Prognostic associations are observational and may be subject to residual confounding..
AI summary of the abstract, published automatically under the strong-evidence tier · Sep 2026; an editor has not yet reviewed it. Describes what this study reported, not medical advice. View on PubMed · Full text
Lab · in vitroMechanismReported positivePreclinical onlyTier 1 · lab
Stem cell research · Dec 2025
alveolar rhabdomyosarcoma
The authors describe a laboratory protocol to generate induced pluripotent stem cell (iPSC)-derived alveolar rhabdomyosarcoma (iARMS) cells during endothelial-directed differentiation by enforced expression of the PAX3::FOXO1 fusion. The resulting cell model is presented as a tool to study how PAX3::FOXO1 transforms endothelial progenitors into aggressive myogenic tumors.
Key findings
- Provided a protocol for generating iPSC-derived alveolar rhabdomyosarcoma cells (iARMS) during endothelial directed differentiation through enforced expression of PAX3::FOXO1 (P3F).
- The iARMS model enables dissection of how P3F mediates transformation of endothelial progenitors into aggressive myogenic tumors.
Limitations: In vitro model only; no in vivo or clinical validation reported in the abstract.; No quantitative results, sample sizes, or experimental details reported in the abstract.; Abstract describes a protocol/model but does not present functional or phenotypic metrics in this text..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Human trialSupportive careReported positiveModerate evidenceTier 4 · clinicaln = 150
JACC. CardioOncology · Dec 2025 · randomized clinical trial
Supportive carebreast cancerprostate cancer
This randomized clinical trial tested a remotely delivered, behaviorally designed gamification intervention versus attention control in Black and Hispanic breast and prostate cancer survivors with cardiovascular risk factors. Over a 24-week intervention, the gamification group increased mean daily steps and weekly minutes of moderate-to-vigorous physical activity more than the control group; some increases persisted at 12-week follow-up but were smaller and one was not statistically significant.
Reported effects: change in mean daily steps during intervention 759 [209–1309], p=0.007, n=150 · change in mean daily steps at follow-up 581 [-47–1208], p=0.07, n=150 · +2 more
Key findings
- Randomized participants: attention control (n = 76) and gamification (n = 74); mean age 64 years; 81% women; 64% Black; 35% Hispanic.
- Greater change from baseline in mean daily steps during the intervention period for gamification vs control: +759 steps (95% CI: 209-1,309; P = 0.007).
- Change from baseline in mean daily steps at follow-up: +581 steps (95% CI: -47 to 1,208; P = 0.070) for gamification vs control.
- Greater increase in weekly minutes of moderate-vigorous physical activity during intervention: +16 minutes (95% CI: 4-29; P = 0.010) for gamification vs control.
- Increase in weekly minutes of moderate-vigorous physical activity at follow-up: +11 minutes (95% CI: 0-22; P = 0.048) for gamification vs control.
- Trial name and registration: RCT of Strategies to Augment Physical Activity in Black and Hispanic Breast and Prostate Cancer Survivors (ALLSTAR); NCT05176756.
Limitations: Follow-up period after the intervention was limited to 12 weeks (postintervention), so longer-term effects are unknown.; Study population was limited to Black and Hispanic breast and prostate cancer survivors who had received cardiotoxic therapy and ≥1 cardiovascular risk factor, which may limit generalizability to other survivor groups.; Outcomes measured were physical activity metrics (steps and weekly MVPA) rather than clinical cardiovascular events or hard clinical endpoints.; The change in mean daily steps at follow-up did not reach conventional statistical significance (P = 0.070)..
Behavioral gamification was tested to increase physical activity in cancer survivors with cardiovascular risk factors, a strategy intended to lower cardiovascular risk in this population.
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Case reportMechanismReported positiveLimited evidenceTier 3 · early humann = 1
Tumori · Dec 2025 · case report
breast cancerlarge-cell neuroendocrine carcinoma
This is a case report of a 34-year-old woman initially treated for HR+/HER2- breast cancer in 2012 who developed a mediastinal large-cell neuroendocrine carcinoma (LCNEC) in 2021. Next-generation sequencing identified the same pathogenic PIK3CA variant in both the breast tumor and the LCNEC, suggesting a possible metastatic relationship. The LCNEC progressed on cisplatin/etoposide but had a remarkable and prolonged response to pembrolizumab until treatment was stopped for grade 3 immune-related colitis; the patient had no clinical evidence of disease as of November 2024.
Reported effects: PD-L1 expression 10%, n=1 · tumor mutational burden (TMB) 9.54, n=1 · +1 more
Key findings
- Next-generation sequencing identified shared tumor PIK3CA pathogenic variants in both breast cancer and LCNEC tissues, suggesting a potential relationship as primary tumor and metastasis.
- The mediastinal tumor was a high-grade LCNEC lacking breast-specific markers (GATA3-, HR-, HER2-, mammoglobin-, GCDFP15-).
- PD-L1 expression was 10% and tumor mutational burden (TMB) was 9.54 mut/MB in the LCNEC specimen.
- First-line chemotherapy (cisplatin plus etoposide) led to rapid disease progression; second-line pembrolizumab produced a remarkable and prolonged disease response.
- Treatment was discontinued in 2023 because of grade 3 immune-related colitis; patient had no clinical evidence of disease as of November 2024.
Limitations: Single-patient case report limits generalizability.; Shared PIK3CA mutation suggests but does not definitively prove clonal origin between the two tumors.; No control group or broader cohort for comparison; findings are observational and hypothesis-generating..
AI summary of the abstract, human-reviewed · Aug 2026. Describes what this study reported, not medical advice. View on PubMed
ReviewMixed resultsModerate evidenceTier 4 · clinical
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
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
Human · observationalMechanismMixed resultsLimited evidenceTier 3 · early humann = 83
Acta neuropathologica communications · Nov 2025 · molecular profiling of tumor cohort (genome-wide copy-number, methylation, targeted sequencing, mRNA expression)
pineoblastoma
Researchers performed genome-wide copy-number, methylation, targeted DNA sequencing, and mRNA expression analyses on pineoblastoma tumors (83 cases). They confirmed four epigenetic PB subtypes and found subtype-specific recurrent genetic events, notably frequent alterations in microRNA-processing genes (DICER1 and DROSHA), recurrent chromosome 7 gains and chromosome 14 losses (the latter associated with DICER1 mutations), frequent OTX2 gains across subtypes, and that PB-MYC/FOXR2 and PB-RB1 in infants had worse outcomes while PB-miRNA subtypes did not differ in survival in this cohort.
Reported effects: cohort_cases_analyzed 83, n=83 · cases_screened_for_mutations 79, n=79 · +15 more
Key findings
- Cytogenetics of 83 PB were analyzed by high-resolution genome-wide molecular inversion probe analysis and methylation profiling.
- Seventy-nine cases were screened for mutations by next-generation DNA panel sequencing and for 25 samples mRNA expression was analyzed using NanoString.
- Clinical data of 63 patients was available.
- Cohort composition: 48 PB-miRNA1, 19 PB-miRNA2, 8 PB-MYC/FOXR2, and 8 PB-RB1 cases.
- PB-miRNA subtype tumors showed frequent microRNA-processing gene alterations: DICER1 mutations (n=19/64), homozygous deletions of the DROSHA locus (n=18/67), and DROSHA mutations (n=12/64).
- Most frequent cytogenetic aberrations in PB-miRNA cases were chromosome 7 gains (n=31/67) and chromosome 14 losses (n=26/67), with 5 of those showing copy-neutral LOH.
- Chromosome 14 losses were significantly associated with DICER1 mutations (p < 0.001).
- OTX2 gain was the most frequent alteration overall, occurring in 37/83 PB across all subtypes.
- Cases with polyploid cytogenetics were identified in the PB-miRNA subtypes (n=16/67).
- No survival difference was found between PB-miRNA subtypes in this cohort; PB-MYC/FOXR2 and PB-RB1 in infants showed worse outcome.
Limitations: Observational molecular profiling study without interventional or functional validation experiments in this abstract.; Clinical outcome data were available for only 63 of 83 cases.; Some epigenetic subtypes had small sample sizes (e.g., PB-MYC/FOXR2 n=8, PB-RB1 n=8), limiting power for outcome comparisons.; Associations reported are correlative and do not establish causation..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Case reportMechanismInconclusiveLimited evidenceTier 3 · early humann = 2
Acta neuropathologica communications · Nov 2025 · case series (2 cases)
pineoblastomagerminomapineal region tumour
The authors report two cases of pineoblastoma in which cerebrospinal fluid (CSF) β-hCG was unexpectedly elevated, a finding that could have suggested intracranial germinoma. They note that histopathology remains the diagnostic gold standard but that pineal biopsy is technically challenging, and they call for novel non-invasive biomarkers to improve diagnostic accuracy.
Key findings
- Two cases of pineoblastoma showed unexpectedly elevated CSF β-hCG levels.
- Elevated CSF β-hCG in these cases could have led to a misdiagnosis of intracranial germinoma.
- Histopathological confirmation remains the diagnostic gold standard for pineal region tumours, but pineal biopsy is challenging.
- The cases highlight the need for development of novel non-invasive biomarkers to improve diagnostic accuracy of intracranial tumours.
Limitations: Very small sample (two case reports) so findings are not generalizable.; No quantitative CSF β-hCG values reported in the abstract.; Observational case descriptions without systematic comparison or prevalence data.; Cannot determine how often pineoblastoma causes elevated CSF β-hCG from these reports alone..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
ReviewInconclusiveLimited evidenceTier 4 · clinical
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
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
Case reportInconclusiveLimited evidenceTier 3 · early humann = 1
Journal of ultrasound · Nov 2025 · case report
uterine serous carcinomaendometrial cancer arising in adenomyosisendometrial carcinoma
This is a case report of a 55-year-old postmenopausal woman who was found to have uterine serous carcinoma arising in adenomyosis. Imaging (CT and ultrasound) showed pelvic cystic masses and a 50 × 36 mm subserous cystic-solid uterine mass that was initially misdiagnosed as a degenerating fibroid; postoperative histopathology established the diagnosis. The authors note that a de novo cystic area in adenomyosis in postmenopausal women may suggest malignant transformation and emphasize ultrasound as the first imaging choice for gynecological masses.
Reported effects: CA125 44.86, n=1 · tumor_size, n=1
Key findings
- A 55-year-old postmenopausal woman presented with anorexia, weight loss and mild abdominal pain; pelvic CT showed cystic masses.
- Serum CA125 was 44.86 u/ml.
- Transvaginal/transabdominal ultrasound detected a 50 × 36 mm subserous cystic-solid mass that was misdiagnosed preoperatively as a subserous uterine fibroid with cystic degeneration.
- Postoperative histopathological diagnosis was uterine serous carcinoma arising from adenomyosis.
- Authors suggest that a de novo cystic area in adenomyosis in postmenopausal women may indicate malignant transformation and present ultrasound images to raise diagnostic awareness.
Limitations: Single case report (n=1), so findings are not generalizable.; No control or comparison group.; Abstract provides limited pathological, immunohistochemical, and follow-up details.; Imaging features described may be nonspecific and susceptible to misdiagnosis.; No data on prevalence, diagnostic performance metrics, or outcomes beyond the single case..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed
Animal studyReported positivePreclinical onlyTier 2 · animal
Molecular pharmaceutics · Nov 2025
cervical cancer
The authors tested DSPE-PEG2000-coated tetragonal-phase barium titanate nanoparticles (BTO@PEG) as ultrasound-activated sonodynamic agents for cervical cancer. In cell studies and in nude mice bearing subcutaneous HeLa-derived tumors, BTO@PEG generated reactive oxygen species under ultrasound via a piezoelectric effect, increased cancer cell apoptosis, and inhibited tumor growth; biocompatibility was reported in cytology and animal experiments.
Studied with: ultrasound.
Key findings
- BTO@PEG could continuously generate ROS through sonodynamic therapy (SDT) and the piezoelectric effect under ultrasound stimulation.
- BTO@PEG promoted apoptosis of cervical cancer cells.
- BTO@PEG inhibited the growth of subcutaneously transplanted HeLa-derived cervical cancer tumors in nude mice.
- BTO@PEG showed good biocompatibility, as confirmed by cytology and animal experiments.
- BTO@PEG was employed to replace conventional nanoacoustic sensitizers to overcome rapid elimination and low water solubility of organic sensitizers.
Limitations: Preclinical work only (cell studies and mouse xenograft); no human data reported.; Tumor model was subcutaneous HeLa xenografts in nude mice which may not fully recapitulate human cervical cancer.; Abstract provides no numeric results, sample sizes, dosing regimens, or statistical measures.; Long-term toxicity, biodistribution, and comparative efficacy versus existing sensitizers are not reported in the abstract..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed
ReviewInconclusiveModerate evidenceTier 4 · clinical
Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · Nov 2025 · clinical guideline
urothelial cancerbladder cancer
This is a 2025 clinical guideline from SEOM-SOGUG that provides evidence-based recommendations for diagnosis, staging, and medical management of urothelial (bladder) cancer. The guideline summarizes current evidence and available therapies across all disease stages. The abstract does not present new numerical results or detailed methods in the summary.
Key findings
- Provides evidence-based recommendations for diagnosis, staging, and management of bladder cancer across all disease stages.
- Updated in 2025 to summarize current evidence and available therapies for the medical management of urothelial cancer.
Limitations: Abstract is a brief guideline summary and does not report methods, levels/grades of evidence, or specific recommendations.; No patient-level data, outcomes, or quantitative results are reported in the abstract.; Details on literature search, guideline development process, and conflicts of interest are not provided in the abstract..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 71
Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · Nov 2025 · Array-based global methylation profiling analysis of tumor samples (71 uterine leiomyosarcoma) compared with several other uterine mesenchymal tumors and soft tissue leiomyosarcoma
uterine leiomyosarcomauterine mesenchymal tumorssoft tissue leiomyosarcoma
Researchers performed array-based global methylation profiling on 71 uterine leiomyosarcoma samples and compared them to other uterine mesenchymal tumors and soft tissue leiomyosarcoma. They found that uLMS have distinct methylation patterns versus other tumor types and that methylation profiling identifies two distinct uLMS subgroups with differing copy number alterations and distinct histologic and clinical behaviors. The authors report this is the first study to describe methylation profiling as a diagnostic tool to differentiate uLMS from its mimics.
Key findings
- uLMS demonstrated distinct methylation patterns differing from all other tumor types.
- Methylation profiling defines 2 distinct subgroups of uLMS with differing copy number alterations.
- The two methylation-defined subgroups exhibit unique histologic and clinical behaviors, supported by differences in methylation pathway analysis.
- This study is the first to report methylation profiling as a useful diagnostic tool in differentiating uLMS from mimics.
Limitations: Observational molecular profiling study without interventional or longitudinal clinical trial data; Sample size limited to 71 uLMS; sizes of comparator tumor groups not reported in abstract; No external validation cohort reported in the abstract; No functional validation experiments described to confirm biological significance of methylation differences; Details on clinical outcome measures, follow-up duration, and statistical metrics are not provided in the abstract.
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed
ReviewMixed resultsPreclinical onlyTier 1 · lab
Advanced drug delivery reviews · Nov 2025
hard-to-treat tumours
This review describes sonodynamic therapy (SDT), which uses low-intensity ultrasound together with sonosensitizers to produce reactive oxygen species (ROS) that can kill tumour cells. The authors focus on sonoluminescence as a major activating mechanism and note that SDT may have deeper tissue penetration and potentially fewer adverse effects than photodynamic therapy. Evidence comes from in vitro, in vivo, and early clinical applications, but the review emphasizes that fundamental studies are still needed and that questions remain about efficiency and safety.
Studied with: ultrasound.
Key findings
- SDT combines sonosensitizers and low-intensity ultrasound to generate ROS and induce tumour cell death.
- Several activation mechanisms are proposed (sonoluminescence, pyrolysis, direct mechanical activation), with sonoluminescence a major focus of this review.
- Sonoluminescence involves light generation from collapsing cavitation bubbles that can activate sensitizers similar to photodynamic therapy.
- Generated ROS species include superoxides, peroxides, singlet oxygen and hydroxyl radicals.
- Compared with photodynamic therapy, SDT may offer deeper tissue penetration, higher accuracy, and potentially fewer adverse effects if well-designed.
- SDT effects have been investigated in vitro, in vivo, and have begun to be applied in clinical settings.
- The authors highlight outstanding questions about SDT efficiency and safety and call for further fundamental studies to understand mechanisms.
Limitations: This is a narrative review rather than primary experimental data.; No quantitative efficacy or safety results are reported in the abstract.; Mechanisms of action remain uncertain and multiple activation pathways are proposed.; Clinical application is described as recent but no clinical trial results or details are provided.; Evidence summarized spans in vitro, animal, and early human work, making translational conclusions uncertain..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed
Human · observationalMechanismMixed resultsLimited evidenceTier 3 · early human
Journal of obstetrics and gynaecology Canada : JOGC = Journal d'obstetrique et gynecologie du Canada : JOGC · Nov 2025 · digital survey of gynaecologic pathologists
endometrial carcinoma
The authors administered a digital survey to gynecologic pathologists at 13 Canadian academic pathology departments to assess use of molecular classification for endometrial carcinoma. They found variability in how molecular classification is applied and that respondents perceived resource restrictions and unclear management implications as barriers. The paper recommends focused research, knowledge translation, and guideline development to improve consistent implementation. The abstract also notes that ongoing clinical trials are investigating treatment paradigms and therapy de-escalation based on molecular classification.
Key findings
- Molecular classification of endometrial carcinoma provides prognostic and predictive information.
- Ongoing clinical trials are investigating different treatment paradigms and therapy de-escalation informed by molecular classification.
- There is variability in the application of molecular classification worldwide, including in Canada.
- A digital survey of gynecologic pathologists in 13 Canadian academic pathology departments identified areas of homogeneity and variability in practice.
- Perceived barriers to universal application included resource restrictions and ambiguity of management implications.
- Authors propose focused research, knowledge translation, and guideline development to facilitate more consistent implementation.
Limitations: Survey-based study with no respondent count or response rate reported in abstract (potential nonresponse/selection bias).; Limited to academic pathology departments in Canada (limited generalizability).; Findings based on perceptions/self-report rather than objective measures of practice or patient outcomes.; Abstract provides no quantitative results or statistical analysis..
AI summary of the abstract, human-reviewed · Aug 2026. Describes what this study reported, not medical advice. View on PubMed
Human · observationalMixed resultsLimited evidenceTier 3 · early humann = 13
International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists · Nov 2025 · retrospective case series (chart review)
mesonephric adenocarcinomamesonephric-like adenocarcinomauterine adenocarcinomaovarian adenocarcinomacervical adenocarcinoma
This retrospective case series describes 13 patients with mesonephric and mesonephric-like adenocarcinomas of the uterus, ovary, and cervix identified from 2016–2024. The report summarizes presentation, stage, treatments (all had upfront surgery; adjuvant therapy recommended), and short-term outcomes, finding that 9 of 13 had no evidence of disease at the time of writing and the cohort median overall survival was 15 months (95% CI: 2.2–27.8 months). The authors note that current literature suggests generally poor prognosis but their series includes several early-stage cases and relatively many patients without recurrence after initial treatment.
Reported effects: Total cases 13, n=13 · Anatomic distribution - uterine 6, n=13 · +12 more
Key findings
- Total cases: 13 new MNAC/MLA cases identified at a single institution between 2016 and 2024.
- Anatomic distribution: 6 uterine, 5 ovarian, and 2 cervical tumors.
- Stage at presentation: 7 stage I, 2 stage II, 3 stage III, and 1 stage IV.
- Treatment: All patients underwent upfront surgical resection; adjuvant therapy was recommended and one patient declined adjuvant treatment.
- Outcomes at time of writing: 9 of 13 patients had completed treatment and had no evidence of disease, 1 was alive with disease, 1 was undergoing treatment, and 2 died of disease.
- Median overall survival (OS) for the cohort was 15 months (95% CI: 2.2-27.8 months).
Limitations: Small sample size (n=13).; Single-institution, retrospective chart-review design.; Short and variable follow-up; outcomes are reported 'at the time of writing' and longer-term prognosis remains uncertain.; No control or comparison group; heterogeneous tumor anatomic sites and treatments limit generalizability.; Potential selection bias in case identification and reporting..
AI summary of the abstract, human-reviewed · Aug 2026. Describes what this study reported, not medical advice. View on PubMed
Human · observationalMechanismMixed resultsLimited evidenceTier 3 · early humann = 65
Journal of gynecologic oncology · Nov 2025
uterine carcinosarcoma
This observational study analyzed 65 uterine carcinosarcoma cases, assigning molecular subtypes by POLE sequencing and IHC for MMR and p53, and quantified PD-L1 and tumor-associated immune cells using QuPath. PD-L1 tumor density and stromal CD8 and CD163 densities were significantly associated with molecular subtype. Patients with POLEmut or dMMR subtypes showed a trend toward better prognosis; high tumor PD-L1 density was associated with better survival while high stromal CD163 density was associated with worse survival.
Reported effects: POLEmut cases (%) 1.5%, n=65 · dMMR cases (%) 16.9%, n=65 · +5 more
Key findings
- Among 65 UCS cases, 1 case (1.5%) was POLEmut, 11 cases (16.9%) were dMMR, 32 cases (49.3%) were p53mut, and 21 cases (32.3%) were NSMP.
- The positive density of PD-L1 in tumor was significantly associated with molecular subtypes (p=0.022).
- The positive density of CD8 in stroma was significantly associated with molecular subtypes (p=0.036).
- The positive density of CD163 in stroma was significantly associated with molecular subtypes (p=0.025).
- Patients with POLEmut and dMMR subtypes had a relatively better prognosis trend than patients with NSMP and p53mut subtypes.
- High positive density of PD-L1 in tumor was associated with significantly better prognosis.
- High positive density of CD163 in stroma was associated with significantly worse prognosis.
Limitations: Observational study design—associations cannot establish causality.; Relatively small sample size (n=65), limiting statistical power and generalizability.; Extremely small number of POLEmut cases (only 1 case), preventing meaningful conclusions for that subtype.; Prognostic associations reported without external validation or reported multivariable adjustment details 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 positiveModerate evidenceTier 4 · clinical
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
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
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
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
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
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
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
Animal studyReported positivePreclinical onlyTier 2 · animal
ACS applied materials & interfaces · Oct 2025 · In vitro assays (ROS generation, cytotoxicity) and in vivo murine tumor model with comparisons to monotherapy and single-membrane-coated controls; PET pretargeting imaging of membrane components.
triple-negative breast cancer
The authors developed a hybrid erythrocyte/tumor cell membrane-coated nanoprobe carrying chlorin e6 for sonodynamic therapy and tirapazamine, a hypoxia-activated prodrug. In vitro the nanoprobe generated reactive oxygen species under ultrasound and showed potent cytotoxicity; in mouse TNBC models it accumulated in tumors and produced greater tumor growth inhibition and prolonged survival versus monotherapy or single-membrane-coated controls. PET pretargeting imaging indicated immune evasion and tumor-specific accumulation of the biomimetic membrane components. Treated mice showed reduced splenomegaly and normalization of aberrant immune cell counts, and negligible toxicity was reported in the absence of ultrasound.
Studied with: sonodynamic therapy (Ce6 + ultrasound), tirapazamine (TPZ).
Key findings
- RBCm/4T1m@D-Ce6-TPZ generated reactive oxygen species (ROS) under ultrasound activation and exerted potent cytotoxicity in vitro.
- Safety evaluation reported negligible toxicity without ultrasound stimulation.
- A click-chemistry-enabled pretargeting PET imaging strategy visualized in vivo distribution of the biomimetic membrane components, validating immune evasion and tumor-specific accumulation.
- Combination sonodynamic therapy and hypoxia-responsive chemotherapy with RBCm/4T1m@D-Ce6-TPZ achieved superior tumor growth inhibition and prolonged survival in murine models compared to monotherapy or single-membrane-coated controls; ultrasound activation further enhanced efficacy.
- Treatment mitigated splenomegaly and normalized aberrant immune cell counts in treated mice, suggesting an immunomodulatory effect.
Limitations: Preclinical only: findings are from in vitro assays and mouse models; no human data reported in the abstract.; Abstract does not report sample sizes, detailed statistical results, or quantitative effect sizes.; No dosing regimen, concentration, or treatment schedule details are provided in the abstract.; Safety assessment appears limited in the abstract (notes negligible toxicity without ultrasound) with no detailed toxicology or long-term safety data.; Translatability to humans is uncertain given the murine model and absence of clinical data..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed
ReviewInconclusiveLimited evidenceTier 4 · clinical
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
ReviewInconclusiveLimited evidenceTier 4 · clinical
JAMA oncology · Oct 2025
ovarian cancer
This viewpoint article summarizes available and emerging approaches for prevention and detection of ovarian cancer. The abstract does not report original experimental or clinical data.
Key findings
- The article describes available and emerging approaches for prevention and detection of ovarian cancer.
- No original data, study methods, or results are reported in the abstract.
Limitations: Viewpoint article without original data reported in the abstract.; Abstract provides no methods, sample size, or specific interventions to evaluate.; Effectiveness or comparative evidence for approaches cannot be assessed from the abstract..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed
Human · observationalMechanismMixed resultsLimited evidenceTier 3 · early human
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
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
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, published automatically under the strong-evidence tier · Jun 2026; an editor has not yet reviewed it. Describes what this study reported, not medical advice. View on PubMed · Full text
Human · observationalMixed resultsLimited evidenceTier 3 · early humann = 97
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
Journal of cancer research and therapeutics · Oct 2025 · case report
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
Animal studyReported positivePreclinical onlyTier 2 · animal
eLife · Sep 2025
uveal melanoma
The abstract reports a novel compound that inhibits the BAF chromatin remodeling complex. In an animal model of uveal melanoma, the compound caused tumor regression. The abstract does not provide the compound name, dosing, species, sample size, or quantitative results.
Key findings
- A novel compound that inhibits the BAF chromatin remodeling complex caused regression in an animal model of uveal melanoma.
- The reported mechanism of action is inhibition of the BAF chromatin remodeling complex (chromatin remodeling).
- The abstract supplies no compound name, dose, species, sample size, comparator, or numeric outcome data.
Limitations: Evidence comes from an animal model only; no human data are reported.; The abstract does not name the compound or report dosing or administration details.; No quantitative results, sample size, control group, or statistical data are provided in the abstract.; Species and study design details are not provided in the abstract..
AI summary of the abstract, human-reviewed · Aug 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Case reportMechanismReported negativeLimited evidenceTier 3 · early humann = 2
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
Case reportReported positiveLimited evidenceTier 3 · early humann = 1
Frontiers in oncology · Sep 2025 · case report
endometrial carcinosarcoma
This case report describes a 21-year-old Chinese woman who presented with vaginal bleeding and was diagnosed by biopsy with endometrial carcinosarcoma containing grade 3 endometrioid carcinoma. She underwent extensive laparoscopic hysterectomy with bilateral adnexectomy, lymphadenectomy, and omentectomy followed by six cycles of paclitaxel-carboplatin; histology confirmed the diagnosis. At two-year follow-up there was no recurrence; a postoperative vesicovaginal fistula was surgically repaired. The case highlights an atypical presentation in a young woman without established risk factors.
Key findings
- Patient presented with persistent vaginal bleeding, anaemia, and lower abdominal pain.
- Laboratory tests showed microcytic hypochromic anaemia and elevated CA125, CA153, CA199, and HE4 (Human Epididymis Protein 4).
- Pelvic MRI revealed a malignant endometrial lesion with vaginal involvement and lymphadenopathy.
- Biopsy confirmed carcinosarcoma with grade 3 endometrioid carcinoma as the epithelial component.
- Multidisciplinary team recommended extensive laparoscopic hysterectomy with bilateral adnexectomy, lymphadenectomy, and omentectomy, followed by six cycles of paclitaxel-carboplatin chemotherapy.
- Histology of the surgical specimen confirmed the diagnosis.
- At two-year follow-up there was no recurrence.
- The patient developed a postoperative vesicovaginal fistula which was surgically repaired.
Limitations: Single-patient case report; findings are not generalizable.; Observational description without control or comparison.; No chemotherapy dosing, scheduling, or toxicity details provided.; No molecular/genetic testing or staging details reported in the abstract.; Follow-up limited to two years; longer-term outcomes unknown..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Human trialTrialReported positiveModerate evidenceTier 4 · clinicaln = 31
Med (New York, N.Y.) · Sep 2025 · Phase 2, single-arm with case-matched control comparison
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, published automatically under the strong-evidence tier · Jul 2026; an editor has not yet reviewed it. Describes what this study reported, not medical advice. View on PubMed
Human · observationalMechanismMixed resultsLimited evidenceTier 3 · early humann = 42
Neuro-oncology · Sep 2025 · retrospective case series (screening institutional datasets and published institutional cases)
central nervous system neuroblastomahigh-grade gliomadiffuse midline glioma (H3 K27M-mutant)radiation-associated tumorembryonal tumorpineoblastoma
Researchers analyzed 42 human CNS tumors with FOXR2 overexpression from institutional datasets and published cases to describe their histologic, molecular, imaging, and clinical features. FOXR2 activation was found across multiple CNS tumor types (including high-grade gliomas, diffuse midline gliomas, embryonal tumors, and pineoblastomas) and arose by mechanisms such as promoter donation, enhancer hijacking, alternative promoter usage, and truncated LINE-1 retrotransposition. Downstream epigenomic and transcriptomic effects were shared across tumor types, but clinical outcomes differed: FOXR2-positive DMGs and pineoblastomas had very poor 2-year survival, while CNS neuroblastomas showed favorable responses to combined chemotherapy and radiation.
Reported effects: n_total_tumors 42, n=42 · HGG_count 21, n=21 · +9 more
Key findings
- 42 CNS tumors with FOXR2 overexpression were analyzed.
- Tumor composition: 21 (50.0%) were high-grade gliomas (HGGs) and 18 (42.9%) were embryonal tumors.
- HGG subgroup included ten H3 K27M-mutant diffuse midline gliomas and eight radiation-associated tumors.
- Embryonal subgroup included 11 CNS neuroblastomas and six pineoblastomas.
- FOXR2 expression was similar between CNS neuroblastoma and other tumor types (P = 0.82).
- Most FOXR2 activation mechanisms involved structural alterations causing promoter donation and enhancer hijacking from active genes essential for brain development; other mechanisms included alternative promoter activation and truncated LINE-1 retrotransposition.
- All but two aberrant FOXR2 transcripts incorporated non-canonical, non-coding exons.
- Gene set enrichment analysis showed shared downstream epigenomic and transcriptomic effects of FOXR2 activation across tumor types.
- Clinical outcomes varied by tumor type: DMGs and pineoblastomas with FOXR2 overexpression had 0% 2-year overall survival, whereas CNS neuroblastomas 'responded well' to combined chemotherapy and radiation.
Limitations: Retrospective case series assembled from institutional datasets and published cases, with potential selection bias.; Small overall sample size (n=42) and small subgroup sizes limit statistical power.; Heterogeneous cohort (multiple tumor histologies and prior radiation–associated tumors) limits generalizability.; Observational molecular analysis without reported prospective validation or functional in vivo confirmation of mechanisms.; Clinical outcome comparisons are descriptive and may be confounded by differing treatments and patient characteristics..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 56
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
ReviewMechanismInconclusiveLimited evidenceTier 4 · clinical
Lung Cancer (Auckland, N.Z.) · Sep 2025
non-small cell lung cancer
This is a review article summarizing how the identification of molecular driver mutations has altered treatment approaches for non-small cell lung cancer (NSCLC). The authors note that many driver mutations and associated targeted therapies have been discovered over the past 20 years, improving survival for some patients, and they highlight ongoing research and emerging molecular targets and strategies for NSCLC.
Key findings
- Identification of molecular driver mutations has changed the therapeutic landscape for NSCLC.
- Over the last 20 years an increasing number of driver mutations and new targeted therapies have been identified, resulting in improved survival for a subset of patients.
- There is ongoing research to identify additional molecular targets and therapeutic strategies to improve outcomes for more patients with lung cancer.
- This review highlights new therapeutic strategies targeting known driver mutations and data regarding emerging molecular targets for NSCLC.
Limitations: Review article with no original experimental or clinical trial data presented in this abstract.; Abstract contains no methodological details (e.g., search strategy), so it is unclear whether this is a systematic review.; No quantitative results, specific agents, or detailed outcomes are reported in the abstract..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
ReviewMechanismInconclusiveLimited evidenceTier 4 · clinical
Cancers · Sep 2025 · review
pleuropulmonary blastomaSertoli-Leydig cell tumorcystic nephromacervical embryonal rhabdomyosarcomacystic lung lesionsthyroid follicular nodular disease
This is a narrative review of DICER1 syndrome, a hereditary cancer predisposition caused by germline loss-of-function variants in DICER1 and characteristic second somatic hotspot mutations in the RNase IIIb domain. The review summarizes the range of associated benign and malignant tumors, describes DICER1's role as an endoribonuclease in RNA interference and microRNA processing, and concludes that the exact molecular mechanisms linking altered DICER1 function to tumorigenesis remain incompletely understood and require further research.
Key findings
- DICER1 syndrome is a hereditary cancer predisposition syndrome with a broad phenotype including pleuropulmonary blastoma, Sertoli-Leydig cell tumor, cystic nephroma, cervical embryonal rhabdomyosarcoma, cystic lung lesions, and thyroid follicular nodular disease.
- The syndrome is caused by loss-of-function germline variants in the DICER1 gene and DICER1-related tumors commonly have second somatic hotspot variants in the RNase IIIb domain.
- DICER1 encodes an endoribonuclease important for RNA interference and microRNA biogenesis.
- The review highlights gaps in knowledge about the precise molecular mechanisms by which altered DICER1 function contributes to tumorigenesis and calls for more research.
Limitations: Narrative review without original experimental or patient-level data.; Conclusions limited by existing incomplete knowledge of molecular mechanisms as noted by the authors.; Review methodology is not described in the abstract (e.g., not specified as a systematic review), so selection bias in covered literature is possible..
AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Case reportSupportive careReported negativeLimited evidenceTier 3 · early humann = 1
Chest · Sep 2025 · case report
Supportive careprostate adenocarcinoma
This case report describes an 85-year-old man with prostate adenocarcinoma who had received bicalutamide and leuprorelin for about 3 years. He presented with dyspnea, respiratory failure, and loss of appetite and was found on chest radiography to have a left pleural effusion. He had a history of COPD and a 20-pack-year smoking history and was admitted for further evaluation of the pleural effusion.
Key findings
- Patient had undergone hormone therapy with bicalutamide and leuprorelin for approximately 3 years for prostate adenocarcinoma with a Gleason score of 4 + 5.
- The patient presented to the emergency department with dyspnea, respiratory failure, and loss of appetite.
- He had a history of COPD with a 20-pack-year smoking history.
- Chest radiography showed a left pleural effusion and he was admitted for further examination of the pleural effusion.
Limitations: Single-patient case report limits generalizability.; No control or comparator; cannot establish causality between therapies and respiratory findings.; Abstract provides limited clinical detail and no follow-up or final diagnostic outcome for the pleural effusion.; Potential confounders (COPD, smoking) are present and not fully explored in the abstract..
Reports a prostate cancer patient on androgen-deprivation therapy who presented with respiratory failure and a left pleural effusion.
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Meta-analysisSupportive careReported positiveModerate evidenceTier 4 · clinical
JNCI cancer spectrum · Sep 2025 · commentary summarizing pooled individual patient data (IPD) analyses from randomized controlled trials
Supportive care
This paper describes the POLARIS initiative, an international pooled individual patient data (IPD) infrastructure that currently includes IPD from 52 exercise randomized trials in patients with cancer. Analyses to date reported that exercise interventions had beneficial effects on physical fitness, fatigue, health-related quality of life, posttreatment self-reported cognition, sleep disturbances, and symptoms of anxiety and depression, and that effects varied by patient and intervention characteristics. The authors highlight the value of pooled IPD for advancing precision exercise medicine and call for pooling data from understudied populations, clinical outcomes, and biomarkers and for using machine learning to identify effect modifiers.
Key findings
- POLARIS currently includes IPD from 52 exercise trials.
- Pooled IPD analyses indicate exercise interventions in patients with cancer have beneficial effects on physical fitness.
- Pooled IPD analyses indicate beneficial effects on fatigue.
- Pooled IPD analyses indicate beneficial effects on health-related quality of life.
- Pooled IPD analyses indicate beneficial effects on self-reported cognition (posttreatment).
- Pooled IPD analyses indicate beneficial effects on sleep disturbances.
- Pooled IPD analyses indicate beneficial effects on symptoms of anxiety and depression.
- Exercise effects varied by patient characteristics (including initial value of the outcome, age, marital status, education level) and intervention characteristics (including exercise supervision and specificity).
- Future opportunities include pooling trials from understudied populations, adding data on clinical outcomes and biomarkers, and applying machine learning to identify combinations of covariables that modify effects and to predict individual treatment effects.
Limitations: This publication is a commentary/synthesis rather than a new primary randomized trial.; Abstract does not report total participant numbers or quantitative effect sizes from the pooled analyses.; Pooled analyses to date may lack data from understudied populations and from clinical outcomes and biomarkers (authors identify these as gaps).; Potential heterogeneity across included exercise interventions and trial populations is implied but not detailed in the abstract..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
ReviewSupportive careMixed resultsLimited evidenceTier 4 · clinical
Journal of the National Cancer Institute. Monographs · Sep 2025
Supportive carepeople diagnosed with cancer
This article discusses considerations for delivering supervised exercise programs remotely via videoconferencing for people with cancer. It describes technological requirements, exercise professional skills, safety, programming features, social interaction, costs, and legal/ethical issues, and notes relevance for clinical trial design and community practice. The authors identify remaining knowledge gaps and opportunities to inform evidence-based and practice-based approaches.
Key findings
- Exercise is safe and beneficial for people diagnosed with cancer.
- Live-remote exercise (exercise delivered by trainers via videoconferencing) has expanded rapidly and can retain key elements of supervised exercise that provide greater benefits than unsupervised programs.
- Adapting in-person supervised exercise to remote delivery poses challenges.
- Key considerations for effective and safe live-remote exercise delivery include technology, exercise professional skills, safety aspects, exercise programming, social interactions, costs, and legal/ethical issues.
- Considerations are described for both exercise oncology clinical trials and community practice, and remaining knowledge gaps are outlined.
Limitations: Narrative/discussion article rather than a primary empirical study—no original quantitative data reported in the abstract.; No study design, sample size, or specific evaluated outcomes are provided in the abstract.; Recommendations are general; applicability to specific patient subgroups or contexts is not quantified in the abstract..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Human · observationalMixed resultsModerate evidenceTier 3 · early humann = 390805
Gynecologic oncology · Sep 2025 · retrospective population-based registry analysis (SEER22, 2000-2019)
endometrial cancerendometrioid carcinomanon-endometrioid carcinomacarcinosarcomaclear cell carcinomaserous carcinomamixed carcinoma
This population-based study used SEER22 data from 2000–2019 (n=390,805) to estimate hysterectomy-corrected, age-specific incidence rates and five-year relative survival for individual endometrial cancer histotypes by race and ethnicity. It found that endometrioid carcinoma incidence was much higher in non-Hispanic White women aged 50+ (104.1 per 100,000) than in other groups, that non-endometrioid histotypes increased sharply around ages 50–54 (especially in non-Hispanic Black women), and that five-year relative survival was highest for endometrioid carcinomas (90.2%) and lower for other histotypes (range 39.6%–59.1%).
Reported effects: endometrioid carcinoma incidence rate, non-Hispanic White women ages 50+ (per 100,000) 104.1 · endometrioid carcinoma incidence rate, other groups ages 50+ (per 100,000) · +3 more
Key findings
- Estimated hysterectomy-corrected, age-specific incidence rates and five-year relative survival for endometrial cancer histotypes using SEER22 (N = 390,805).
- Endometrioid carcinoma rates were similar by race/ethnicity in younger women but much higher in non-Hispanic White women ages 50+ years (104.1 per 100,000) versus other groups (51.1-68.5).
- Non-endometrioid histotypes were rare in younger women, with mixed carcinomas being the most common among the non-endometrioid types.
- Carcinosarcoma, clear cell, and serous carcinoma rates increased sharply at ages 50-54, especially in non-Hispanic Black women.
- Median age at diagnosis was youngest in Hispanic and non-Hispanic Asian/Pacific Islander women, particularly for endometrioid carcinomas.
- Five-year relative survival: endometrioid carcinomas 90.2%; mixed carcinomas 77.0%; other non-endometrioid histotypes range 39.6%–59.1%.
Limitations: Observational registry study — cannot establish causal relationships between age/race/ethnicity and incidence or survival.; Potential for histotype or stage misclassification in registry data.; SEER lacks detailed individual-level risk factor, treatment, or molecular data to explain observed differences.; Hysterectomy-correction methods are estimations and may introduce uncertainty in incidence rates.; Findings are limited to populations covered by SEER and may not generalize to all US regions or internationally..
AI summary of the abstract, human-reviewed · Aug 2026. Describes what this study reported, not medical advice. View on PubMed
Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 381
Virchows Archiv : an international journal of pathology · Sep 2025
ovarian mucinous tumorsovarian epithelial carcinomas
The authors examined FOXA1 protein expression by immunohistochemistry and KRAS mutation status across normal/benign ovarian tissues, mucinous ovarian tumors, and other ovarian epithelial carcinomas (total n=381). FOXA1 was commonly expressed in mucinous tumors and its expression correlated with MUC2; KRAS mutations increased with malignancy but were relatively enriched in FOXA1-negative cystadenomas. The authors propose that co-occurrence of KRAS mutation and FOXA1 expression may relate to tumor progression and intestinal-type differentiation.
Reported effects: FOXA1 expression in cystadenomas 73.6% · FOXA1 expression in borderline tumors 91.4% · +7 more
Key findings
- FOXA1 expression was significantly associated with mucinous histology in ovarian epithelial carcinomas (P < 0.001).
- In mucinous tumors, FOXA1 was expressed in 73.6% of cystadenomas, 91.4% of borderline tumors, 100% of borderline tumors with intraepithelial carcinomas, and 87.5% of carcinomas.
- MUC2 expression progressively increased from mucinous cystadenomas to borderline tumors (P < 0.050) and significantly correlated with FOXA1 expression (P = 0.024).
- The prevalence of KRAS mutations tended to increase with the malignancy of mucinous tumors (P < 0.050).
- KRAS mutations were significantly enriched in FOXA1-negative cystadenomas compared with FOXA1-positive cystadenomas (P < 0.050).
- A stepwise increase was noted in the percentage of both KRAS mutations and FOXA1 expression from cystadenoma to carcinoma.
Limitations: Observational analysis of tumor specimens only (no functional or mechanistic experiments reported).; No clinical outcome or survival data were reported to link findings to prognosis.; Causality between FOXA1 expression, KRAS mutation, and tumor progression or differentiation cannot be established from the methods described..
AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed
ReviewSupportive careReported positiveStrong evidenceTier 4 · clinical
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
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
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
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
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
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
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
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
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
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
Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 6
Frontiers in immunology · Aug 2025 · Single-cell RNA sequencing (scRNA-seq) of metastatic lesions from a treatment-naïve uterine leiomyosarcoma patient compared to normal uterine myometrium samples (MMM, n=5); integrated analyses including CNV, pseudotime, cell-cell communication, functional enrichment, and mpIF validation; survival correlations with TCGA-SARC cohort.
uterine leiomyosarcoma
The authors performed single-cell RNA sequencing on metastatic lesions from one treatment-naïve uterine leiomyosarcoma patient and compared the data to five normal myometrium samples. They found an immunosuppressed tumor microenvironment characterized by exhausted CD8+ T cells, M2-like tumor-associated macrophages, and immature N2 neutrophils enriched in metastatic foci; these features correlated with poorer prognosis in TCGA-SARC analyses. The study also identified cell-cell communication axes (MIF-(CD74+CD44), CXCL8) and candidate biomarkers (EDARADD, CLDN10, TMIGD2) and dysregulated pathways (TGF-beta, angiogenesis, MIF signaling).
Key findings
- The tumor microenvironment showed prominent immunosuppression with exhausted CD8+ T cells, with initial markers (CCR7, MAL) diminishing over time and exhaustion markers (LAG3, HAVCR2, TIGIT) enriched.
- M2-polarized macrophages were mainly composed of M2-like TAMs with tumor-promoting characteristics (CD163, FTH1, FTL, TIMP1) and there was a polarization trajectory from M1 to M2.
- Immature, tumor-promoting N2 neutrophils (CD15+EDARADD+) were enriched in metastatic foci and associated with poor prognosis.
- Cell-cell communication analyses highlighted MIF-(CD74+CD44) interactions between T/B cells and a role for the CXCL8 signaling axis in promoting angiogenesis, TAM polarization, and immunosuppression.
- Constructed a comprehensive single-cell map of ULSA, defined a metastasis-susceptible cell subset (U11-EDARADD), and nominated biomarkers (EDARADD, CLDN10, TMIGD2) and dysregulated pathways (TGF-β, angiogenesis, MIF signaling) as possible targets for future combined-immunotherapy development.
Limitations: Tumor single-cell data derive from a single ULSA patient (metastatic lesions from one individual), limiting generalizability.; Normal comparator samples are limited (MMM, n=5) and cohort sizes are small.; Observational single-cell profiling cannot establish causal relationships between identified cell states/pathways and clinical outcomes or therapy resistance.; Survival associations were assessed using TCGA-SARC correlations (indirect validation) rather than validation in an independent ULSA cohort.; No interventional or functional experiments reported to validate that identified biomarkers/pathways drive immunosuppression or therapy resistance..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Animal studyReported positivePreclinical onlyTier 2 · animal
Cancers · Aug 2025
chronic myelogenous leukemia
This animal study tested voluntary wheel running in immunodeficient mice given human donor lymphocytes with or without human leukemia cells. Exercise reduced leukemia tumor burden, extended tumor-free survival, decreased graft-versus-host disease severity, and increased survival in the GvHD model. Bone marrow RNA sequencing showed downregulation of genes linked to mitochondrial function, protein synthesis, and metabolism in tumors from exercised mice. The authors conclude exercise improved DLI outcomes in this xenogeneic mouse model.
Reported effects: overall survival extended 60% · tumor-free survival extended in DLI group 44.5%, p significantly · +1 more
Key findings
- In the GvHD model, exercise extended overall survival by 60% and reduced GvHD severity.
- In the GvL model, exercise significantly lowered tumor burden and extended tumor-free survival in both DLI and vehicle control groups by 44.5% and 37.5%, respectively.
- RNA sequencing of bone marrow from saline-injected mice revealed downregulation of genes associated with mitochondrial function, protein synthesis, and metabolic processes in tumors from exercised mice.
- Voluntary wheel running improved DLI outcomes by enhancing GvL and reducing GvHD.
Limitations: Preclinical study in mice; no human efficacy data; Xenogeneic model (human PBMCs into immunodeficient mice) may not fully replicate human immune/tumor interactions; Sample sizes and randomization/blinding not reported in abstract; Relatively short follow-up (~40 days); Mechanistic link (metabolic reprogramming) is correlative from RNA sequencing and not proven causal.
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Lab · in vitroReported positivePreclinical onlyTier 1 · lab
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
Cell reports · Aug 2025 · mouse models and NSCLC cell lines; gut microbiota comparison in patients with NSCLC and healthy controls
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
Animal studyReported positivePreclinical onlyTier 2 · animal
Journal of nanobiotechnology · Aug 2025
hepatocellular carcinoma
This preclinical study combined the vasodilator isosorbide mononitrate with a BTz organic nanosonosensitizer and ultrasound in mouse models of hepatocellular carcinoma. Isosorbide mononitrate increased tumor accumulation of the nanosonosensitizer by about 1.8-fold, and the combined sonodynamic approach produced 78% tumor growth inhibition versus sonodynamic therapy alone, with no detectable systemic toxicity reported. The nanosonosensitizer's near-infrared fluorescence allowed image-guided tracking of uptake and response.
Reported effects: nanosonosensitizer accumulation fold-change 1.8 · tumor growth inhibition 78%
Studied with: BTz nanosonosensitizer, sonodynamic therapy (ultrasound).
Key findings
- Isosorbide mononitrate increases nanosonosensitizer accumulation by ~ 1.8-fold.
- Under ultrasound irradiation, nanosonosensitizer produced high ROS generation.
- Combined treatment resulted in 78% tumor growth inhibition in murine HCC models—nearly double that of SDT alone—without detectable systemic toxicity.
- Near-infrared fluorescence of the nanosonosensitizer enabled real-time, image-guided tracking of sonosensitizer uptake and therapeutic response.
Limitations: Preclinical animal study only (murine models); no human data reported.; Abstract does not report sample sizes or detailed experimental design.; Dose, schedule, and administration details for isosorbide mononitrate and nanosonosensitizer are not provided in the abstract.; Primary endpoint reported is tumor growth inhibition; survival and long-term outcomes are not described.; Unclear whether multiple tumor models or replicates were used; generalizability to other models is unknown..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
ReviewMechanismInconclusiveLimited evidenceTier 4 · clinical
Brain communications · Aug 2025
meningiomavestibular schwannomaintra-axial brain tumours
This narrative review summarizes meningeal structure and function, including the meningeal lymphatic network and its connections to the skull bone marrow and peripheral immune system. It discusses how these meningeal immune features may relate to extra-axial brain tumours (meningioma and vestibular schwannoma), potentially influencing tumour immune infiltration, meningeal inflammation, and symptoms such as headache and anxiety.
Key findings
- The meninges (dura, arachnoid, pia) are structurally and functionally connected to neighbouring structures including the skull.
- The meningeal lymphatic network places the meninges at a nexus between the brain, peripheral immune system, and skull bone marrow.
- Meningeal lymphatics can regulate immune responses in models of health and disease, including intra-axial brain tumours, and thereby affect tumour behaviour.
- A diverse array of resident and circulating immune cells (macrophages, T-cells, B-cells) inhabit the meninges, with specialized hubs around dural venous sinuses and cranial nerves.
- Meningioma and vestibular schwannoma commonly arise near meningeal immune hubs, suggesting possible bidirectional interactions influencing immune infiltration and meningeal inflammation and symptoms.
Limitations: Narrative review rather than primary experimental or clinical data; no original quantitative results reported.; Abstract does not state whether this is a systematic review or the methods used for literature selection.; Many links between meningeal features and tumour behavior are discussed conceptually or based on models rather than demonstrated causally in patients.; No evaluation of interventions, therapies, or clinical outcomes in treated patients presented in the abstract..
AI summary of the abstract, human-reviewed · Aug 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
ReviewReported positiveLimited evidenceTier 4 · clinical
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
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
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
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
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
ReviewMechanismReported positivePreclinical onlyTier 2 · animal
Cancer cell · Aug 2025
bladder cancer
This commentary summarizes two recent papers reporting that bladder cancer immunotherapy with Bacillus Calmette-Guerin (BCG), alone or combined with β‑glucan, involves reprogramming of bone marrow hematopoiesis. The authors state these findings provide additional evidence that bone marrow–mediated trained immunity (TRIM) has therapeutic potential against cancer. The abstract itself does not present experimental details, species, sample sizes, or quantitative results.
Studied with: beta-glucan.
Key findings
- Two articles (in Immunity and Cancer Cell) report that BCG alone or combined with β‑glucan involves reprogramming of bone marrow hematopoiesis.
- These observations are presented as additional evidence for the therapeutic potential of bone marrow–mediated trained immunity (TRIM) against cancer.
Limitations: This abstract is a commentary summarizing other articles and does not present original experimental data.; No species, sample sizes, experimental methods, doses, or quantitative results are provided in this abstract.; Translatability to human clinical outcomes is not addressed in the abstract..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed
OtherMechanismReported positiveLimited evidenceTier 3 · early human
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
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
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
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
Animal studyFormulationReported positivePreclinical onlyTier 2 · animal
Journal of nanobiotechnology · Jul 2025
pancreatic cancer
The authors developed a PLGA/polydopamine nanoparticle carrying manganese porphyrin and the hypoxia-activated prodrug tirapazamine, labeled with 131I for dual MRI/SPECT imaging. In preclinical experiments the platform generated ROS under ultrasound combined with 131I beta emissions, exacerbated tumor hypoxia to activate TPZ, and produced synergistic tumor-cell killing while inhibiting tumor stem cell formation. The nanoparticle showed good biocompatibility, stable radionuclide labeling, and enabled real-time imaging of its metabolism and therapeutic effect.
Studied with: 131I radionuclide therapy, sonodynamic therapy (ultrasound).
Key findings
- MnTTP and tirapazamine (TPZ) were encapsulated in PLGA spheres and coated with polydopamine to allow labeling with 131I, creating a theranostic nanoplatform.
- The nanoplatform demonstrated excellent biocompatibility, stable labeling efficiency, and dual-modal MRI/SPECT imaging capabilities.
- Under ultrasound activation the nanoplatform generated ROS, and in combination with beta-rays emitted by 131I synergistically eradicated tumor cells and exacerbated tumor hypoxia.
- TPZ was activated under hypoxic conditions to produce toxic free radicals, enabling synergistic radionuclide and sonodynamic therapy.
- The combined approach effectively inhibited tumor stem cell formation and enhanced anti-tumor efficacy, with in vivo metabolism and therapeutic effect monitored by MRI/SPECT.
Limitations: Preclinical study reported in the abstract (in vivo models) with no human data.; Abstract does not report species, sample sizes, or quantitative effect sizes.; No details on controls, comparator groups, or statistical significance are provided in the abstract.; Safety, long-term outcomes, and translatability to humans are not addressed in the abstract..
Preclinical study of a theranostic nanoparticle combining radionuclide and sonodynamic approaches with a hypoxia-activated prodrug for pancreatic cancer.
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Human trialTrialReported positiveStrong evidenceTier 4 · clinicaln = 571
Journal of clinical oncology : official journal of the American Society of Clinical Oncology · Jul 2025 · randomized, open-label, phase III, multicenter
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, published automatically under the strong-evidence tier · Jul 2026; an editor has not yet reviewed it. Describes what this study reported, not medical advice. View on PubMed
Human · observationalMechanismReported negativeLimited evidenceTier 3 · early human
Discover oncology · Jul 2025 · Whole-genome sequencing in a three-generation family; immunohistochemistry on tumor, adjacent, and CPAM tissues; Kaplan-Meier survival analysis comparing GPC3 expression groups
pleuropulmonary blastoma
The authors performed whole-genome sequencing in a three-generation family with pleuropulmonary blastoma and identified a novel missense mutation in GPC3. Immunohistochemistry showed higher GPC3 expression in PPB tissues than in CPAM or adjacent non-tumor tissues. Kaplan–Meier analysis found lower two-year survival among patients with high GPC3 expression (30%) versus moderate (75%) and low (90.9%) expression (p = 0.0035). The authors propose GPC3 as a potential prognostic marker in PPB.
Reported effects: two-year survival (GPC3+++) 30%, p p = 0.0035 · two-year survival (GPC3++) 75%, p p = 0.0035 · +1 more
Key findings
- Seventeen candidate genes were identified by WGS, including GPC3, and a novel missense mutation in GPC3 was confirmed.
- GPC3 expression was significantly higher in PPB tissues than in CPAM or adjacent non-tumor tissues by immunohistochemistry.
- Survival analysis: two-year survival was 30% for high GPC3 expression (GPC3+++), 75% for moderate (GPC3++), and 90.9% for low (GPC3+) expression (p = 0.0035).
Limitations: Whole-genome sequencing was performed on a single three-generation family (limited genetic sample for segregation/causality).; Abstract does not report the total sample size or numbers in each expression group.; Observational association (IHC and survival analysis) without functional validation of the mutation's biological effects.; IHC expression categories (GPC3+, ++, +++) are semiquantitative and may be subjective..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Human · observationalMechanismMixed resultsLimited evidenceTier 3 · early humann = 300
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
ReviewSupportive careReported positiveLimited evidenceTier 3 · early human
American journal of lifestyle medicine · Jul 2025 · narrative review
Supportive care
This narrative review summarizes how lifestyle medicine (nutrition, physical activity, stress management, sleep, social connections, and risk reduction) has been implemented in cancer survivorship programs around the world. The authors describe several hospital- and community-based models and report that structured lifestyle interventions have been associated with improved treatment tolerance, quality of life, and potential reductions in cardiometabolic risk factors, while noting barriers to wider adoption.
Key findings
- The review examines global implementation models including Mass General Cancer Center's Lifestyle Medicine Clinic, the Clinical Oncology Society of Australia's exercise oncology framework, the Cleveland Clinic Abu Dhabi's Lifestyle Medicine Oncology Program, and Kansas City's Cancer Wellness for Life initiative.
- Across diverse clinical settings, structured lifestyle interventions have been associated with improved treatment tolerance and quality of life, and have the potential to reduce cardiometabolic risk factors.
- Hospital-based programs tend to integrate multidisciplinary support, whereas community-driven initiatives can expand access to lifestyle interventions.
- Barriers to widespread adoption include gaps in clinician training, limited institutional support, and disparities in patient access.
- Authors conclude that increasing access, overcoming implementation challenges, and using technology may improve survivorship outcomes.
Limitations: Narrative review (not a systematic review or meta-analysis) with potential selection and reporting bias.; No primary data or pooled quantitative synthesis presented in the abstract.; Heterogeneity of programs and settings limits generalizability of specific outcomes.; Abstract does not specify study-level methods, sample sizes, or objective outcome measures for the cited programs..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Lab · in vitroMechanismReported positivePreclinical onlyTier 1 · lab
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
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
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
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 trialTrialMixed resultsLimited evidenceTier 4 · clinicaln = 22
Journal of neuro-oncology · Jul 2025 · Retrospective analysis of tumor volumes from patients prospectively treated with bevacizumab on a phase II clinical trial (NF104)
Bevacizumabmeningiomanon-vestibular schwannoma (NVS)NF2-related schwannomatosis Researchers retrospectively analyzed volumes of intracranial non-vestibular schwannomas (NVS) and meningiomas in NF2-related schwannomatosis patients who received bevacizumab for two years on trial NF104. Best radiographic response occurred in 13% of meningiomas (5/40) and 42% of NVS (5/12); per-patient response rates were 38% for meningioma (3/8) and 67% for NVS (4/6). During two years, progression occurred in 55% of meningiomas (22/40) and 8% of NVS (1/12). Median time to progression was 15 months for meningiomas and was not reached for NVS.
Reported effects: Best-response RR (meningiomas) 13%, n=40 · Best-response RR (non-vestibular schwannomas, NVS) 42%, n=12 · +6 more
Key findings
- Best-response radiographic response (RR) occurred in 13% (5/40) of meningiomas.
- Best-response radiographic response (RR) occurred in 42% (5/12) of non-vestibular schwannomas (NVS).
- Per-patient RR for meningioma: 38% (3/8) of patients.
- Per-patient RR for NVS: 67% (4/6) of patients.
- During two years of treatment, progression (PD) occurred in 55% (22/40) of meningiomas.
- During two years of treatment, progression (PD) occurred in 8% (1/12) of NVS.
- Median time to tumor progression was 15 months for meningiomas and was not reached for NVS.
Limitations: Retrospective analysis of a subset of trial participants (non-target tumors) rather than a pre-specified primary endpoint for these tumors.; Small numbers of patients/tumors evaluated (40 meningiomas in 8 patients; 12 NVS in 6 patients).; Single-arm trial with no randomized control group.; Endpoints are radiographic volumetric responses and progression; clinical outcomes (e.g., survival, functional status) are not reported here.; Potential selection bias because all patients were enrolled for progressive vestibular schwannoma..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed
Case reportReported negativeLimited evidenceTier 3 · early humann = 1
Neurology India · Jul 2025 · case report
schwannomamalignant peripheral nerve sheath tumortentorial schwannomaintracranial schwannomabrain neoplasm
This case report describes a 45-year-old man who presented with a giant tentorial schwannoma with supra- and infratentorial extension. The tumor recurred on follow-up and, per the authors, underwent malignant transformation to a malignant peripheral nerve sheath tumor (MPNST). The patient had no clinical features of neurofibromatosis. The authors state this is the first reported case of malignant transformation of a tentorial schwannoma.
Key findings
- Intracranial schwannomas are uncommon; intracranial schwannomas account for approximately 6.8%-8.0% of intracranial tumors (background statement).
- Tentorial schwannomas are rare—only 18 cases had been reported prior to this report (background statement).
- The authors present a single case of a giant tentorial schwannoma in a 45-year-old man with supra- and infratentorial growth.
- The tumor recurred on follow-up and was reported to have transformed into a malignant peripheral nerve sheath tumor (MPNST).
- The patient had no features of neurofibromatosis.
Limitations: Single-patient case report — findings may not be generalizable.; Abstract provides limited clinical, pathological, and follow-up detail (diagnostic criteria and timing of recurrence/transformation not specified).; No control or comparative data; cannot establish incidence or causality of malignant transformation..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed
Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 45
Indian journal of pathology & microbiology · Jul 2025
ovarian high-grade serous carcinoma (HGSC)
This observational pathology study examined BRCA1 and BRCA2 protein expression by immunohistochemistry in 45 cases of ovarian high-grade serous carcinoma and assessed the presence of SET (solid, pseudoendometrioid, transitional) growth pattern. SET morphology was present in 64.4% (29/45) of cases; BRCA1 loss was seen in 35.5% (16/45) and BRCA2 loss in 17.7% (8/45). Tumor-infiltrating lymphocytes, necrosis, lymphovascular invasion and BRCA1 loss positively correlated with SET morphology. The authors conclude BRCA1 IHC can be an effective alternative method to detect BRCA1 dysfunction and correlate with HGSC histomorphology.
Reported effects: SET pattern prevalence 64.4%, n=45 · BRCA1 loss prevalence 35.5%, n=45 · +1 more
Key findings
- SET growth pattern was seen in 64.4% (29/45) cases.
- 35.5% (16/45) of the total cases showed BRCA1 loss.
- 17.7% (8/45) cases showed BRCA2 loss.
- Tumor-infiltrating lymphocytes (TILs), necrosis, lymphovascular invasion, and BRCA1 loss positively correlated with SET pattern morphology.
- Immunohistochemical analysis for BRCA1 is reported as an effective and alternative method for detection of BRCA1 dysfunction and can be correlated with the histomorphological pattern of HGSC.
Limitations: Small sample size (n=45).; Observational clinicopathological correlation — association does not prove causation.; BRCA dysfunction was assessed by immunohistochemistry; no genetic (germline/somatic mutation) or promoter methylation testing is reported to confirm underlying BRCA1/2 alterations.; No clinical outcome or treatment-response data reported to link immunoexpression with prognosis or therapy..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed
ReviewSupportive careInconclusiveLimited evidenceTier 3 · early human
Exercise and sport sciences reviews · Jul 2025
Supportive care
This review article discusses that completing the full intended course of anticancer treatment is important for efficacy, recurrence risk, and survival. The authors state that engaging in an exercise program during cancer treatment has the potential to improve completion of those treatments. They also note a need for standardized terminology for reporting treatment completion as cancer therapies evolve.
Key findings
- Receipt of the entire course of intended anticancer treatment is critical to maximize treatment efficacy, reduce risk of disease recurrence, and improve survival.
- Engaging in an exercise program during cancer treatment has the potential to improve treatment completion.
- Standardization in terminology for reporting on cancer treatment completion is needed, especially as types of cancer treatments continue to evolve.
Limitations: This is a review article and the abstract does not present primary experimental or trial data.; The abstract provides no quantitative effect sizes or outcome data on exercise and treatment completion.; Review methodology (search strategy, inclusion criteria) is not described in the abstract, so potential bias or incompleteness cannot be assessed from the abstract alone.; Recommendations are general and acknowledge evolving cancer treatments, which may limit direct applicability without standardized reporting..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
ReviewMechanismInconclusiveModerate evidenceTier 4 · clinical
Pediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology Society · Jul 2025 · narrative review
pleuropulmonary blastomaSertoli-Leydig cell tumorcystic nephromauterine cervical embryonal rhabdomyosarcomathyroid follicular nodular disease
This narrative review summarizes the spectrum of benign and malignant tumors associated with germline heterozygous pathogenic DICER1 variants and emphasizes DICER1's role in miRNA processing and RNA interference. It highlights the most prevalent tumor types (pleuropulmonary blastoma, Sertoli-Leydig cell tumor, cystic nephroma, uterine cervical embryonal rhabdomyosarcoma, and thyroid follicular nodular disease), notes that these neoplasms are rare and often occur in children, and focuses on their histological features and molecular pathogenesis. The authors recommend that pathologists consider additional molecular testing and referral for genetic counseling and testing to facilitate earlier diagnosis.
Key findings
- DICER1 syndrome is caused by germline heterozygous pathogenic variants in DICER1 and is essential in miRNA processing and RNA interference.
- The syndrome is heterogeneous and includes a large variety of benign and malignant tumor types.
- The most prevalent tumor types include pleuropulmonary blastoma, Sertoli-Leydig cell tumor, cystic nephroma, uterine cervical embryonal rhabdomyosarcoma, and thyroid follicular nodular disease.
- These neoplasms are rare and particularly occur in the pediatric population.
- Pathologists should be aware of the potential relationship to DICER1 syndrome to perform or suggest additional molecular pathologic analysis and refer patients and their parents for genetic counseling and testing.
- The review emphasizes histological features of DICER1-related tumors and reflects on DICER1 molecular pathogenesis to raise awareness and facilitate earlier diagnosis.
Limitations: Review article that does not present new primary data.; Rarity of the tumor types limits the available evidence base and generalizability.; Focus is on histological features and molecular pathogenesis; the review does not provide primary clinical outcome or treatment data..
AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
ReviewReported negativeModerate evidenceTier 4 · clinical
Dermatologic clinics · Jul 2025
melanoma
This narrative review summarizes recent trends in melanoma incidence and mortality. The authors report that incidence rates and the total number of melanoma deaths continue to increase annually and discuss how sex, age, race, socioeconomic status, and tanning bed use relate to those trends across subpopulations.
Key findings
- Melanoma incidence rate and the total number of associated deaths continue to increase annually.
- Melanoma outcomes are impacted by sex, age, race, socioeconomic status, and tanning bed use.
- The article explores trends in changing melanoma incidence and mortality by modifiable variables and subpopulation.
Limitations: Narrative review—no original data reported in the abstract; Abstract provides no methods, data sources, or quantitative results; Geographic scope and time period of the trends are not specified in the abstract; Potential heterogeneity of included studies and lack of systematic methods (not stated).
AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed
Human trialSupportive careInconclusiveLimited evidenceTier 4 · clinical
JAMA oncology · Jul 2025 · pilot randomized clinical trial
Supportive careprostate cancer
This pilot randomized clinical trial evaluated acupuncture versus usual care for nocturia in survivors of prostate cancer. The abstract states the study objective but does not report any results, effect sizes, sample size, or safety data.
Key findings
- The trial randomized survivors of prostate cancer with nocturia to acupuncture versus usual care.
- The abstract provides no outcome data, effect estimates, sample size, or safety results.
Limitations: Abstract provides no results or quantitative outcome data.; Pilot study (likely small) — limited sample size and statistical power (sample size not reported).; Key trial details (sample size, randomization method, blinding, follow-up duration, endpoints, and safety data) 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
Human · observationalMechanismInconclusiveLimited evidenceTier 3 · early human
JAMA network open · Jul 2025 · cohort study
prostate cancer
This cohort study examined whether patients with prostate cancer who had preexisting depression had different survival compared with those without preexisting depression. The abstract states the study objective but provides no details on methods, sample size, follow-up, or the study's results.
Key findings
- The study evaluated survival differences between prostate cancer patients with versus without preexisting depression.
- The abstract does not report quantitative results, sample size, or methodological details.
Limitations: Observational cohort design subject to confounding and cannot establish causality.; Abstract provides no sample size, follow-up time, methods, covariate adjustment, or outcome results.; Insufficient reporting in the abstract prevents assessment of effect estimates or statistical significance..
AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed
Human · observationalReported positiveLimited evidenceTier 3 · early human
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
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
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
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
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
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
Case reportReported negativeLimited evidenceTier 3 · early humann = 1
BMJ case reports · Jun 2025 · case report
large-cell neuroendocrine carcinoma of the trachea
This case report describes a man in his 70s who presented with dyspnoea and was found to have a primary large-cell neuroendocrine carcinoma of the trachea. Bronchoscopic debulking immediately relieved his dyspnoea; PET suggested the trachea as the primary site. After an incidental COVID-19 infection delayed a second bronchoscopy for 1 month, regrowth of the tracheal lesion with multiple disseminated airway lesions was found; the patient is receiving chemotherapy. The authors note primary tracheal LCNEC is very rare and may be aggressive, and recommend systemic evaluation for metastases.
Reported effect: delay to second bronchoscopy 1, n=1
Key findings
- Patient: man in his 70s presenting with dyspnoea
- Imaging revealed an intratracheal tumour; a small lesion was also detected in the left main bronchus
- Bronchoscopic debulking of the intratracheal tumour resulted in immediate relief of dyspnoea
- Pathological diagnosis was large-cell neuroendocrine carcinoma (LCNEC)
- Positron emission tomography suggested the trachea was the primary site
- Incidental COVID-19 infection delayed the second bronchoscopy for 1 month
- Second bronchoscopy revealed regrowth of the residual tracheal lesion with multiple disseminated lesions in the airways
- The patient is currently undergoing chemotherapy
- Authors conclude primary tracheal LCNEC is very rare and may be aggressive; systemic evaluation for metastases should be considered
Limitations: Single-patient case report; results are not generalizable; No long-term follow-up or outcome data reported beyond initiation of chemotherapy; No controlled comparison or systematic data on frequency, prognosis, or optimal management; Timeline potentially confounded by incidental COVID-19 infection delaying care.
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed
Human trialTrialReported positiveStrong evidenceTier 4 · clinicaln = 381
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
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
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
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
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
Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 64
Clinical cancer research : an official journal of the American Association for Cancer Research · Jun 2025 · systematic proteogenomic analysis of tumor and stromal tissue sections
synchronous endometrioid endometrial and ovarian cancerendometrioid endometrial cancerendometrioid ovarian cancer
The authors performed proteogenomic profiling (panel DNA sequencing plus mass-spectrometry proteomics) on tumors from 64 patients, including 29 with synchronous endometrioid endometrial and ovarian cancer (SEOC) and single-site endometrioid ovarian and endometrial cancers for comparison. DNA sequencing showed most SEOCs are clonally related, proteome profiling revealed clear differences between SEOCs and single-site tumors and highlighted a distinctive stromal proteome in SEOCs that was more similar to single endometrial cancers. The authors derived a proteomic predictor that distinguishes SEOCs from single-site ovarian and uterine tumors and conclude most SEOCs likely represent primary endometrial cancers that metastasized to the ovary.
Key findings
- DNA-based panel sequencing confirmed that most SEOCs are clonally related.
- Global proteome profiling uncovered pronounced differences between SEOCs and single tumors.
- The stromal proteome is important in defining and identifying SEOCs; SEOC stromal proteomes were globally more related to single endometrial cancers.
- A proteomic predictor distinguishing SEOCs from single-site ovarian and uterine tumors was derived.
Limitations: Modest sample size (64 patients total; 29 SEOC cases).; Observational, tissue-based proteogenomic study without interventional or longitudinal outcome data reported.; No independent validation cohort or external validation of the derived proteomic predictor is reported in the abstract.; Inference that SEOCs represent primary endometrial cancers metastasized to the ovary is based on proteogenomic similarity rather than direct lineage/functional validation..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
ReviewFormulationReported positiveLimited evidenceTier 4 · clinical
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
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
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
ReviewMechanismInconclusiveLimited evidenceTier 4 · clinical
American Society of Clinical Oncology educational book. American Society of Clinical Oncology. Annual Meeting · Jun 2025
uterine neoplasmsleiomyosarcomauterine stromal tumorsmesonephric-like carcinomaserous carcinoma
This is a review of rare uterine malignancies (including leiomyosarcomas, uterine stromal tumors, mesonephric-like and serous carcinomas). The authors summarize recent advances in diagnostic precision, risk stratification, and identification of biomarker-guided therapeutic options, and note that improved molecular understanding has led to development of targeted approaches. They conclude that further progress requires coordinated global efforts and enrollment of patients on biomarker-driven clinical trials.
Key findings
- Rare uterine malignancies are clinically and biologically heterogeneous, creating treatment challenges.
- The rarest uterine cancers discussed include leiomyosarcomas, uterine stromal tumors, and mesonephric-like and serous carcinomas.
- Recent advancements have improved diagnostic precision and risk stratification for these rare subtypes.
- Identification of biomarker-guided therapeutic options and improved molecular profiling have led to development of targeted treatment approaches.
- Further progress depends on coordinated, global characterization efforts and enrollment of patients on biomarker-driven clinical trials.
Limitations: Review article — does not present new primary experimental or clinical trial data.; Focuses on rare, heterogeneous tumor subtypes for which evidence is often limited.; Conclusions are broad and dependent on availability of biomarker-driven trials rather than on definitive trial results..
AI summary of the abstract, human-reviewed · Aug 2026. Describes what this study reported, not medical advice. View on PubMed
ReviewInconclusiveModerate evidenceTier 4 · clinical
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
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
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, published automatically under the strong-evidence tier · Jul 2026; an editor has not yet reviewed it. Describes what this study reported, not medical advice. View on PubMed · Full text
ReviewMechanismInconclusiveLimited evidenceTier 4 · clinical
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
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
Gynecologic oncology · Jun 2025 · archival tissue analysis plus patient-derived organoid and xenograft preclinical study
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
OtherFormulationReported positivePreclinical onlyTier 1 · lab
Scientific reports · May 2025 · experimental bench study using heterogeneous phantoms, the Gustav voxel model, and head tissue‑simulating liquid
The authors developed a metamaterial-integrated applicator operating at 2.45 GHz for focused clinical hyperthermia. They evaluated it using heterogeneous phantoms, a computational voxel model, and head tissue‑simulating liquid and report that the applicator reached 44 °C in tumors with 3 W input power. SAR measurements at 0.1 W showed consistent energy distribution across depths, and simulation and experimental results were strongly aligned. The device was encased in Teflon and tested with a water bolus including a 1 mm PVC layer to protect superficial tissues.
Reported effects: operating frequency 2.45 · tumor temperature at 3 W input 44 · +2 more
Key findings
- Applicator operates at 2.45 GHz and integrates a double spiral antenna (DSA), spiral frequency selective surface (SFSS), and artificial magnetic conductor (AMC).
- The applicator achieves a therapeutic temperature of 44 °C in tumors with just 3 W of input power.
- Specific absorption rate (SAR) measurements at 0.1 W input confirm consistent energy distribution across varying depths.
- Thermal efficiency analyzed with a water bolus including a 1 mm PVC layer to protect superficial tissues and enable uniform heat distribution.
- Impedance matching and resonance at 2.45 GHz ensure effective energy delivery; simulation and experimental results showed strong alignment.
Limitations: Evaluation limited to heterogeneous phantoms, a computational voxel model, and tissue‑simulating liquid — no in vivo or clinical testing reported.; Abstract does not report sample sizes or experimental replication details.; Performance shown at a single operating frequency (2.45 GHz) and specific test conditions, which may limit generalizability to clinical settings..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
ReviewMechanismReported positiveModerate evidenceTier 4 · clinical
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
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
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
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
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
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
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
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
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
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
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
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
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
Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 9
Clinical cancer research : an official journal of the American Association for Cancer Research · Apr 2025 · germline and tumor sequencing with cohort prevalence analysis in population biobanks
pineoblastomaWilms tumor
The study sequenced germline and tumor DNA and identified nine children from eight families with heterozygous pathogenic germline DROSHA variants who had pineoblastoma (8) or Wilms tumor (1). A somatic second hit in DROSHA was detected in all eight tumors analyzed, and all pineoblastomas were classified as the miRNA processing-altered 1 subtype. The authors estimated population prevalence of germline DROSHA loss-of-function variants at about 1:3,875 to 1:4,843 and found no evidence for increased adult cancer risk. They suggest considering genetic testing and research-based surveillance for individuals with DROSHA GPVs.
Reported effects: case_count_total 9 · pineoblastoma_count 8 · +3 more
Key findings
- Nine children from eight families were described with heterozygous germline pathogenic DROSHA variants and diagnoses of pineoblastoma (n = 8) or Wilms tumor (n = 1).
- A somatic second hit in DROSHA was detected in all eight tumors analyzed.
- All pineoblastoma tumors analyzed were classified as miRNA processing-altered 1 subtype.
- Estimated population prevalence of germline DROSHA loss-of-function variants is 1:3,875 to 1:4,843 based on UK Biobank and Geisinger DiscovEHR analyses.
- No evidence was found for increased adult cancer risk in the datasets analyzed.
- Authors recommend consideration of genetic testing for DROSHA GPVs in patients with pineoblastoma, Wilms tumor, or related conditions and propose research-based surveillance recommendations.
Limitations: Small case series (nine children from eight families) limits generalizability.; Observational genetic study design cannot prove causality.; Abstract does not provide details of the number of adult cases or follow-up, limiting assessment of adult cancer risk.; Population prevalence estimates are reported without detailed methods or confidence intervals in the abstract..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Human · observationalMechanismReported negativeLimited evidenceTier 3 · early humann = 406
Pathology, research and practice · Apr 2025 · retrospective study
ovarian mucinous tumormucinous ovarian carcinomaborderline mucinous tumor
Investigators retrospectively reviewed slides from 406 patients (417 tumors) with primary ovarian mucinous tumors to look for mesonephric-like components and performed immunohistochemistry (GATA3, TTF-1) on suspicious areas. They found 64 cases with morphology that could be considered mesonephric-like, but only two foci were TTF-1 positive and one showed weak focal GATA3 staining, which the authors judged nonspecific. Overall, they report no associated mesonephric-like components in this series and conclude such association is probably too rare to support a mesonephric origin.
Reported effects: patients_included 406, n=406 · mean age at diagnosis 47.4, n=406 · +10 more
Key findings
- Included 406 patients with primary ovarian mucinous tumors (417 tumors, 15 bilateral cases).
- Tumor breakdown: 305 mucinous cystadenomas/cystadenofibromas, 84 borderline mucinous tumors, 28 mucinous carcinomas.
- Associated Brenner tumors present in 16 cases and teratomas in 8 cases.
- Morphological analysis revealed 64 cases with a component that could be considered mesonephric-like.
- Two of these were TTF-1 positive and one of them expressed GATA3 weakly and very focally; these were interpreted as non-specific for mesonephric differentiation.
- Conclusion: no associated mesonephric-like components identified in this series; such association is likely too rare to imply a role in histogenesis.
Limitations: Retrospective study design; Immunohistochemical analysis limited to two markers (GATA3 and TTF-1) as reported in the abstract; Interpretation of mesonephric-like differentiation and IHC positivity described as non-specific, which is subjective; No molecular/genetic testing reported in the abstract to further characterize suspicious foci.
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed
Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 195
JCI insight · Apr 2025 · retrospective multiinstitutional cohort
uterine serous carcinomauterine neoplasm
Researchers scored GATA2 protein levels by immunohistochemistry in a retrospective cohort of 195 uterine serous carcinomas and related GATA2 levels to clinical outcomes. They found that FIGO stage I tumors with high GATA2 (GATA2hi) had 100% recurrence-free and 100% cancer-related survival, and among patients who omitted adjuvant chemotherapy, GATA2hi tumors had 100% 5-year recurrence-free survival versus 60% in GATA2lo tumors. In patient-derived USC cells, depletion of GATA2 increased invasion in vitro. The authors propose GATA2 IHC could identify a subgroup (~33%) of stage I patients with greatly reduced recurrence risk.
Reported effects: recurrence-free survival (FIGO stage I, GATA2hi) 100% · cancer-related survival (FIGO stage I, GATA2hi) 100% · +2 more
Key findings
- Patients with FIGO stage I GATA2hi USCs had 100% recurrence-free and 100% cancer-related survival, which was significantly better than patients with GATA2lo USCs.
- In patients for whom adjuvant chemotherapy was omitted, patients with GATA2hi USC had 100% recurrence-free 5-year survival compared with 60% recurrence-free survival in patients with GATA2lo USC.
- Depletion of GATA2 in patient-derived USC cells increased invasion in vitro.
- Routine GATA2 IHC identifies 33% of patients with FIGO stage I USC who have a greatly reduced risk of posthysterectomy USC recurrence.
Limitations: Retrospective cohort design (nonrandomized) limits causal inference and is susceptible to selection and unmeasured confounding.; Mechanistic data demonstrating increased invasion were limited to in vitro depletion of GATA2 in patient-derived cells (no in vivo validation).; Abstract does not report follow-up duration, subgroup sizes, confidence intervals, or p-values for the quoted percentages.; No prospective or external validation cohort reported in the abstract to confirm prognostic performance before clinical implementation..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Case reportReported positiveLimited evidenceTier 3 · early humann = 1
Journal of obstetrics and gynaecology of India · Apr 2025 · case report
peritoneal endometrioid adenocarcinomaendometriosis-associated neoplasm
This single-patient case report describes a 43-year-old woman with grade IV endometriosis and a peritoneal nodule that was histologically diagnosed as endometrioid adenocarcinoma. The lesion (5.5×4.5 cm) was removed by en bloc wide local excision and complete surgical staging was performed; no adjuvant therapy was given. The patient has been disease-free for the last 3 years.
Reported effects: patient age 43, n=1 · peritoneal nodule size, n=1 · +1 more
Key findings
- Background: Endometriosis-associated neoplasms develop in 0.7-2.5% of women with endometriosis (background statement).
- A 43years female presented with menorrhagia, dysmenorrhoea and dyspareunia.
- Imaging showed an endometriotic cyst in the left ovary and an iso- to hyperechoic nodular area in the right iliac fossa.
- Laparoscopy showed grade IV endometriosis and a peritoneal nodule of 5.5
x
4.5cm in the right iliac fossa.
- The peritoneal nodule was removed en bloc with wide local excision and clinically disease-free margin.
- Histopathology of the peritoneal nodule showed endometrioid adenocarcinoma.
- Complete surgical staging for peritoneal cancer was performed and no adjuvant therapy was advised.
- The patient remained disease-free at 3 years of follow-up.
Limitations: Single case report — results are not generalizable.; No molecular, genetic, or immunohistochemical data presented to further characterize the tumor.; No discussion or data on rationale for omitting adjuvant therapy or on long-term surveillance beyond 3 years.; No control or comparator; cannot inform prognosis or management guidance broadly..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
ReviewInconclusiveLimited evidenceTier 4 · clinical
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
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