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
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 · 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
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
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
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
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
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
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
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
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
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
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
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
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
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 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
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