These are reviewed studies whose abstracts concern Ovarian Carcinoma. Each describes only what that study reported. This is not a claim by OncoForge that any compound helps or harms Ovarian Carcinoma. Most are early lab, animal, or small human studies, and findings often conflict.
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 · 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
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
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
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
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
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
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 · 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
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