These are reviewed studies whose abstracts concern Endometrial Cancer. Each describes only what that study reported. This is not a claim by OncoForge that any compound helps or harms Endometrial Cancer. Most are early lab, animal, or small human studies, and findings often conflict.
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 · 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
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 · 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
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
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
ReviewMixed resultsLimited evidenceTier 4 · clinical
Medicina (Kaunas, Lithuania) · Dec 2024 · literature review
uterine serous carcinoma (serous endometrial carcinoma)endometrial cancer
This literature review summarizes current HER2-directed therapies for HER2-positive uterine serous (serous endometrial) carcinoma. The authors note that about one-third of serous endometrial cancers overexpress HER2 or have ERBB2 amplification and that clinical trials combining chemotherapy with anti-HER2 agents (mainly trastuzumab, alone or with pertuzumab) have shown promising results and been incorporated into international guidelines. The review also describes ongoing research into antibody–drug conjugates and tyrosine kinase inhibitors and highlights that acquired resistance and other unmet needs remain.
Studied with: chemotherapy, pertuzumab.
Key findings
- Approximately one-third of patients with serous endometrial carcinoma may overexpress HER2/neu protein and/or show c-erBb2 (ERBB2) gene amplification.
- HER2-directed treatments, especially trastuzumab alone or combined with pertuzumab and chemotherapy, have shown promising results in clinical trials and have been incorporated into international guidelines.
- Antibody-drug conjugates and tyrosine kinase inhibitors targeting HER2 are under active investigation in endometrial cancer.
- Acquired resistance to HER2-targeted therapies is an important unresolved problem in endometrial cancer and its mechanisms are mostly unknown.
- Research is exploring earlier use of HER2-directed therapy in this disease.
Limitations: This is a literature review and does not present new primary experimental or trial data.; The abstract does not state this is a systematic review, so selection and synthesis methods are not described in the abstract.; No quantitative effect sizes or detailed trial outcome data are presented in the abstract.; Mechanistic understanding of acquired resistance in endometrial cancer is reported as largely unknown..
AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
ReviewMechanismInconclusiveLimited evidenceTier 3 · early human
Cancer investigation · Nov 2024
endometrial cancer
This narrative review summarizes published evidence about circulating tumor cells (CTCs) and disseminated tumor cells (DTCs) in endometrial cancer. The authors report that a growing body of evidence suggests CTCs may provide a more complete tumor profile, help understand molecular mechanisms, and assist individual patient management. The review emphasizes the presence and clinical applications of CTCs/DTCs for prognosis and management and highlights the diagnostic value of tumor cells detected in urine.
Key findings
- Endometrial cancer mortality has been increasing over the last twenty years (statement of clinical context).
- A growing body of evidence suggests that circulating tumor cells (CTCs) may provide a more complete tumor profile and facilitate understanding of molecular mechanisms and individual management of endometrial cancer patients.
- The review presents the presence and clinical applications of CTCs and disseminated tumor cells (DTCs) in endometrial cancer, with particular emphasis on prognosis and management.
- The authors highlight the diagnostic value of tumor cells found in the urine of endometrial cancer patients.
Limitations: Narrative review only—no original primary data reported in this article.; Abstract does not specify search methods or criteria, so potential for selection bias or incomplete coverage of the literature.; No quantitative synthesis (meta-analysis) or new numerical results presented in the abstract..
AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed
Human · observationalInconclusiveLimited evidenceTier 3 · early human
JAMA network open · Oct 2024 · case-control
endometrial cancer
This is a case-control analysis of UK Biobank data that examined eight early-life factors in relation to risk of early-onset endometrial cancer among UK residents. The abstract states the study aim and design but does not report any results or effect estimates.
Key findings
- The study investigated associations between 8 early-life factors and early-onset endometrial cancer risk using a case-control design in UK Biobank data.
Limitations: Abstract does not report any results, effect sizes, sample sizes, or statistical significance.; Observational case-control design is susceptible to confounding and bias.; Generalisability may be limited to UK Biobank participants/UK residents..
AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
ReviewInconclusiveLimited evidenceTier 4 · clinical
Cancer treatment reviews · Sep 2024
endometrial cancer
This is a narrative review summarizing historical, current, and emerging therapies for locally advanced and metastatic endometrial cancer. It describes how tumor sequencing and The Cancer Genome Atlas classification have informed clinical practice and clinical trials, and highlights targeted therapies, hormonal therapies, and immunotherapy, including combinatorial approaches to overcome resistance.
Studied with: targeted therapies, immune checkpoint inhibitors, hormonal therapies.
Key findings
- Tumor sequencing and The Cancer Genome Atlas classification have been major advancements informing management.
- Clinical trials are investigating targeted therapies against signaling pathways, immune checkpoints, DNA integrity, growth factors, hormonal signaling, and metabolism.
- Numerous trials are testing combinations of targeted therapies to overcome tumoral resistance, compensatory mechanisms, and tumor polyclonality.
- The review particularly highlights clinical research on targeted and hormonal therapies, and also immunotherapy, reflecting an evolving treatment landscape.
Limitations: Narrative review without primary patient-level data or new experimental results presented in this article.; No quantitative treatment outcomes or effect sizes reported in the abstract.; Not a systematic review or meta-analysis (methodology for study identification/selection not described in abstract)..
AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed
Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 18
Cell death & disease · Aug 2024 · Single-cell RNA sequencing of 18 human endometrial cancer samples across multiple pathological types, with patient-derived organoid drug testing and in vitro validation experiments
endometrial canceruterine clear cell carcinomaendometrioid endometrial carcinomauterine serous carcinoma
The authors performed single-cell RNA sequencing on 18 endometrial cancer samples across different pathological subtypes to map tumor-cell and microenvironment heterogeneity. They report pathology-specific tumor cell programs (immune-, proliferation-, or metabolism-modulating) and distinct microenvironment compositions, identified candidate drugs for each pathological group and confirmed drug activity in patient-derived organoids, and validated oncogenic effects of SOD2+ inflammatory cancer-associated fibroblasts in vitro. These findings provide descriptive molecular and cellular maps that may guide future, but not yet clinical, personalized approaches.
Reported effect: n_samples 18, n=18
Key findings
- scRNA-seq was performed on 18 endometrial cancer samples from multiple pathological types.
- Cancer cells showed pathology-associated hallmarks: immune-modulating in uterine clear cell carcinoma (UCCC), proliferation-modulating in well-differentiated endometrioid endometrial carcinoma (EEC-I), and metabolism-modulating in uterine serous carcinoma (USC).
- Cancer cells from UCCC exhibited the greatest heterogeneity among the groups studied.
- Potential effective drugs were predicted for each pathological group and their effectiveness was confirmed using patient-derived endometrial cancer organoids.
- Tumor microenvironment differences: normal endometrium had prognostically favorable CD8+ cytotoxic T cells and NK cells, whereas tumors were dominated by CD4+ regulatory T cells, CD4+ exhausted T cells, and CD8+ exhausted T cells.
- CXCL3+ macrophages with an M2 signature and angiogenesis association were found exclusively in tumors.
- Epithelium-specific CAFs (eCAFs) predominated in EEC-I while SOD2+ inflammatory CAFs (iCAFs) predominated in UCCC.
- The oncogenic effects of SOD2+ iCAFs were validated in vitro.
Limitations: Relatively small sample size (18 samples) limits generalizability.; Observational single-cell profiling: no prospective clinical outcome data or in vivo validation reported.; Drug effectiveness was confirmed in patient-derived organoids (ex vivo) but not in patients or animal models.; In vitro validation of SOD2+ iCAFs does not establish causality in vivo or clinical relevance.; Abstract does not report specific drug names, doses, or safety data..
AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
ReviewMechanismInconclusiveLimited evidenceTier 4 · clinical
Clinical advances in hematology & oncology : H&O · Jul 2024
endometrial canceruterine serous carcinomauterine carcinosarcoma
This is a narrative review summarizing genomic and molecular features of uterine serous carcinoma (USC) and uterine carcinosarcoma (UCS). The authors note that USC and UCS are a small but increasing fraction of endometrial cancers and contribute disproportionately to endometrial cancer mortality, and that both subtypes have poor prognoses. The review summarizes clinical advances in primary advanced and recurrent disease and discusses emerging molecularly driven treatment strategies.
Key findings
- Endometrial cancer, including high-grade subtypes, has a rising incidence and mortality.
- Uterine serous carcinoma (USC) and uterine carcinosarcoma (UCS) account for a small but increasing proportion of endometrial cancer cases and a significant portion of endometrial cancer mortality.
- USC and UCS are molecularly and clinically distinct but both have a poor prognosis.
- There have been few therapeutic strategies directed specifically at these endometrial cancer subtypes to date.
- The review summarizes genomic/molecular features, clinical advances for primary advanced and recurrent disease, and novel molecularly driven treatment strategies.
Limitations: Review article only — does not present new, patient-level primary data.; Abstract does not indicate this is a systematic review or meta-analysis, so selection and synthesis methods are not described.; Does not report specific quantitative efficacy data or comparative clinical trial results in the abstract..
AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed