Research Radartracking 1,762 published studies · 471 human · 11 safety signals · 58 clinical trials · 44 cancer pages · updated Sep 2026Open the Research Map →

Endometrial Cancer

A plain-English summary of the published research on Endometrial Cancer, reviewed and approved by our editors — not a hand-curated clinical overview.

Research summary · reviewed
Educational only: This page is not medical advice. Coordinate decisions with your oncology team.

Reviewed Jun 2026 · OncoForge editorial · How we review →

AI extractedhuman reviewedsources checkedretractions suppressed· last updated Jun 2026

Evidence at a glanceHuman trial / meta-analysisMixed results⚠ Studies disagree
97 published studies that name Endometrial Cancer15 human studies approved & graded (trial, observational, or meta-analysis)285 human clinical studies in the Endometrial Cancer corpus1355 source documents in the Endometrial Cancer corpus

last checked June 19, 2026

Why this grade?

Human trial / meta-analysis — Includes human trial or meta-analysis evidence.

Computed deterministically from the studies’ types and reported outcomes — not written by AI, and not a claim that anything works.

What the guidelines say

NCI PDQESMONCCNASCO

We link the authoritative guidelines rather than reproduce them. Below, the treatments on this page are split into standard care, guideline or regulatory options, supportive care, and studied but not standard so established care is not mixed with experimental or supportive items.

Guideline / FDA options - context-specific
  • pembrolizumab
  • durvalumab
  • dostarlimab
  • lenvatinib
Studied, not standard - investigational
  • surgery
  • Lymphadenectomy
  • chemotherapy
  • radiotherapy
  • Vaginal brachytherapy
  • hormone therapy
  • Novel targeted therapies
  • vaginal cuff brachytherapy
  • postoperative intensity-modulated pelvic radiotherapy
  • vaginal dilation
  • nurse-led programs
  • soy isoflavones
  • atezolizumab
  • avelumab
  • carboplatin
  • paclitaxel
  • tamoxifen

Read the guidelines

Cancer-specific deep links aren’t curated yet — these search the authoritative sources for Endometrial Cancer.

Treatment map: Endometrial Cancer

Open as a full page →

Standard care plus every compound studied in the literature (each cited) and graded by evidence, organized by clinical readiness. A category, not a verdict that anything works — confirm anything here with your oncology team.

23
Interventions
0
Standard of care
6
Tested in people
3
Lab / animal
10
Named in lit.
8
Classes
Standard of care (0) Guideline option (4) Tested in people (6) Lab / animal only (3) Named in the literature (10)

Tested in people, by trial phase: phase not reported ×6

Clinical evidence
Preclinical evidence
Standard of care
Guideline option
Tested in people
Lab / animal only
Named in the literature
Surgery & procedures
—
—
1
—
3
Radiotherapy
—
—
1
—
3
Chemotherapy
—
—
—
2
2
Targeted therapy
—
1
—
—
1
Immunotherapy
—
3
2
—
—
Hormonal therapy
—
—
—
1
1
Supplements & natural agents
—
—
1
—
—
Other
—
—
1
—
—

Columns group into clinical evidence (used in, or tested on, people) and preclinical evidence (lab/animal, or only named in the literature). Cell = number of interventions; a dashed cell means none recorded there.

Established care — detail (4)
Targeted therapy
lenvatinib
FDA-approved for this cancer.
—Guideline option
Immunotherapy
pembrolizumab
FDA-approved for this cancer.
—Guideline option
durvalumab
FDA-approved for this cancer.
—Guideline option
dostarlimab
FDA-approved for this cancer.
—Guideline option
Investigational & adjunct compounds — detail (19)
Meta-analysis (4)
nurse-led programsradiotherapysoy isoflavonesvaginal dilation
Named in the literature
surgeryLymphadenectomychemotherapyradiotherapy· Adjuvant (after surgery)Vaginal brachytherapy· Adjuvant (after surgery)hormone therapyNovel targeted therapieschemotherapy· Recurrent or later-linevaginal cuff brachytherapy· Adjuvant (after surgery)postoperative intensity-modulated pelvic radiotherapy· Adjuvant (after surgery)

"Tested in people" rows show the highest trial phase found in that compound's cited human studies (Phase I–IV; "phase not reported" = a human study with no phase tag). "Studied" = named in the cited literature for this cancer. "FDA ✓" = FDA-approved for this cancer; "off-label" = an FDA-approved drug used outside its approved indications (per openFDA). Not a claim that anything works.

Reported figures

Get cited updates on Endometrial Cancer
A monthly email when the research changes — $10/mo. Manage follows
Follow Endometrial Cancer

Snapshot

The essentials in ~60 seconds — every line is drawn from the cited sources below.

What it is
Endometrial carcinoma is the most common gynecologic malignancy in the United States and worldwide; most patients are diagnosed at an early stage. [1][2][3]
Survival
Most patients are diagnosed at an early stage with a low risk of relapse; overall 5-year survival is greater than 85%. [3]
Standard treatment
Diagnosis uses endometrial sampling (office biopsy, hysteroscopy, or dilatation and curettage) and initial management is surgical (including consideration of lymphadenectomy); transvaginal ultrasound and cross-sectional imaging (MRI) are used for staging and planning, and fertility‑sparing options are considered for selected patients. [4][1][5][6]
Key test
A molecular classification that identifies POLE‑ultramutated, mismatch repair‑deficient, p53‑abnormal, and tumors with no specific molecular profile is described in the literature. [7]
Biggest challenge
Key clinical challenges are uncertainty about which patients should receive adjuvant therapy (chemotherapy, radiotherapy, or both) and poor outcomes for metastatic or recurrent disease related to poor chemotherapy responses and limited second‑line options. [3]

Ask about Endometrial Cancer

Answers come only from the cited sources on this page — with the supporting evidence shown. If the sources here don't cover your question, it will say so. Educational information, not medical advice.

Key numbers & factors

Risk factors

  • ▲ increases riskLynch syndrome carrier status — Estimated prevalence of endometrial cancer was 20% among female Lynch syndrome carriers. [8]
  • ▲ increases riskInfertility — Guidelines state infertile women may be at an increased risk of invasive ovarian, endometrial, and breast cancer. [9]
  • ◆ mixedEndocrine-disrupting chemicals (EDCs) — Epidemiological data are inconsistent and studies reported both positive and null associations for different EDC exposures. [7]
  • ◆ mixedFertility drug use — Based on available data, use of fertility drugs does not appear to increase the risk of invasive ovarian cancer, breast cancer, or endometrial cancer. [9]

Biomarkers

  • MSH6 · Gene-specific risk marker in Lynch syndrome carriers (increased endometrial cancer risk). [8]
  • PMS2 · Gene-specific risk marker in Lynch syndrome carriers (reduced endometrial cancer risk relative to other Lynch genes). [8]
  • Tumor molecular classification (POLE, MMR-deficient, p53-abnormal, NSMP) · Classifies endometrial tumors into POLE‑ultramutated, mismatch repair‑deficient, p53‑abnormal, or no specific molecular profile. [7]

10 sections — tap any heading to expand its cited detail. Key points are above.

OverviewEndometrial carcinoma is the most common gynecologic malignancy and is often diagnosed at an early stage with overall survival at 5 years greater than 85%. It is the sixth most frequently diagnosed malignancy in women, with approximately 417,000 new cases and nearly 97,000 deaths reported each year, and has historically been classified into Type I and Type II subtypes.4 points
  • Endometrial carcinoma (adenocarcinoma of the endometrium) is the most common gynecologic malignancy; it is the most common malignancy of the female genital tract in the United States and the most common gynaecological tumour in developing countries. [1][2][3]3 sources
  • Endometrial cancer is the sixth most frequently diagnosed malignancy in women, with approximately 417,000 new cases worldwide and nearly 97,000 deaths reported each year. [7]
  • Historically endometrial cancer has been classified into two main histopathological subtypes: Type I tumors (about 85%) are predominantly low-grade endometrioid carcinomas with high ER-α expression, while Type II tumors include high-grade and non-endometrioid histologies and are less dependent on hormonal signaling. [7]
  • Most patients with endometrial cancer are diagnosed at an early stage with a low risk of relapse and overall survival at 5 years greater than 85%. [3]
EpidemiologyAn estimated 49,560 new uterine cancer cases and 8190 deaths were reported for 2013. Among known risk factors, female Lynch syndrome carriers have an estimated endometrial cancer prevalence of 20%, while epidemiological evidence linking endocrine-disrupting chemicals (EDCs) to endometrial cancer is inconsistent — a systematic review identified eight human studies with both positive and null associations.4 points

Key figures

Survival & outcomes
OutcomeValue95% CI
estimated deaths from uterine cancer in 20138190—
endometrial_cancer_studies7—
Source quotes
  • “An estimated 49,560 new uterine cancer cases will occur in 2013, with 8190 deaths resulting from the disease.”
  • “Eleven studies focused on cervical cancer, 7 on endometrial cancer, and 8 included mixed gynecologic malignancies.”
  • A systematic review of radiation therapy patient-reported outcomes in gynecologic cancer included 26 studies comprising 5646 patients and reported that seven studies focused on endometrial cancer. [10]
  • An estimated 49,560 new uterine cancer cases will occur in 2013, with 8190 deaths resulting from the disease. [2]
  • Among female Lynch syndrome carriers the estimated prevalence of endometrial cancer was 20%. [8]
  • A systematic review of endocrine-disrupting chemicals (EDCs) and endometrial cancer identified eight human studies that met the inclusion criteria and concluded that epidemiological data linking EDC exposure to endometrial cancer risk remain inconsistent and fragmented; individual studies reported both positive and null associations for different EDC exposures. [7]
Standard managementEvaluation and management of endometrial cancer commonly includes endometrial sampling and imaging, with surgery as a mainstay for early and advanced disease and ongoing questions about adjuvant therapy. Consensus guidance exists for postoperative radiotherapy target volumes and for vaginal-cuff brachytherapy technique and reporting; fertility-sparing approaches and ultrasound assessment of asymptomatic endometrial thickening are discussed in guidelines and reviews.9 points
  • Women with possible endometrial cancer can undergo an endometrial evaluation by office biopsy, hysteroscopy, or dilatation and curettage. [4]
  • Surgical management of early and advanced cancer, including lymphadenectomy in early cancer, is examined in practice recommendations. [1]
  • Fertility-sparing treatment is one of the topics examined in contemporary reviews of management strategies. [6]
  • There has been no consensus regarding adjuvant treatment in endometrial cancer patients, with many open questions about which patients should receive it and whether chemotherapy, radiotherapy, or both are best. [3]
  • Consensus recommendations for delineation of the clinical target volume for postoperative pelvic intensity-modulated radiotherapy for endometrial cancer specify that the CTV should include the common, external, and internal iliac lymph node regions; the upper 3.0 cm of the vagina and paravaginal soft tissue lateral to the vagina; and, for endometrial cancer with cervical stromal invasion, the presacral lymph node region. [11]
  • The American Brachytherapy Society made specific recommendations for applicator selection, insertion techniques, target volume definition, dose fractionation, and specifications for postoperative adjuvant vaginal cuff therapy; the ABS recommends that applicator selection should be based on patient anatomy, target volume geometry, and physician judgment, and that doses should be reported at the vaginal surface and at 0.5-cm depth. [12]
  • There are published clinical practice guidelines addressing assessment of asymptomatic endometrial thickening found on ultrasound in postmenopausal patients without bleeding. [13]
  • In women with polycystic ovary syndrome, who share many risk factors associated with endometrial cancer, the guideline suggests against routine ultrasound screening for endometrial thickness. [14]
  • Cross-sectional imaging plays a vital role in pretreatment assessment of endometrial cancers and should be viewed as a complementary tool for surgical evaluation and planning; transvaginal ultrasound remains the preferred examination for screening purposes. [5]
Staging & riskMagnetic resonance imaging (MRI) is the preferred imaging modality for staging endometrial cancer. Combining dynamic contrast-enhanced and diffusion-weighted MRI provides the highest accuracy for staging.2 points
  • MRI has emerged as the modality of choice for the staging of endometrial cancer. [5]
  • A combination of dynamic contrast-enhanced and diffusion weighted MRI provides the highest accuracy for staging. [5]
PrognosisPrognosis in endometrial cancer varies: a subgroup of patients has a very poor prognosis linked to pathological and molecular features, and survival for metastatic or recurrent disease is described as quite short, in part because of poor chemotherapy responses and lack of second-line treatments. Uterine sarcomas are uncommon, accounting for approximately 3% of all uterine cancers.3 points
  • Uterine sarcomas are uncommon and account for approximately 3% of all uterine cancers. [2]
  • A subgroup of endometrial cancer patients has a very poor prognosis due to pathological features and molecular characteristics. [3]
  • Survival of patients with metastatic or recurrent endometrial cancer is described as quite short, related to poor chemotherapy responses and lack of second-line treatments. [3]
Safety & interactionsInfertility is associated with a possible increased risk of invasive ovarian, endometrial, and breast cancer, while available data indicate that use of fertility drugs does not appear to increase the risk of those cancers. Radiation therapy for gynecologic cancers can cause enduring adverse effects on sexual health, affecting both physical and psychosocial dimensions.3 points
  • Guidelines state that infertile women may be at an increased risk of invasive ovarian, endometrial, and breast cancer. [9]
  • Based on available data, use of fertility drugs does not appear to increase the risk of invasive ovarian cancer, breast cancer, or endometrial cancer. [9]
  • Radiation therapy for gynecologic cancers has enduring adverse effects on sexual health that involve both physical and psychosocial dimensions. [10]
Treatments & compounds studiedFourteen therapeutic entries across procedure_device, chemotherapy, radiotherapy, hormonal_therapy, targeted_therapy, other, and supplement_natural are summarized below.14 treatments

Chemotherapy

  • Chemotherapy · 2 findings
    • Chemotherapy is discussed as a therapy for advanced disease. [6]
    • Recurrent or later-lineSEOM notes that responses to standard first-line chemotherapy are poor in metastatic or recurrent disease and that second-line options are lacking. [3]

Targeted therapy

  • Novel targeted therapies: Novel targeted therapies are mentioned as a topic of interest in reviews of endometrial cancer treatment. [6]

Hormonal therapy

  • Hormone therapy: Hormone therapy is discussed as a therapy option for advanced disease. [6]

Radiotherapy

  • Radiation therapy · radiotherapy · 2 findings
    • Adjuvant (after surgery)Radiation therapy is discussed as an adjuvant treatment. [6]
    • Radiation therapy was consistently associated with long-term sexual dysfunction, including vaginal dryness, dyspareunia, and diminished sexual satisfaction. [10]
  • Vaginal brachytherapy: Adjuvant (after surgery)Vaginal brachytherapy is listed among adjuvant therapy options. [6]
  • postoperative intensity-modulated pelvic radiotherapy: Adjuvant (after surgery)Postoperative intensity-modulated pelvic radiotherapy has consensus CTV definitions intended as a template for planning postoperative radiotherapy in endometrial cancer. [11]

Supplements & natural agents

  • soy isoflavones: A randomized trial of soy isoflavones (a phytoestrogen supplement) reported a null finding for endometrial cancer outcomes in the trial entry reported in the review. [7]

Procedures & devices

  • Surgery: Surgical management, including surgery for early and advanced disease, is examined in practice recommendations. [1]
  • Lymphadenectomy: Lymphadenectomy is described as part of surgical management in early endometrial cancer. [1]
  • vaginal cuff brachytherapy: Adjuvant (after surgery)Adjuvant vaginal cuff brachytherapy is addressed in ABS consensus recommendations that include guidance on applicator selection, insertion technique, target volume definition, and dose fractionation for postoperative therapy after hysterectomy. [12]
  • vaginal dilation: Regular vaginal dilation was associated with maintained vaginal length and enhanced sexual function but had no effect on vaginal elasticity. [10]

Other

  • nurse-led programs: Nurse-led programs may help preserve vaginal health, though adherence is low and benefits are modest. [10]
What we don't know yetKey uncertainties in endometrial cancer include methodological limitations in epidemiological studies of exposures (for example, fertility drugs and endocrine-disrupting chemicals) and unresolved questions about optimal adjuvant treatment, with clinical trials ongoing to address some of these issues.3 points
  • Methodological limitations in studying the association between fertility drug use and cancer include increased baseline cancer risk in women who never conceive, low incidence of many cancers, and long latency between exposure and diagnosis. [9]
  • Available human studies of exposure to endocrine-disrupting chemicals (EDCs) are heterogeneous in design and exposure assessment; a systematic and critical evaluation of the epidemiological evidence is required to clarify any association with endometrial cancer risk and to identify key knowledge gaps. [7]
  • There remain many open questions about adjuvant treatment in endometrial cancer, and relevant clinical trials are in progress to address them. [3]
Key biomarkersEndometrial cancer biomarker classification includes a molecular system dividing tumors into POLE-ultramutated, mismatch repair-deficient, p53-abnormal, and no specific molecular profile groups; separately, within Lynch syndrome carriers, MSH6 is associated with increased endometrial cancer risk and PMS2 with reduced risk compared with other Lynch genes.2 points
  • Gene-specific analyses in Lynch syndrome carriers showed increased endometrial cancer risk with MSH6 and reduced risk with PMS2, relative to other Lynch genes. [8]
  • A molecular classification has been described that identifies POLE-ultramutated, mismatch repair-deficient, p53-abnormal, and tumors with no specific molecular profile. [7]
Biology & pathwaysSome endocrine-disrupting chemicals that resemble estradiol can interact with estrogen receptors and modulate estrogen-dependent signaling; experimental studies report they can activate ER-dependent transcription, induce oxidative stress, and stimulate proliferative and anti-apoptotic pathways relevant to endometrial carcinogenesis.1 point
  • Some endocrine-disrupting chemicals share structural similarities with endogenous steroid hormones such as estradiol and may bind hormone receptors to modulate estrogen-dependent signaling pathways; experimental studies report that selected EDCs can activate ER-dependent transcription, induce oxidative stress, and promote proliferative and anti-apoptotic signaling pathways relevant to endometrial carcinogenesis. [7]

Common questions

What is Endometrial Cancer?

Endometrial carcinoma is the most common gynecologic malignancy and is often diagnosed at an early stage with overall survival at 5 years greater than 85%. It is the sixth most frequently diagnosed malignancy in women, with approximately 417,000 new cases and nearly 97,000 deaths reported each year, and has historically been classified into Type I and Type II subtypes.

How common is Endometrial Cancer?

An estimated 49,560 new uterine cancer cases and 8190 deaths were reported for 2013. Among known risk factors, female Lynch syndrome carriers have an estimated endometrial cancer prevalence of 20%, while epidemiological evidence linking endocrine-disrupting chemicals (EDCs) to endometrial cancer is inconsistent — a systematic review identified eight human studies with both positive and null associations.

Which biomarkers are important in Endometrial Cancer?

Endometrial cancer biomarker classification includes a molecular system dividing tumors into POLE-ultramutated, mismatch repair-deficient, p53-abnormal, and no specific molecular profile groups; separately, within Lynch syndrome carriers, MSH6 is associated with increased endometrial cancer risk and PMS2 with reduced risk compared with other Lynch genes.

What is the biology of Endometrial Cancer?

Some endocrine-disrupting chemicals that resemble estradiol can interact with estrogen receptors and modulate estrogen-dependent signaling; experimental studies report they can activate ER-dependent transcription, induce oxidative stress, and stimulate proliferative and anti-apoptotic pathways relevant to endometrial carcinogenesis.

How is Endometrial Cancer treated?

Evaluation and management of endometrial cancer commonly includes endometrial sampling and imaging, with surgery as a mainstay for early and advanced disease and ongoing questions about adjuvant therapy. Consensus guidance exists for postoperative radiotherapy target volumes and for vaginal-cuff brachytherapy technique and reporting; fertility-sparing approaches and ultrasound assessment of asymptomatic endometrial thickening are discussed in guidelines and reviews.

What treatments are studied for Endometrial Cancer?

Fourteen therapeutic entries across procedure_device, chemotherapy, radiotherapy, hormonal_therapy, targeted_therapy, other, and supplement_natural are summarized below.

Sources

Every statement above is drawn from these reviewed sources. This page reports what they describe. Sources last checked June 19, 2026.

  1. GuidelineEndometrial cancer: a review and current management strategies: part I · 2014
  2. GuidelineUterine neoplasms, version 1.2014 · 2014
  3. GuidelineSEOM guidelines for endometrial cancer · 2012
  4. GuidelineEpidemiology and investigations for suspected endometrial cancer · 2013
  5. GuidelineACR Appropriateness Criteria® pretreatment evaluation and follow-up of endometrial cancer · 2014
  6. GuidelineEndometrial cancer: a review and current management strategies: part II · 2014
  7. Systematic reviewEnvironmental endocrine disruptors and endometrial cancer: a systematic review of epidemiological studies · 2026
  8. Meta-analysisGene-specific cancer risks in female Lynch syndrome carriers: A copula-based meta-analysis · 2026
  9. GuidelineFertility drugs and cancer: a guideline · 2016
  10. Systematic reviewA Systematic Review of Patient-Reported Outcomes on the Impact of Radiation Therapy on Sexual Health in Patients With Gynecologic Cancer · 2026
  11. GuidelineConsensus guidelines for delineation of clinical target volume for intensity-modulated pelvic radiotherapy in postoperative treatment of endometrial and cervical cancer · 2008
  12. GuidelineAmerican Brachytherapy Society consensus guidelines for adjuvant vaginal cuff brachytherapy after hysterectomy · 2012
  13. GuidelineAsymptomatic endometrial thickening · 2010
  14. GuidelineDiagnosis and treatment of polycystic ovary syndrome: an Endocrine Society clinical practice guideline · 2013

What supports this page

The kinds of sources behind this page, strongest at the top. Faint rungs show what is not here yet.

Guideline
44
Meta-analysis
224
Systematic review
36
Randomized trial
5
Clinical trial
24
Observational
6
Case report
45
Review
958
Preclinical
0
Other
13

Living document — last change June 19, 2026: Cancer page updated. 2 recent updates logged.

Pooled evidence across studies

PubMed
  • PFS: HR 0.51 (0.34–0.87 across studies) · pembrolizumab + carboplatin-paclitaxel chemotherapy
    6 studies · 0% agree · heterogeneous38422895
  • OS: 29.4 months (27.9–74.8 across studies) · (regimen unspecified)
    3 studies · 67% agree · moderate · 1 flagged39837013
  • ASCVD incidence: HR 1.56 (0.91–2.8 across studies) · (regimen unspecified)
    3 studies · 33% agree · heterogeneous40445187
  • Five-year relative survival: 83.6% (77–90.2 across studies) · (regimen unspecified)
    2 studies · 100% agree · consistent40752271
  • Colorectal cancer incidence: RR 1.135 (1.1–1.17 across studies) · red meat
    2 studies · 100% agree · consistent34455534
  • Colon cancer incidence: RR 1.19 (1.17–1.21 across studies) · red meat
    2 studies · 100% agree · consistent34455534
  • Rectal cancer incidence: RR 1.24 (1.22–1.26 across studies) · red meat
    2 studies · 100% agree · consistent34455534
  • Lung cancer incidence: RR 1.23 (1.2–1.26 across studies) · red meat
    2 studies · 100% agree · consistent34455534
  • PFS: HR 2.6695 (2.033–3.306 across studies) · (regimen unspecified)
    2 studies · 0% agree · heterogeneous29731976
  • OS: HR 1.65 (1.3–2 across studies) · (regimen unspecified)
    2 studies · 0% agree · heterogeneous39837013
  • ORR: 8.05% (5.3–10.8 across studies) · durvalumab + tremelimumab
    2 studies · 0% agree · heterogeneous36512912

Numbers pooled deterministically across 81 published studies that passed our figure-accuracy checks — a quick synthesis, not a formal meta-analysis. Updated 9/7/2026.

Compounds compared by evidence

PubMed

How to read this: Ranked by the strength and volume of the evidence — NOT by how well a treatment works. A higher rank means a compound has been studied more, or in stronger study designs (e.g. randomized trials over lab studies), not that it produces better outcomes. The effect column shows the largest pooled figure reported, not a head-to-head comparison.

#CompoundEvidence strengthStudiesLargest pooled effect
1Pembrolizumab ImmunotherapyHuman trial / meta-analysis3PFS: HR 0.51
2Durvalumab ImmunotherapyHuman trial / meta-analysis2ORR: 8.05%
3Atezolizumab ImmunotherapyHuman trial / meta-analysis1—
4Avelumab Targeted therapyHuman trial / meta-analysis1—
5Dostarlimab Targeted therapyHuman trial / meta-analysis1—
6Carboplatin ChemotherapyInsufficient evidence2—
7Lenvatinib Targeted therapyInsufficient evidence1—
8Paclitaxel ChemotherapyInsufficient evidence1—
9Tamoxifen Hormonal therapyInsufficient evidence1—

Ranked across 9 compounds with published studies for this cancer. Updated 9/7/2026.

Medicines & supplements studied for Endometrial Cancer

PubMedFDAClinicalTrials.gov

Every drug, supplement, and other agent the published studies cover for Endometrial Cancer, ranked by how strong the evidence is — what studies report, not a recommendation. Tap any to see its full profile.

Medicines · 9

PembrolizumabHuman trial / meta-analysisMixed results1 human

Includes human trial or meta-analysis evidence.

Largest credible effect: pooled HR overall 0.63 [0.52–0.76], p <.001, n=2456 PMID 38422895 · hazard ratios 0.34–0.87 across 6 studies

Most authoritative study: Incorporation of anti-PD1 or anti PD-L1 agents to platinum-based chemotherapy for the primary treatment of advanced or recurrent endometrial cancer. A meta-analysis

Findings conflict across studies · Effect sizes reported in only 1 of 4 studies.
ImmunotherapyFDA approved4 studiesFull profile →
DurvalumabHuman trial / meta-analysisMixed results2 human

Includes human trial or meta-analysis evidence.

Largest credible effect: pooled HR overall 0.63 [0.52–0.76], p <.001, n=2456 PMID 38422895 · hazard ratios 0.34–0.87 across 6 studies

Most authoritative study: Incorporation of anti-PD1 or anti PD-L1 agents to platinum-based chemotherapy for the primary treatment of advanced or recurrent endometrial cancer. A meta-analysis

Findings conflict across studies.
ImmunotherapyFDA approvedPhase 22 studiesFull profile →
AtezolizumabHuman trial / meta-analysisReported positive1 human

Includes human trial or meta-analysis evidence.

Largest credible effect: pooled HR overall 0.63 [0.52–0.76], p <.001, n=2456 PMID 38422895 · hazard ratios 0.34–0.87 across 6 studies

Most authoritative study: Incorporation of anti-PD1 or anti PD-L1 agents to platinum-based chemotherapy for the primary treatment of advanced or recurrent endometrial cancer. A meta-analysis

Based on a single study.
ImmunotherapyFDA off-label1 studyFull profile →
AvelumabHuman trial / meta-analysisReported positive1 human

Includes human trial or meta-analysis evidence.

Largest credible effect: pooled HR overall 0.63 [0.52–0.76], p <.001, n=2456 PMID 38422895 · hazard ratios 0.34–0.87 across 6 studies

Most authoritative study: Incorporation of anti-PD1 or anti PD-L1 agents to platinum-based chemotherapy for the primary treatment of advanced or recurrent endometrial cancer. A meta-analysis

Based on a single study.
ImmunotherapyFDA off-label1 studyFull profile →
DostarlimabHuman trial / meta-analysisReported positive1 human

Includes human trial or meta-analysis evidence.

Largest credible effect: pooled HR overall 0.63 [0.52–0.76], p <.001, n=2456 PMID 38422895 · hazard ratios 0.34–0.87 across 6 studies

Most authoritative study: Incorporation of anti-PD1 or anti PD-L1 agents to platinum-based chemotherapy for the primary treatment of advanced or recurrent endometrial cancer. A meta-analysis

Based on a single study.
ImmunotherapyFDA approved1 studyFull profile →
CarboplatinInsufficient evidenceMixed results

No primary experimental studies yet.

Largest credible effect: annual percent change 1.7% [1.2–2.2] PMID 33183764 · response rates 5.5–37.5 across 4 studies

Most authoritative study: Uterine carcinosarcoma: Contemporary clinical summary, molecular updates, and future research opportunity

No human studies yet · Findings conflict across studies · Effect sizes reported in only 1 of 2 studies.
ChemotherapyFDA off-label2 studiesFull profile →
LenvatinibInsufficient evidenceReported positive

No primary experimental studies yet.

Most authoritative study: Uterine serous carcinoma: key advances and novel treatment approaches

No human studies yet · No numeric effect sizes reported.
Targeted therapyFDA approved2 studiesFull profile →
PaclitaxelInsufficient evidenceReported positive

No primary experimental studies yet.

Most authoritative study: Targeted therapy in uterine serous carcinoma: an aggressive variant of endometrial cancer

No human studies yet · No numeric effect sizes reported · Based on a single study.
ChemotherapyFDA off-label1 studyFull profile →
TamoxifenInsufficient evidenceMixed results

No primary experimental studies yet.

Most authoritative study: Tamoxifen and Endometrial Cancer: A Janus-Headed Drug

No human studies yet · No numeric effect sizes reported · Based on a single study.
Hormonal therapyFDA off-label1 studyFull profile →

What recent studies report in Endometrial Cancer

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.

60 studies12 human1 animal⚠ Conflicting evidenceMechanism (32)Supportive care (3)Trial (2)

Tracking 60 published studies of Endometrial Cancer: 12 in humans, 1 in animals, 47 reviews/other.

Reported direction across studies: 19 positive, 15 mixed, 3 negative, 23 inconclusive.

Findings conflict — both supportive and negative/mixed results exist (see below). Human evidence is limited.

These counts summarize what the studies reported; they are not a measure of whether anything works for Endometrial Cancer.

Compounds with studies mentioning Endometrial Cancer

Pembrolizumab (3)Durvalumab (2)Lenvatinib (2)Atezolizumab (1)Avelumab (1)Dostarlimab (1)Carboplatin (1)Tamoxifen (1)
Case reportInconclusiveLimited evidenceTier 3 · early humann = 1

Uterine serous carcinoma arising in adenomyosis: a case report

Journal of ultrasound · Nov 2025 · case report

uterine serous carcinomaendometrial cancer arising in adenomyosisendometrial carcinoma

This is a case report of a 55-year-old postmenopausal woman who was found to have uterine serous carcinoma arising in adenomyosis. Imaging (CT and ultrasound) showed pelvic cystic masses and a 50 × 36 mm subserous cystic-solid uterine mass that was initially misdiagnosed as a degenerating fibroid; postoperative histopathology established the diagnosis. The authors note that a de novo cystic area in adenomyosis in postmenopausal women may suggest malignant transformation and emphasize ultrasound as the first imaging choice for gynecological masses.

Reported effects: CA125 44.86, n=1 · tumor_size, n=1

Key findings
  • A 55-year-old postmenopausal woman presented with anorexia, weight loss and mild abdominal pain; pelvic CT showed cystic masses.
  • Serum CA125 was 44.86 u/ml.
  • Transvaginal/transabdominal ultrasound detected a 50 × 36 mm subserous cystic-solid mass that was misdiagnosed preoperatively as a subserous uterine fibroid with cystic degeneration.
  • Postoperative histopathological diagnosis was uterine serous carcinoma arising from adenomyosis.
  • Authors suggest that a de novo cystic area in adenomyosis in postmenopausal women may indicate malignant transformation and present ultrasound images to raise diagnostic awareness.
Limitations: Single case report (n=1), so findings are not generalizable.; No control or comparison group.; Abstract provides limited pathological, immunohistochemical, and follow-up details.; Imaging features described may be nonspecific and susceptible to misdiagnosis.; No data on prevalence, diagnostic performance metrics, or outcomes beyond the single case..

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

ReviewReported positiveModerate evidenceTier 4 · clinical

Processed Meat Health Risks: Pathways and Dietary Solutions

The Journal of nutrition · Nov 2025 · review

colorectal cancerbreast cancerendometrial cancerlung cancer

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

Studied with: plant proteins, poultry, fish.

Key findings
  • Observational studies and meta-analyses show positive associations between red/processed meat consumption and multiple chronic diseases, including colorectal, breast, endometrial, and lung cancers, type 2 diabetes, cardiovascular disease, and all-cause mortality.
  • Dose-response relationships indicate elevated risks even at moderate intakes.
  • Processed meats consistently show stronger detrimental associations than unprocessed red meats.
  • Mechanistic pathways discussed include carcinogen formation, proinflammatory effects, gut microbiome dysbiosis, heme iron, trimethylamine N-oxide (TMAO), saturated fats, and effects on lipid metabolism and insulin resistance.
  • Replacing red/processed meats with plant proteins, poultry, or fish is associated with reduced disease risk according to the review.
  • Evidence complexities include inconsistent randomized controlled trial findings on short-term biomarkers and substantial modification of risk by processing, cooking methods, overall diet, lifestyle, and genetic factors.
Limitations: Predominantly observational epidemiologic evidence, which is susceptible to confounding and cannot establish causality.; Inconsistent randomized controlled trial findings limited to short-term biomarkers rather than clinical endpoints.; Heterogeneity introduced by differences in processing methods, cooking techniques, and definitions of processed versus unprocessed meat.; Potential modification of associations by overall diet, lifestyle, and genetic factors, complicating interpretation.; Identified gaps include need for greater mechanistic specificity, more diverse populations, and integrated health-environment assessments..

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

Human · observationalMixed resultsModerate evidenceTier 3 · early humann = 390805

Age-specific incidence and five-year relative survival of endometrial cancer histotypes by race and ethnicity among US women, 2000 to 2019

Gynecologic oncology · Sep 2025 · retrospective population-based registry analysis (SEER22, 2000-2019)

endometrial cancerendometrioid carcinomanon-endometrioid carcinomacarcinosarcomaclear cell carcinomaserous carcinomamixed carcinoma

This population-based study used SEER22 data from 2000–2019 (n=390,805) to estimate hysterectomy-corrected, age-specific incidence rates and five-year relative survival for individual endometrial cancer histotypes by race and ethnicity. It found that endometrioid carcinoma incidence was much higher in non-Hispanic White women aged 50+ (104.1 per 100,000) than in other groups, that non-endometrioid histotypes increased sharply around ages 50–54 (especially in non-Hispanic Black women), and that five-year relative survival was highest for endometrioid carcinomas (90.2%) and lower for other histotypes (range 39.6%–59.1%).

Reported effects: endometrioid carcinoma incidence rate, non-Hispanic White women ages 50+ (per 100,000) 104.1 · endometrioid carcinoma incidence rate, other groups ages 50+ (per 100,000) · +3 more

Key findings
  • Estimated hysterectomy-corrected, age-specific incidence rates and five-year relative survival for endometrial cancer histotypes using SEER22 (N = 390,805).
  • Endometrioid carcinoma rates were similar by race/ethnicity in younger women but much higher in non-Hispanic White women ages 50+ years (104.1 per 100,000) versus other groups (51.1-68.5).
  • Non-endometrioid histotypes were rare in younger women, with mixed carcinomas being the most common among the non-endometrioid types.
  • Carcinosarcoma, clear cell, and serous carcinoma rates increased sharply at ages 50-54, especially in non-Hispanic Black women.
  • Median age at diagnosis was youngest in Hispanic and non-Hispanic Asian/Pacific Islander women, particularly for endometrioid carcinomas.
  • Five-year relative survival: endometrioid carcinomas 90.2%; mixed carcinomas 77.0%; other non-endometrioid histotypes range 39.6%–59.1%.
Limitations: Observational registry study — cannot establish causal relationships between age/race/ethnicity and incidence or survival.; Potential for histotype or stage misclassification in registry data.; SEER lacks detailed individual-level risk factor, treatment, or molecular data to explain observed differences.; Hysterectomy-correction methods are estimations and may introduce uncertainty in incidence rates.; Findings are limited to populations covered by SEER and may not generalize to all US regions or internationally..

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

Human · observationalMechanismReported negativeModerate evidenceTier 3 · early humann = 6036

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

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

endometrial cancerendometrial carcinosarcoma

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

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

Key findings
  • 6036 women were included (mean age 67 years; 86% White) with mean follow-up of 48 months.
  • 45% of patients experienced recurrence and 39% of patients died due to any cause.
  • Median rwDFS from initiation of adjuvant therapy: 4.56 years (95% CI: 4.14-5.12).
  • Median OS from initiation of adjuvant therapy: 8.85 years (95% CI: 8.15-9.82).
  • Estimated 2-year and 5-year probabilities: rwDFS 0.64 (95% CI: 0.63-0.65) and 0.49 (95% CI: 0.48-0.50); OS 0.78 (95% CI: 0.77-0.79) and 0.60 (95% CI: 0.58-0.61).
  • Disease recurrence was associated with a 3.23-fold higher risk of death (p < 0.001).
  • Kendall's τ between rwDFS and OS was 0.75 (95% CI: 0.69-0.80, p < 0.001), supporting rwDFS as a surrogate for OS.
Limitations: Retrospective observational design (potential for confounding and bias).; Use of registry data (NCRAS) may limit availability of detailed clinical variables and introduces potential data-recording limitations).; rwDFS was operationalized as time to next treatment or death, a surrogate endpoint rather than confirmed radiographic/pathologic recurrence.; Findings are from England and may not generalize to other settings or populations..

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

ReviewMechanismInconclusiveLimited evidenceTier 3 · early human

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

Cells · Aug 2025 · review

uterine serous carcinomaendometrial cancerbreast cancer

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

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

Key findings
  • HER2/neu coordinates cell growth and differentiation and when overexpressed and/or amplified its downstream tyrosine kinase can become constitutively activated, causing dysregulated gene transcription.
  • HER2/neu has been successfully targeted in breast cancer with monoclonal antibodies and antibody-drug conjugates.
  • Use of HER2-directed therapies in gynecologic malignancies has been slower, in part due to unique characteristics of HER2 protein expression and gene amplification in USC such as major heterogeneity and lack of apical staining compared to breast cancer.
  • Optimal testing algorithms for HER2/neu status in USC may have important implications for developing targeted therapies.
  • The review evaluates efficacy of HER2-directed therapies in both preclinical and clinical settings and discusses possible mechanisms of resistance.
Limitations: Narrative review rather than original experimental or systematic/meta-analytic data.; Abstract contains no quantitative results or study-level sample sizes.; Conclusions depend on heterogeneous preclinical and clinical studies in the literature rather than a single controlled dataset.; Field limitations noted (e.g., heterogeneity of HER2 expression in USC) may limit generalizability of testing and therapeutic approaches..

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

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

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

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

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

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

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

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

Key findings
  • During up to 36 years of follow-up, 4,334 new-onset ASCVD events among 49,603 incident cancer cases were documented.
  • Cervical cancer was associated with increased ASCVD incidence (HR = 1.56, 95% CI = 1.06 to 2.29).
  • Hodgkin lymphoma was associated with increased ASCVD incidence (HR = 2.80, 95% CI = 1.89 to 4.15).
  • Prostate cancer was associated with lower ASCVD incidence (HR = 0.91, 95% CI = 0.85 to 0.97).
  • Breast cancer survivors experienced lower ASCVD risk during the first 7.5 years after diagnosis, but risk gradually increased afterward (Pnonlinearity = .01).
  • ASCVD risk increased over time among patients with cancers of the colorectum (P = .003), lung (P = .002), and endometrium (P = .04).
  • No statistically significant association with ASCVD risk was observed for cancers of the oral cavity and pharynx, kidney, or ovary; sarcoma; melanoma; or leukemia.
Limitations: Observational cohort design cannot establish causality.; Potential for residual confounding despite multivariable adjustment.; Cohorts consist of nurses and health professionals, which may limit generalizability to other populations.; Abstract does not report details on cancer stage or treatments, which could influence ASCVD risk..

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

ReviewMechanismInconclusiveLimited evidenceTier 4 · clinical

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

Medicina (Kaunas, Lithuania) · Jun 2025 · review

endometrial carcinosarcomaendometrial cancercarcinosarcoma of the endometrium

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

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

Key findings
  • ECS is a rare, aggressive biphasic metaplastic carcinoma with a monoclonal origin composed of epithelial and mesenchymal components.
  • The tumor originates from epithelial components that undergo epithelial-to-mesenchymal transition.
  • Approximately half of patients are diagnosed at early stage and half at advanced stage.
  • More than one-third of women present with metastatic lymph nodes and approximately 10% have distant metastases.
  • ECS has the worst prognosis among endometrial cancers compared with other high-grade endometrial carcinomas.
  • Surgical resection with adjuvant therapy remains the standard of care in most cases.
  • Rarity of ECS limits prospective clinical trials and the development of specific management guidelines.
  • The review discusses molecular characteristics and new treatment regimens for primary (early and advanced) and recurrent ECS.
Limitations: This article is a review and presents no new primary data.; The rarity of ECS limits the ability to conduct prospective clinical trials and to establish optimal treatment regimens (stated in abstract).; No specific treatment guidelines exist for ECS, reflecting limited high-quality evidence (stated in abstract)..

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

Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 64

A Proteogenomic View of Synchronous Endometrioid Endometrial and Ovarian Cancer

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

Human · observationalMechanismMixed resultsLimited evidenceTier 3 · early humann = 18

Exploring the Genetic and Clinical Landscape of Dedifferentiated Endometrioid Carcinoma

International journal of molecular sciences · Apr 2025

dedifferentiated endometrioid carcinomaendometrial cancer

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

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

Key findings
  • Incidence of DDEC was 2.0% among endometrial cancers.
  • The 5-year progression-free survival for DDEC was approximately 40%.
  • The 5-year overall survival for DDEC was approximately 30%.
  • Immunohistochemistry indicated 66.7% of patients were mismatch repair deficient.
  • The rate of p53 mutations in this series was higher than reported previously, and p53 mutations in undifferentiated components were associated with poor prognosis.
  • Whole-exome sequencing (n = 3) showed different gene mutations and mutation signatures between well-differentiated and undifferentiated components.
  • New genetic mutations in undifferentiated regions were uncommon in the three sequenced cases.
  • Among the three sequenced cases: one showed homologous recombination deficiency, and the other two had MSI-high and hypermutator phenotypes.
  • Authors suggest that immune checkpoint inhibitors, PARP inhibitors, and drugs targeting the p53 pathway may be therapeutically relevant to DDEC based on the genetic findings.
Limitations: Small overall sample size (18 cases); Whole-exome sequencing performed in only 3 cases; Observational, descriptive design with no interventional testing of suggested therapies; Single-country (Japanese) cohort which may limit generalizability; No functional validation of suggested therapeutic targets reported in the abstract.

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

Human · observationalMechanismMixed resultsModerate evidenceTier 3 · early humann = 2235

Not all uterine carcinosarcomas are created equal: Survival outcomes according to molecular characterization of uterine carcinosarcoma

Gynecologic oncology · Feb 2025

uterine carcinosarcomaendometrioid endometrial cancer

The authors analyzed ProMisE molecular subtypes in 2235 uterine carcinosarcoma (UCS) samples and compared survival to 6469 endometrioid endometrial cancer (EEC) tumors using sequencing and real-world overall survival from a clinical database. They report that TP53-mutant is the most common UCS subtype and that POLE-mutant UCS had substantially longer median overall survival than other UCS subtypes. TP53-mutant and TP53-wildtype UCS had worse median overall survival than their respective EEC counterparts, while POLE-mutant and MSI-H UCS showed no statistically significant survival difference when compared to the same EEC subtypes. HER2-negative UCS also had worse post-chemotherapy overall survival than HER2-negative EEC.

Reported effects: UCS subtype distribution 2.7%, n=48 · UCS subtype distribution 7.4%, n=132 · +11 more

Key findings
  • Of 2235 UCS samples, 2.7% (n=48) were POLE mutant, 7.4% (n=132) MSI-H, 78.2% (n=1402) TP53 mutant, and 11.7% (n=210) TP53 wild type.
  • In UCS POLE MT tumors, median OS was 74.8 months (95% CI: 30.5-not reached; p < 0.01), significantly longer than other UCS subtypes.
  • There was no difference in median post-chemo OS between POLE MT UCS and POLE MT EEC (p = 0.75) or between MSI-H UCS and MSI-H EEC (p = 0.14).
  • TP53 MT UCS had median OS 27.9 vs 35.3 months in the respective EEC subtype (HR 1.3, 95% CI 1.1-1.5; p = 0.01).
  • TP53 WT UCS had median OS 29.4 vs 70.7 months in the respective EEC subtype (HR 2.0, 95% CI 1.5-2.7; p < 0.01).
  • HER2-negative UCS had worse post-chemo OS than HER2-negative EEC (32.9 vs 77 months; HR 1.60, 95% CI 1.092-2.348; p = 0.02).
Limitations: Observational real-world database analysis (non-randomized); Abstract does not report treatment heterogeneity or how treatments were controlled for in comparisons; Median follow-up duration not reported in the abstract; Some molecular subgroups were small (e.g., POLE MT n=48), limiting precision for those comparisons.

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

ReviewMixed resultsLimited evidenceTier 4 · clinical

HER2-Positive Serous Endometrial Cancer Treatment: Current Clinical Practice and Future Directions

Medicina (Kaunas, Lithuania) · Dec 2024 · literature review

uterine serous carcinoma (serous endometrial carcinoma)endometrial cancer

This literature review summarizes current HER2-directed therapies for HER2-positive uterine serous (serous endometrial) carcinoma. The authors note that about one-third of serous endometrial cancers overexpress HER2 or have ERBB2 amplification and that clinical trials combining chemotherapy with anti-HER2 agents (mainly trastuzumab, alone or with pertuzumab) have shown promising results and been incorporated into international guidelines. The review also describes ongoing research into antibody–drug conjugates and tyrosine kinase inhibitors and highlights that acquired resistance and other unmet needs remain.

Studied with: chemotherapy, pertuzumab.

Key findings
  • Approximately one-third of patients with serous endometrial carcinoma may overexpress HER2/neu protein and/or show c-erBb2 (ERBB2) gene amplification.
  • HER2-directed treatments, especially trastuzumab alone or combined with pertuzumab and chemotherapy, have shown promising results in clinical trials and have been incorporated into international guidelines.
  • Antibody-drug conjugates and tyrosine kinase inhibitors targeting HER2 are under active investigation in endometrial cancer.
  • Acquired resistance to HER2-targeted therapies is an important unresolved problem in endometrial cancer and its mechanisms are mostly unknown.
  • Research is exploring earlier use of HER2-directed therapy in this disease.
Limitations: This is a literature review and does not present new primary experimental or trial data.; The abstract does not state this is a systematic review, so selection and synthesis methods are not described in the abstract.; No quantitative effect sizes or detailed trial outcome data are presented in the abstract.; Mechanistic understanding of acquired resistance in endometrial cancer is reported as largely unknown..

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

ReviewMechanismReported positiveModerate evidenceTier 4 · clinical

FIGO 2023 staging for endometrial cancer, when, if it is not now?

European journal of cancer (Oxford, England : 1990) · Dec 2024 · review

endometrial cancer

This is a review article discussing the FIGO 2023 staging system for endometrial cancer and responding to concerns raised by some pathologists and clinicians. The authors note that FIGO 2023 incorporates pathological and optional molecular features. They state that several recent validation studies reported higher prognostic precision for FIGO 2023 compared with FIGO 2009.

Key findings
  • FIGO 2023 incorporates pathological and (not mandatory) molecular features into the staging system.
  • Several recent validation studies demonstrated higher prognostic precision of FIGO 2023 versus FIGO 2009.
  • The article responds to concerns raised by pathologists and clinicians about the new staging system.
Limitations: Review article rather than primary data or a systematic study.; Abstract provides no methodological details or description of the validation studies referenced.; No quantitative results or sample sizes are reported in the abstract..

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

Browse all studies mentioning Endometrial Cancer →

Where the evidence is

What has been studied, and how strong it is, by topic. A dashed cell means no studies were found for that combination — a gap, not evidence of no effect. Open a row to see its studies.

CompoundHuman evidenceMechanismSafetyTrial
Pembrolizumab13—1
Durvalumab22—2
Atezolizumab11—1
Avelumab11—1
Dostarlimab11—1
Carboplatin—2——
Lenvatinib—1——
Paclitaxel—1——
Tamoxifen—1——

Study mix

97 published studies by what they were done in. Lab and animal findings often do not carry over to people.

15 Human1 Animal1 Lab80 Review/other
Reported directionReported positive31Mixed results19Reported negative5Inconclusive42

Compounds with reported-positive results in Endometrial Cancer

Where at least one study reported a positive result, shown with the full picture, not just the wins. Positive results are more likely to be published, and most of these are early lab or animal studies that may not translate to people. This reports what studies found, not what works.

Human evidence

Pembrolizumab2 positive1 negative/mixed1 human
Limitations: Meta-analysis focused on progression-free survival (PFS); impact on overall survival (OS) is not reported and remains uncertain.; Subgroup analyses by dMMR/pMMR and by drug class (anti-PD-1 vs anti-PD-L1) are based on pooled trial-level data and may be limited by heterogeneity and lack of patient-level data.; Three of five trials included endometrial carcinosarcoma, which may affect generalizability to typical endometrial carcinoma populations.; The abstract does not report safety/toxicity or follow-up duration, limiting assessment of risks and long-term outcomes.; This is a review article summarizing prior studies and does not present new primary patient-level data.; Some clinical evidence cited (e.g., a phase II study) is early-phase and may have limited sample size or non-randomized design..
Cited positive studies (2)
Atezolizumab1 positive1 human
Limitations: Meta-analysis focused on progression-free survival (PFS); impact on overall survival (OS) is not reported and remains uncertain.; Subgroup analyses by dMMR/pMMR and by drug class (anti-PD-1 vs anti-PD-L1) are based on pooled trial-level data and may be limited by heterogeneity and lack of patient-level data.; Three of five trials included endometrial carcinosarcoma, which may affect generalizability to typical endometrial carcinoma populations.; The abstract does not report safety/toxicity or follow-up duration, limiting assessment of risks and long-term outcomes..
Cited positive studies (1)
Avelumab1 positive1 human
Limitations: Meta-analysis focused on progression-free survival (PFS); impact on overall survival (OS) is not reported and remains uncertain.; Subgroup analyses by dMMR/pMMR and by drug class (anti-PD-1 vs anti-PD-L1) are based on pooled trial-level data and may be limited by heterogeneity and lack of patient-level data.; Three of five trials included endometrial carcinosarcoma, which may affect generalizability to typical endometrial carcinoma populations.; The abstract does not report safety/toxicity or follow-up duration, limiting assessment of risks and long-term outcomes..
Cited positive studies (1)
Durvalumab1 positive1 negative/mixed2 human
Limitations: Meta-analysis focused on progression-free survival (PFS); impact on overall survival (OS) is not reported and remains uncertain.; Subgroup analyses by dMMR/pMMR and by drug class (anti-PD-1 vs anti-PD-L1) are based on pooled trial-level data and may be limited by heterogeneity and lack of patient-level data.; Three of five trials included endometrial carcinosarcoma, which may affect generalizability to typical endometrial carcinoma populations.; The abstract does not report safety/toxicity or follow-up duration, limiting assessment of risks and long-term outcomes..
Cited positive studies (1)
Dostarlimab1 positive1 human
Limitations: Meta-analysis focused on progression-free survival (PFS); impact on overall survival (OS) is not reported and remains uncertain.; Subgroup analyses by dMMR/pMMR and by drug class (anti-PD-1 vs anti-PD-L1) are based on pooled trial-level data and may be limited by heterogeneity and lack of patient-level data.; Three of five trials included endometrial carcinosarcoma, which may affect generalizability to typical endometrial carcinoma populations.; The abstract does not report safety/toxicity or follow-up duration, limiting assessment of risks and long-term outcomes..
Cited positive studies (1)
Preclinical only: lab / animal (3)
Lenvatinib1 positive
Limitations: This is a review article summarizing prior studies and does not present new primary patient-level data.; Some clinical evidence cited (e.g., a phase II study) is early-phase and may have limited sample size or non-randomized design.; The abstract does not provide sample sizes, statistical details, or full trial designs for the cited studies.; Uterine serous carcinoma is an uncommon subtype, which can limit the size and generalizability of studies..
Cited positive studies (1)
Carboplatin1 positive1 negative/mixed
Limitations: This is a review article and does not present new primary clinical trial data.; The abstract reports genomic findings but provides no quantitative results, sample sizes, or outcome data.; No direct evidence of clinical efficacy of targeted agents in USC is provided in the abstract..
Cited positive studies (1)
Paclitaxel1 positive
Limitations: This is a review article and does not present new primary clinical trial data.; The abstract reports genomic findings but provides no quantitative results, sample sizes, or outcome data.; No direct evidence of clinical efficacy of targeted agents in USC is provided in the abstract..
Cited positive studies (1)

Evidence at a glance: compounds studied in Endometrial Cancer

A deterministic grade of what published studies report for each: strength of evidence, the reported direction, and the largest credible effect, strongest-evidence first. This summarizes findings; it is not a claim that anything works.

PembrolizumabHuman trial / meta-analysisMixed results1 human

Includes human trial or meta-analysis evidence.

Largest credible effect: pooled HR overall 0.63 [0.52–0.76], p <.001, n=2456 PMID 38422895 · hazard ratios 0.34–0.87 across 6 studies

Most authoritative study: Incorporation of anti-PD1 or anti PD-L1 agents to platinum-based chemotherapy for the primary treatment of advanced or recurrent endometrial cancer. A meta-analysis

Findings conflict across studies · Effect sizes reported in only 1 of 4 studies.
DurvalumabHuman trial / meta-analysisMixed results2 human

Includes human trial or meta-analysis evidence.

Largest credible effect: pooled HR overall 0.63 [0.52–0.76], p <.001, n=2456 PMID 38422895 · hazard ratios 0.34–0.87 across 6 studies

Most authoritative study: Incorporation of anti-PD1 or anti PD-L1 agents to platinum-based chemotherapy for the primary treatment of advanced or recurrent endometrial cancer. A meta-analysis

Findings conflict across studies.
AtezolizumabHuman trial / meta-analysisReported positive1 human

Includes human trial or meta-analysis evidence.

Largest credible effect: pooled HR overall 0.63 [0.52–0.76], p <.001, n=2456 PMID 38422895 · hazard ratios 0.34–0.87 across 6 studies

Most authoritative study: Incorporation of anti-PD1 or anti PD-L1 agents to platinum-based chemotherapy for the primary treatment of advanced or recurrent endometrial cancer. A meta-analysis

Based on a single study.
AvelumabHuman trial / meta-analysisReported positive1 human

Includes human trial or meta-analysis evidence.

Largest credible effect: pooled HR overall 0.63 [0.52–0.76], p <.001, n=2456 PMID 38422895 · hazard ratios 0.34–0.87 across 6 studies

Most authoritative study: Incorporation of anti-PD1 or anti PD-L1 agents to platinum-based chemotherapy for the primary treatment of advanced or recurrent endometrial cancer. A meta-analysis

Based on a single study.
DostarlimabHuman trial / meta-analysisReported positive1 human

Includes human trial or meta-analysis evidence.

Largest credible effect: pooled HR overall 0.63 [0.52–0.76], p <.001, n=2456 PMID 38422895 · hazard ratios 0.34–0.87 across 6 studies

Most authoritative study: Incorporation of anti-PD1 or anti PD-L1 agents to platinum-based chemotherapy for the primary treatment of advanced or recurrent endometrial cancer. A meta-analysis

Based on a single study.
CarboplatinInsufficient evidenceMixed results

No primary experimental studies yet.

Largest credible effect: annual percent change 1.7% [1.2–2.2] PMID 33183764 · response rates 5.5–37.5 across 4 studies

Most authoritative study: Uterine carcinosarcoma: Contemporary clinical summary, molecular updates, and future research opportunity

No human studies yet · Findings conflict across studies · Effect sizes reported in only 1 of 2 studies.
LenvatinibInsufficient evidenceReported positive

No primary experimental studies yet.

Most authoritative study: Uterine serous carcinoma: key advances and novel treatment approaches

No human studies yet · No numeric effect sizes reported.
PaclitaxelInsufficient evidenceReported positive

No primary experimental studies yet.

Most authoritative study: Targeted therapy in uterine serous carcinoma: an aggressive variant of endometrial cancer

No human studies yet · No numeric effect sizes reported · Based on a single study.
TamoxifenInsufficient evidenceMixed results

No primary experimental studies yet.

Most authoritative study: Tamoxifen and Endometrial Cancer: A Janus-Headed Drug

No human studies yet · No numeric effect sizes reported · Based on a single study.

What the research shows for Endometrial Cancer

A plain-language summary of the reviewed studies OncoForge tracks for Endometrial Cancer. It reports what those studies described, not a claim that any compound or therapy helps or harms Endometrial Cancer. Most of this evidence is early, and findings often conflict.

  • A moderate‑strength meta‑analysis pooled five randomized trials (about 2,456 patients) and reported that adding anti‑PD‑1/PD‑L1 immune checkpoint blockade to standard platinum‑based first‑line chemotherapy improved outcomes in advanced or recurrent endometrial cancer compared with chemotherapy alone.
  • Reviews of uterine carcinosarcoma and aggressive endometrial cancers summarize that carboplatin‑based regimens (commonly carboplatin plus paclitaxel) are widely used and that some reviewed series reported improved progression‑free survival with such multimodal chemotherapy, though the review evidence was described as limited or mixed.
  • A narrative review of endometrial carcinosarcoma highlighted biological features (for example epithelial‑to‑mesenchymal transition) and generally poor prognosis of this subtype, emphasizing that molecular heterogeneity complicates treatment decisions.
  • Across the included publications, the strength of evidence varied: the immunotherapy benefit comes from randomized trials synthesized in a meta‑analysis (moderate strength), while much of the other literature is narrative or limited observational data.

Compounds studied in Endometrial Cancer

Atezolizumab1 study
In these studies, a meta-analysis that pooled five randomized trials (about 2,456 patients) reported that adding anti‑PD‑1/PD‑L1 immune checkpoint inhibitors to first‑line platinum‑based chemotherapy for advanced or recurrent endometrial cancer improved outcomes versus chemotherapy alone; the analysis was rated moderate strength but pooled different trials/agents and leaves uncertainty about effects for any single drug or specific patient subgroups.
Carboplatin1 study
In these studies, narrative and clinical reviews report that carboplatin — commonly combined with paclitaxel — is used as adjuvant or first‑line chemotherapy for uterine carcinosarcoma and endometrial cancer, with some reviewed data showing improved progression‑free survival, but the evidence described was limited, mixed, and based largely on retrospective series and small studies.

Supportive & alternative options discussed

  • Exercise / prehabilitation: Also discussed as a supportive option for people with endometrial cancer to help with overall fitness, quality of life, and survivorship issues, though the studies above do not evaluate it directly.
  • Mind–body (MBSR / CBT): Also discussed as a supportive option for symptom management and psychological well‑being in endometrial cancer care; the provided studies do not assess mind–body interventions.
  • Acupuncture: Also discussed as a supportive option for managing treatment‑related symptoms (for example pain or nausea) in cancer care; the studies above do not provide evidence on acupuncture for endometrial cancer.
  • Ketogenic / metabolic therapy: Also discussed by some patients and practitioners as a dietary approach in cancer care, but the included studies do not evaluate ketogenic diets for endometrial cancer.

What we don’t know yet

  • Which specific patients (molecular subtypes, PD‑L1 status, MSI status, or other biomarkers) derive the most benefit from adding immune checkpoint inhibitors to chemotherapy is not established by these publications.
  • Direct evidence on the efficacy and safety of single named agents (for example atezolizumab specifically) versus other checkpoint inhibitors in endometrial cancer is limited because the meta‑analysis pooled different anti‑PD‑1/PD‑L1 agents.
  • Long‑term outcomes, optimal sequencing with other systemic or local therapies, and effects on overall survival versus progression‑free survival are not fully defined in the provided studies.
  • For uterine carcinosarcoma, high‑quality prospective trial data are limited; the magnitude of benefit from carboplatin/paclitaxel and the best adjuvant regimen remain uncertain.
  • Toxicity profiles and quality‑of‑life tradeoffs when adding immunotherapy to chemotherapy across diverse patient populations are incompletely characterized in these reports.
The available evidence includes a moderate‑strength meta‑analysis of randomized trials supporting added immune checkpoint blockade to chemotherapy in advanced/recurrent disease but otherwise relies on limited or mixed review and observational data, so conclusions about specific drugs, subgroups, and long‑term outcomes remain preliminary.

Clinical trials in Endometrial Cancer

61 ongoing · 86 completed · tracked from ClinicalTrials.gov. Recruiting is not the same as proven, and completed is not the same as positive — read the results. Not a recommendation.

Completed
20 stopped (terminated / withdrawn / suspended)

Search all trials on ClinicalTrials.gov →

Getting care & support

Nonprofit / Gov

Practical, vetted help for Endometrial Cancer — advocacy, paying for treatment, second opinions, and caregivers.

If you’re struggling emotionally, you don’t have to wait.

Advocacy & community

No dedicated organization for this specific cancer is curated yet — these general organizations can help in the meantime.

Financial help

  • PAN Foundation ↗ — Copay assistance funds by diagnosis (funds open and close as money allows). · status changes often — check the fund’s site
  • HealthWell Foundation ↗ — Copay and premium assistance funds by disease. · status changes often — check the fund’s site
  • CancerCare — financial assistance ↗ — Limited grants plus free financial counseling. · status changes often — check the fund’s site
  • Family Reach ↗ — Help with everyday living costs (rent, transport, food) during treatment. · status changes often — check the fund’s site
  • NeedyMeds ↗ — Searchable directory of drug patient-assistance and discount programs. · status changes often — check the fund’s site
What you’ll typically need to apply
  • Your diagnosis and, if you have it, the specific drug/treatment name (from your care team).
  • Insurance details — your member ID card, or a note that you're uninsured (some funds require active insurance, some don't).
  • Proof of income and household size (recent pay stubs, a tax return, or a benefits letter) — most funds are income-based.
  • Your prescriber's contact information; some programs need the clinic to submit part of the application.
  • Apply early and re-check: funds open and close as money is available, so a closed fund may reopen.

General guidance — each program sets its own eligibility. Confirm requirements on the program’s site.

Help paying for the medicines on this page

Second opinions

Caregiver support

We list only non-profit and government resources — never product sellers — and take no affiliate fees. If a link is broken or a resource doesn't meet that bar, tell us.

Heading to an appointment? Get a printable one-page summary — studied compounds, open trials, interactions, and questions to ask.
Bring this to your appointment →