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Endometrial Carcinoma

A plain-English summary of the published research on Endometrial Carcinoma, 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
109 published studies that name Endometrial Carcinoma30 human studies approved & graded (trial, observational, or meta-analysis)92 human clinical studies in the Endometrial Carcinoma corpus963 source documents in the Endometrial Carcinoma 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
  • durvalumab
  • pembrolizumab
Studied, not standard - investigational
  • radiotherapy
  • lymphadenectomy
  • office endometrial biopsy
  • hysteroscopy
  • dilatation + curettage
  • fertility preservation
  • Robotic single-site hysterectomy (RSSH)
  • Minimally invasive surgery (MIS) for recurrent endometrial carcinoma
  • carboplatin + paclitaxel
  • hormone therapy
  • External-beam radiation therapy
  • Vaginal brachytherapy
  • Fertility-sparing treatment
  • Novel targeted therapies
  • Total hysterectomy + bilateral salpingo-oophorectomy + pelvic lymphadenectomy
  • levonorgestrel intrauterine system + oral progestins
  • oral progestins
  • chemotherapy
  • pelvic + para‑aortic lymph node dissection
  • surgery
  • adjuvant therapy
  • carboplatin
  • paclitaxel
  • cisplatin
  • Curcumin / Theracurmin
  • sacituzumab govitecan
  • sulfasalazine

Read the guidelines

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

Treatment map: Endometrial Carcinoma

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.

29
Interventions
0
Standard of care
12
Tested in people
4
Lab / animal
11
Named in lit.
9
Classes
Standard of care (0) Guideline option (2) Tested in people (12) Lab / animal only (4) Named in the literature (11)

Tested in people, by trial phase: phase not reported ×12

Clinical evidence
Preclinical evidence
Standard of care
Guideline option
Tested in people
Lab / animal only
Named in the literature
Surgery & procedures
—
—
4
—
6
Radiotherapy
—
—
1
—
2
Chemotherapy
—
—
4
1
—
Targeted therapy
—
—
—
1
1
Immunotherapy
—
2
—
—
—
Hormonal therapy
—
—
2
—
1
Repurposed drugs
—
—
—
1
—
Supplements & natural agents
—
—
—
1
—
Other
—
—
1
—
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 (2)
Immunotherapy
durvalumab
FDA-approved for this cancer.
—Guideline option
pembrolizumab
FDA-approved for this cancer.
—Guideline option
Investigational & adjunct compounds — detail (27)
Meta-analysis (10)
carboplatin + paclitaxelchemotherapy· Adjuvant (after surgery)fertility preservationlevonorgestrel intrauterine system + oral progestinsMinimally invasive surgery (MIS) for recurrent endometrial carcinoma· Recurrent or later-lineoral progestinspelvic + para‑aortic lymph node dissectionradiotherapyRobotic single-site hysterectomy (RSSH)Total hysterectomy + bilateral salpingo-oophorectomy + pelvic lymphadenectomy
Named in the literature
lymphadenectomyoffice endometrial biopsyhysteroscopydilatation + curettagehormone therapyExternal-beam radiation therapy· Adjuvant (after surgery)Vaginal brachytherapy· Adjuvant (after surgery)Fertility-sparing treatmentNovel targeted therapiessurgeryadjuvant therapy· 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

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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 and in the United States accounts for 7% of all cancers in women; most cases are diagnosed at an early stage and are identified when women undergo endometrial evaluation (office biopsy, hysteroscopy, or D&C) prompted by symptoms. [1][2][3]
Survival
Overall prognosis is often favorable for many tumors; randomized PORTEC trials reported POLE‑mutated tumors with ten-year cancer-specific survival reaching 100% (PORTEC‑1 and PORTEC‑2) and ten-year recurrence-free survival of 98.0% (PORTEC‑3). [4][5]
Standard treatment
Initial management is primarily surgical for most patients; diagnostic evaluation uses office endometrial biopsy, hysteroscopy, or D&C and imaging to plan treatment, with MRI preferred when pretreatment assessment of local tumor extent is indicated. [2][6][3][7]
Key test
Molecular testing (as recommended in the WHO 5th edition and recent guidelines) is used to define prognostic risk groups and inform management decisions; when possible, progesterone and estrogen receptor status is also assessed in stage I–II disease. [8][4][2]
Biggest challenge
A major challenge is implementing and integrating molecular testing and molecular-based risk groups into routine practice to guide preoperative surgical and adjuvant decision-making. [8][4]

Ask about Endometrial Carcinoma

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

Survival by stage

StageSurvivalNotes
Clinical stages I-II3-year disease-free survival 93% for progesterone receptor level ≥100 vs 36% for level <100 [2]

Risk factors

  • ▲ increases riskHigher BMI — Genetic association reported in Mendelian randomization studies [9][1][10]
  • ▲ increases riskEarly menarche [9][1]
  • ▲ increases riskNulliparity [9][1]
  • ▲ increases riskGenetic predisposition [9][1]
  • ▲ increases riskPostmenopausal status — Increased malignant potential compared with premenopausal women [11]
  • ▲ increases riskTamoxifen use — Associated with increased risk of uterine malignancies [2]

Biomarkers

  • POLE exonuclease-domain mutationActionableIdentifies an ultramutated phenotype with strong immune activation and excellent long-term outcomes [5][8]
  • p53‑abnormalActionableMarks a group with the highest reported rate of lymph node metastases [12][4]
  • Mismatch repair–deficient (MMR‑deficient)ActionableDefines a molecular subgroup with an intermediate pooled prevalence of lymph node metastases [12][4]
  • Progesterone receptor · Prognostic indicator in clinical stages I–II (large differences in 3‑year disease-free survival by level) [2]

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

OverviewEndometrial carcinoma is the most common gynecologic malignancy and, in the United States, accounts for 7% of cancers in women. Molecular classification is increasingly used in diagnosis and provides information with therapeutic implications, including for tailoring preoperative surgical treatment.2 points
  • Endometrial carcinoma is the most common gynecologic malignancy; in the United States it accounts for 7% of all cancers in women. [1][2]
  • Molecular classification of endometrial carcinoma is increasingly integrated into diagnostic evaluation and provides information with direct therapeutic implications, including to help tailor preoperative surgical treatment. [8][12]
EpidemiologyEndometrial carcinoma is a common gynecologic cancer worldwide, with over 417,000 new cases and 97,000 deaths reported in 2020; the lifetime likelihood of developing the disease is approximately 3% and the average age at diagnosis is reported as 61 years. Established risk factors include older age, obesity, reproductive factors and family history/genetic predisposition, and hypertension has been associated with an increased risk.6 points

Key figures

Survival & outcomes
OutcomeValue95% CI
Estimated deaths in 202513860—
Prognostic factors
FactorEffectHR (95% CI)p
risk ratio (hypertension vs no hypertension)▲ worse1.37 (1.27–1.47)< 0.001
Source quotes
  • “Estimated new cases and deaths from cancer of the uterine corpus, which includes the endometrium, in the United States in 2025:[ 1 ] New cases: 69,120. Deaths: 13,860.”
  • “Accordingly, the risk of endometrial cancer in patients with hypertension is 1.37 times higher (95% CI: 1.27–1.47, p < 0.001).”
  • Sources describe risk factors including early menarche, nulliparity, and higher BMI; reviews also note genetic predisposition. A Mendelian randomization study reports a genetic association between higher BMI and multiple female reproductive tumors, including endometrial cancer. [9][1][10]3 sources
  • Estimated new cases and deaths from cancer of the uterine corpus (which includes the endometrium) in the United States in 2025 are New cases: 69,120 and Deaths: 13,860. [2]
  • Endometrial cancer was reported as the sixth most frequently diagnosed cancer in women and the 15th most prevalent cancer overall, with over 417,000 new cases and 97,000 deaths in 2020; the lifetime likelihood of developing endometrial cancer is approximately 3% and the average age at diagnosis is reported as 61 years. [9]
  • A guideline objective was to review the evidence relating to the epidemiology of endometrial cancer and its diagnostic workups. [6]
  • Women with possible endometrial cancer can undergo an endometrial evaluation by office biopsy, hysteroscopy, or dilatation and curettage, and pelvic ultrasound, CT, or MRI may be considered to assist treatment planning. [3]
  • Postmenopausal women are at increased risk of malignant potential as compared to premenopausal women. [11]
Key biomarkersMolecular testing is recommended for endometrial carcinoma in the WHO 5th edition and has been incorporated into recent international prognostic risk-group guidelines. Distinct molecular subtypes (including POLE‑mutated, mismatch repair‑deficient, no specific molecular profile, and p53‑abnormal) have different biological features and differing rates of lymph node metastasis.5 points
  • Molecular testing of endometrial carcinomas is recommended in the latest (5th) edition of the WHO classification of Female Genital Tumors, and recent international guidelines define prognostic risk groups that integrate molecular markers. [8][4]
  • Pooled prevalence of lymph node metastases differed by molecular subgroup: 4% for POLE‑mutated, 22% for no specific molecular profile, 23% for mismatch repair‑deficient, and 31% for p53‑abnormal; the authors concluded that molecular classification appears to influence the presence of lymph node metastases with p53‑abnormal showing the highest and POLE‑mutated the lowest rates, and the reviewed studies reported lymph node metastases according to the molecular classification categories as defined in the ESGO‑ESMO‑ESP guidelines. [12]
  • POLE exonuclease-domain mutations create an ultramutated phenotype with abundant neoantigens and are associated with strong immune activation. [5]
  • Elevated lymph node to primary tumor standardized uptake value ratio (NTR) was significantly associated with worse overall survival, disease-free survival, and distant metastasis-free survival. [13]
  • When possible, progesterone and estrogen receptor statuses are included in the evaluation of patients with stage I and stage II disease. [2]
Standard managementMost endometrial carcinoma cases are diagnosed at an early stage and are often treated with surgery alone. Diagnostic evaluation uses endometrial sampling (office biopsy, hysteroscopy, or dilatation and curettage) and imaging (transvaginal ultrasound, pelvic CT, or MRI) to assist treatment planning; MRI is preferred to assess local tumor extent and cross-sectional imaging or PET/CT may be used if distant metastasis is suspected.8 points
  • Diagnostic options to evaluate patients with suspected endometrial cancer include office endometrial biopsy, hysteroscopy, or dilatation and curettage; transvaginal ultrasonography, pelvic examination, pelvic ultrasound, CT, or MRI may be used to assist treatment planning. [6][3][2]3 sources
  • When pretreatment assessment of local tumor extent is indicated, MRI is the preferred imaging modality. [7]
  • Recurrence rates in patients with endometrial carcinoma are infrequent, and radiologic evaluation is typically used only to investigate suspicion of recurrent disease based on symptoms or physical examination rather than for routine surveillance after treatment. [7]
  • The Society of Gynecologic Oncology reviewed the literature through March 2014 and produced evidence-based practice recommendations covering adjuvant therapy, therapy for advanced disease, fertility-sparing treatment, surveillance, and novel targeted therapies. [14]
  • Studies of positive peritoneal cytology in early-stage endometrial cancer reported limited and conflicting evidence about the benefit of adjuvant therapy. [15]
  • A network meta-analysis concluded that LNG-IUS–based treatments are feasible for conservative therapy in patients with endometrial carcinoma and endometrial hyperplasia and recommended LNG-IUS–based treatments as the best conservative therapy. [16]
  • Most cases are diagnosed at an early stage and are amenable to treatment with surgery alone. [2]
  • If distant metastatic disease is clinically suspected, preoperative assessment with cross-sectional imaging or PET/CT may be performed; most patients with low-grade disease are at low risk of lymph node and distant metastases and thus may not require a routine pretreatment evaluation for distant metastases. [7]
Staging & riskMultidisciplinary guidelines address staging for endometrial carcinoma. Risk of lymph node metastasis varies by prognostic group and depth of myometrial invasion, with reported values ranging from <5% to 20%–60% and an overall rate of 7.5% in one surgical series.2 points
  • Risk of lymph node metastasis varies with prognostic group and depth of myometrial invasion: one series of 228 surgical patients reported an overall lymph node metastasis rate of 7.5% and noted increasing rates with deeper myometrial invasion; in clinical stage I disease the risk is reported as '<5%' for Grade 1 tumors involving only endometrium and '20%–60% pelvic nodes' for deep muscle invasion. [17][2]
  • Recent multidisciplinary guidelines comprehensively cover endometrial carcinoma staging. [4]
PrognosisPrognostic risk groups for endometrial carcinoma incorporate molecular markers that stratify outcomes — for example, POLE‑mutated tumors show excellent long‑term survival while p53‑abnormal tumors are associated with more nodal involvement. Other prognostic considerations include noncancer comorbidity (cardiovascular disease is the most common cause of death) and tumor markers such as progesterone receptor level, which predicts 3‑year disease‑free survival in early‑stage disease.3 points

Key figures

Survival & outcomes
OutcomeValue95% CI
ten-year cancer-specific survival (PORTEC-1 and PORTEC-2)100%—
10-year recurrence-free survival (PORTEC-3)98%—
3-year disease-free survival rate (PR ≥100) vs progesterone receptor level ≥100 vs <10093%—
3-year disease-free survival rate (PR <100) vs progesterone receptor level ≥100 vs <10036%—
Source quotes
  • “For instance, ten-year cancer-specific survival reached 100% for POLE-mutated tumors in PORTEC-1 and PORTEC-2 [5,6], and the 10-year recurrence-free survival was 98.0% in PORTEC-3 [7].”
  • “Patients with progesterone receptor levels of 100 or greater had a 3-year disease-free survival rate of 93%, compared with 36% for those with a level below 100.”
  • Guidelines define prognostic risk groups that integrate molecular markers; randomized PORTEC trials found POLE‑mutated endometrial tumors had excellent long-term outcomes (ten-year cancer-specific survival reaching 100% in PORTEC-1 and PORTEC-2 and 10-year recurrence-free survival of 98.0% in PORTEC-3), and a molecular-profile meta-analysis reported that the p53‑abnormal group presented the highest rate of nodal involvement while POLE‑mutated tumors presented the lowest. [4][5][12]3 sources
  • The most common cause of death in patients with endometrial cancer is cardiovascular disease because of related metabolic risk factors. [2]
  • One report found progesterone receptor levels to be the single most important prognostic indicator of 3-year survival in clinical stages I and II disease, with patients with progesterone receptor levels of 100 or greater having a 3-year disease-free survival rate of 93% compared with 36% for those with a level below 100. [2]
What we don't know yetSeveral important uncertainties remain in endometrial carcinoma diagnosis, prognosis, and treatment. These include limited or conflicting evidence for some treatment approaches, the need to implement and standardize molecular testing in routine practice, and incomplete understanding of biological risk factors and prognostic markers, all of which require further study.7 points
  • In the absence of clear scientific evidence on some points, guideline judgments were based on professional experience and consensus. [4]
  • Because of the need to implement molecular testing recommendations in practice, professional societies organized a meeting that produced a joint recommendation for molecular testing in routine diagnostic practice. [8]
  • Data on minimally invasive surgery for recurrent endometrial carcinoma are limited and need confirmation by additional studies. [18]
  • The review of adjuvant therapy for patients with early-stage endometrial cancer and positive peritoneal cytology concluded that evidence is limited and conflicting, indicating the need for continued evaluation. [15]
  • The causal association between BMI and female tumor susceptibility, including endometrial cancer subtypes, was described as not fully understood and a topic for further study using Mendelian randomization approaches. [10]
  • Future studies should aim to validate the prognostic association between elevated NTR and survival outcomes in larger and more diverse patient populations and to investigate underlying mechanisms. [13]
  • Authors of the LNG‑IUS network meta-analysis stated that future studies with larger sample sizes and more outcomes are required to further evaluate treatment selection differences. [16]
Treatments & compounds studied23 therapeutics and procedures are reported across radiotherapy, surgical/procedural, chemotherapy, hormonal, targeted, repurposed drug, and other classes.21 treatments

Chemotherapy

  • adjuvant chemotherapy · chemotherapy: Adjuvant (after surgery)Adjuvant chemotherapy has been reported in at least one nationwide study to be associated with reduced risk of death among patients with stage I–II endometrial cancer presenting positive peritoneal cytology, while another study reported no association and overall evidence was judged limited and conflicting. [15]
Show 1 lab & early-research entry
  • carboplatin plus paclitaxel: A case report described induction chemotherapy with six cycles of carboplatin plus paclitaxel every 3 weeks and reported a partial response after six cycles. [5]

Targeted therapy

  • Novel targeted therapies: Novel targeted therapies are discussed as a topic in the review of endometrial carcinoma management. [14]

Hormonal therapy

  • Hormone therapy: Hormone therapy is listed among options for therapy for advanced endometrial cancer. [14]
  • levonorgestrel intrauterine system + oral progestins: LNG-IUS combined with oral progestins (LNG-IUS + OP) was ranked as the best treatment to improve complete response (SUCRA = 67.2%) in patients with endometrial carcinoma in a network meta-analysis. [16]
    CR rate RR (LNG-IUS vs OP) 1.21 (95% CI 1.11–1.34) vs OPCR rate RR (LNG-IUS + MET vs OP) 323.57 vs OP
    Source quotes
    • “As for EH patients, LNG-IUS (RR 1.21; 95% CrI [1.11, 1.34]) and LNG-IUS + MET (RR 323.57; 95% CrI [1.61, 214,223,188.1])] significantly increased CR rate in comparison with OP.”
    • “As for EH patients, LNG-IUS (RR 1.21; 95% CrI [1.11, 1.34]) and LNG-IUS + MET (RR 323.57; 95% CrI [1.61, 214,223,188.1])] significantly increased CR rate in comparison with OP.”
  • oral progestins: Oral progestins (OP) were reported to have a higher progression rate than LNG-IUS in patients with endometrial hyperplasia (RR 4, 95% CI 1.89–8.46). [16]
    CR rate RR (LNG-IUS vs OP) 1.21 (95% CI 1.11–1.34) vs OPCR rate RR (LNG-IUS + MET vs OP) 323.57 vs OP
    Source quotes
    • “As for EH patients, LNG-IUS (RR 1.21; 95% CrI [1.11, 1.34]) and LNG-IUS + MET (RR 323.57; 95% CrI [1.61, 214,223,188.1])] significantly increased CR rate in comparison with OP.”
    • “As for EH patients, LNG-IUS (RR 1.21; 95% CrI [1.11, 1.34]) and LNG-IUS + MET (RR 323.57; 95% CrI [1.61, 214,223,188.1])] significantly increased CR rate in comparison with OP.”

Radiotherapy

  • radiotherapy: The guidelines define principles of radiotherapy in the management of endometrial carcinoma. [4]
  • External-beam radiation therapy: Adjuvant (after surgery)Adjuvant therapy options include radiation, vaginal brachytherapy, and chemotherapy. [14]
  • Vaginal brachytherapy: Adjuvant (after surgery)Vaginal brachytherapy is named as an adjuvant therapy option in endometrial carcinoma. [14]

Procedures & devices

  • lymphadenectomy: Surgical management of early and advanced endometrial cancer is described and includes lymphadenectomy in early cancer. [1]
  • office endometrial biopsy: Women with possible endometrial cancer can undergo an endometrial evaluation by office biopsy as part of diagnostic and management pathways. [6]
  • hysteroscopy: Hysteroscopy is listed as an option to evaluate the endometrium in women with possible endometrial cancer. [6]
  • dilatation and curettage: Dilatation and curettage is listed as an option to evaluate the endometrium in women with possible endometrial cancer. [6]
  • Robotic single-site hysterectomy (RSSH): Robotic single-site hysterectomy (RSSH) was compared with laparoendoscopic single-site hysterectomy (LESS-H), with RSSH associated with a longer operative time and modestly lower estimated blood loss. [19]
    MD in operative time 16.02, p=0.05 vs LESS-H
    Source quote
    • “RSSH was associated with a longer operative time compared to LESS-H (MD = 16.02 min, 95% CI [-0.07, 32.11], P = 0.05), with significant heterogeneity (I² = 89%).”
  • Minimally invasive surgery (MIS) for recurrent endometrial carcinoma: Recurrent or later-lineMinimally invasive surgery (MIS) for recurrent endometrial carcinoma was reported as feasible and safe in a small series, with all patients undergoing successful MIS and a reported disease-free survival rate of 63.6%. [18]
    mean follow-up duration 23.6 monthsdisease-free survival rate 63.6%
    Source quotes
    • “The mean follow-up duration was 23.6 months, with a disease-free survival rate of 63.6%.”
    • “The mean follow-up duration was 23.6 months, with a disease-free survival rate of 63.6%.”
  • Fertility-sparing treatment: Fertility-sparing treatment is addressed as a management option in endometrial carcinoma. [14]
  • Total hysterectomy with bilateral salpingo-oophorectomy and pelvic lymphadenectomy: Total hysterectomy with bilateral salpingo-oophorectomy and pelvic lymphadenectomy was performed in the reported POLE-mutated case. [5]
  • pelvic and para‑aortic lymph node dissection: Pelvic and para‑aortic lymph node dissection has been investigated for its effect on prognosis in endometrial cancer. [17]
  • surgery: Most cases of endometrial cancer are described as amenable to treatment with surgery alone. [2]

Other

  • fertility preservation: Guidelines address fertility preservation as a topic in the management of endometrial carcinoma. [4]
  • adjuvant therapy: Adjuvant (after surgery)Patients with pathological features predictive of a high rate of relapse and patients with extrauterine spread at diagnosis have a high rate of relapse despite adjuvant therapy. [2]
Biology & pathwaysPOLE exonuclease‑domain mutations are linked to strong immune activation that is thought to contribute to a favorable prognosis. Hypertension has been proposed to influence endometrial tumor biology and prognosis through mechanisms such as altered angiogenesis (via MMP2 and MMP9), insulin resistance with effects on IGF‑1, and hypertension‑related inflammation and extracellular matrix remodeling.2 points
  • POLE exonuclease-domain mutations are associated with strong immune activation that is thought to contribute to the favorable prognosis of POLE‑mutated endometrial carcinomas. [5]
  • Hypertension has been proposed to influence endometrial tumor biology and prognosis through multiple mechanisms, including disruption of angiogenesis via matrix metalloproteinases 2 and 9, an association with insulin resistance linked to IGF‑1 signaling, and hypertension‑related inflammation and extracellular matrix remodeling. [9]
Safety & interactionsA comparison of RSSH and LESS-H found no significant difference in overall complication rates. In patients with endometrial hyperplasia, oral progestins had higher reported nausea while LNG-IUS was associated with lower irregular vaginal bleeding compared with oral progestins; tamoxifen is associated with an increased risk of endometrial/uterine malignancies and the FDA has issued a black box warning regarding this risk.3 points
  • The comparison of RSSH and LESS-H found no significant difference in overall complication rates (risk ratio = 1.161, 95% CI [0.588, 2.291], P = 0.667). [19]
  • In patients with endometrial hyperplasia, oral progestins had a higher reported nausea rate compared with LNG-IUS (RR 1.93, 95% CI 1.24–3.01), and LNG-IUS was associated with lower irregular vaginal bleeding rates compared with oral progestins (RR 0.76, 95% CI 0.64–0.90). [16]
  • Tamoxifen is associated with an increased risk of endometrial cancer related to the estrogenic effect of tamoxifen on the endometrium, and the U.S. Food and Drug Administration has issued a black box warning that includes data about the increase in uterine malignancies associated with tamoxifen use. [2]

Common questions

What is Endometrial Carcinoma?

Endometrial carcinoma is the most common gynecologic malignancy and, in the United States, accounts for 7% of cancers in women. Molecular classification is increasingly used in diagnosis and provides information with therapeutic implications, including for tailoring preoperative surgical treatment.

How common is Endometrial Carcinoma?

Endometrial carcinoma is a common gynecologic cancer worldwide, with over 417,000 new cases and 97,000 deaths reported in 2020; the lifetime likelihood of developing the disease is approximately 3% and the average age at diagnosis is reported as 61 years. Established risk factors include older age, obesity, reproductive factors and family history/genetic predisposition, and hypertension has been associated with an increased risk.

Which biomarkers are important in Endometrial Carcinoma?

Molecular testing is recommended for endometrial carcinoma in the WHO 5th edition and has been incorporated into recent international prognostic risk-group guidelines. Distinct molecular subtypes (including POLE‑mutated, mismatch repair‑deficient, no specific molecular profile, and p53‑abnormal) have different biological features and differing rates of lymph node metastasis.

What is the biology of Endometrial Carcinoma?

POLE exonuclease‑domain mutations are linked to strong immune activation that is thought to contribute to a favorable prognosis. Hypertension has been proposed to influence endometrial tumor biology and prognosis through mechanisms such as altered angiogenesis (via MMP2 and MMP9), insulin resistance with effects on IGF‑1, and hypertension‑related inflammation and extracellular matrix remodeling.

How is Endometrial Carcinoma treated?

Most endometrial carcinoma cases are diagnosed at an early stage and are often treated with surgery alone. Diagnostic evaluation uses endometrial sampling (office biopsy, hysteroscopy, or dilatation and curettage) and imaging (transvaginal ultrasound, pelvic CT, or MRI) to assist treatment planning; MRI is preferred to assess local tumor extent and cross-sectional imaging or PET/CT may be used if distant metastasis is suspected.

What treatments are studied for Endometrial Carcinoma?

23 therapeutics and procedures are reported across radiotherapy, surgical/procedural, chemotherapy, hormonal, targeted, repurposed drug, and other classes.

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. GuidelinePDQ(R) Endometrial Cancer Treatment — National Cancer Institute · n.d.
    Source: PDQ(R) Adult Treatment Editorial Board. PDQ Cancer Information Summaries. Bethesda, MD: National Cancer Institute. The NCI does not endorse this site or its content.
  3. GuidelineEpidemiology and investigations for suspected endometrial cancer · 2013
  4. GuidelineESGO/ESTRO/ESP Guidelines for the management of patients with endometrial carcinoma · 2021
  5. Systematic reviewUnusual Case of Neuromeningeal Late Relapse of POLE Mutated Endometrioid Carcinoma: A Case Report and Systematic Review · 2026
  6. GuidelineNo. 291-Epidemiology and Investigations forSuspected Endometrial Cancer · 2018
  7. GuidelineACR Appropriateness Criteria® Pretreatment Evaluation and Follow-Up of Endometrial Cancer · 2020
  8. GuidelineMolecular testing in endometrial carcinoma (Joint recommendation of Czech Oncological Society, Oncogynecological Section of the Czech Gynecological and Obstetrical Society, Society of Radiation Oncology, Biology and Physics, and the Society of Czech Pathologists) · 2021
  9. Meta-analysisAssociation of endometrial cancer risk with hypertension- an updated meta-analysis of observational studies · 2024
  10. Meta-analysisBody Mass Index and Risk of Female Reproductive System Tumors Subtypes: A Meta-Analysis Using Mendelian Randomization · 2024
  11. Systematic reviewAssociation of endometrial pathologies with infertility and malignant potential in pre- and postmenopausal women-a systematic review · 2026
  12. Meta-analysisMolecular profile in endometrial carcinoma: can we predict the lymph node status? A systematic review and meta-analysis · 2024
  13. Meta-analysisThe prognostic value of lymph node to primary tumor standardized uptake value ratio in cancer patients: a meta-analysis · 2024
  14. GuidelineEndometrial cancer: a review and current management strategies: part II · 2014
  15. Systematic reviewA qualitative systematic review of the significance of adjuvant therapy in patients with low-risk endometrial cancer presenting positive peritoneal cytology: a relevant study to the guideline update for endometrial cancer by the Japan society of gynecologic oncology guideline committee · 2024
  16. Meta-analysisComparative effects of different treatments based on the levonorgestrel intrauterine system in endometrial carcinoma and endometrial hyperplasia patients: a network meta-analysis · 2024
  17. Meta-analysisA meta-analysis of the effect of pelvic and para-aortic lymph node dissection on the prognosis of patients with endometrial cancer · 2024
  18. Systematic reviewMinimally invasive surgical treatment of recurrent endometrial carcinoma: A systematic review · 2026
  19. Meta-analysisComparison of the Efficacy and Safety of Single-Site Laparoscopic Hysterectomy with and without Robotic Assistance: A Meta-Analysis · 2026

What supports this page

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

Guideline
17
Meta-analysis
68
Systematic review
16
Randomized trial
2
Clinical trial
12
Observational
2
Case report
136
Review
685
Preclinical
0
Other
25

Living document — last change June 19, 2026: Cancer page updated. 4 recent updates logged.

Pooled evidence across studies

PubMed
  • PRAME immunoreactivity rate: 76% (60–90 across studies) · PRAME (Preferentially expressed antigen in melanoma)
    13 studies · 62% agree · moderate35973038
  • Interobserver agreement rate: 62% (53–90 across studies) · (regimen unspecified)
    3 studies · 67% agree · moderate · 1 flagged26166718
  • Interobserver kappa: 0.55 kappa (0.48–0.9 across studies) · (regimen unspecified)
    3 studies · 67% agree · moderate · 1 flagged26166718
  • Interobserver outcome counts: 14 count (6–55 across studies) · (regimen unspecified)
    3 studies · 33% agree · heterogeneous · 1 flagged26166718
  • ORR: 8.05% (5.3–10.8 across studies) · durvalumab + tremelimumab
    2 studies · 0% agree · heterogeneous36512912
  • PFS: HR 2.6695 (2.033–3.306 across studies) · (regimen unspecified)
    2 studies · 0% agree · heterogeneous29731976

Numbers pooled deterministically across 82 published studies that passed our figure-accuracy checks — a quick synthesis, not a formal meta-analysis. Updated 9/6/2026.

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
1Durvalumab ImmunotherapyHuman trial / meta-analysis1ORR: 8.05%
2Sacituzumab Govitecan Targeted therapyAnimal only1—
3Pembrolizumab ImmunotherapyInsufficient evidence1—

Ranked across 3 compounds with published studies for this cancer. Updated 9/6/2026.

Medicines & supplements studied for Endometrial Carcinoma

PubMedFDAClinicalTrials.gov

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

Medicines · 7

DurvalumabHuman trial / meta-analysisReported negative1 human

Includes human trial or meta-analysis evidence.

Largest credible effect: ORR Arm 2 5.3% [1.4–100], p one-sided 90% CI, n=38 PMID 36512912 · effect sizes 4–82 across 4 studies

Most authoritative study: Durvalumab with or without tremelimumab in patients with persistent or recurrent endometrial cancer or endometrial carcinosarcoma: A randomized open-label phase 2 study

Based on a single study.
ImmunotherapyFDA approvedPhase 21 studyFull profile →
CarboplatinHuman · observationalMixed results1 human

Human observational evidence only — no trials.

Largest credible effect: median age 66, n=24 PMID 30036218 · response rates 11–63 across 7 studies

Most authoritative study: Undifferentiated Endometrial Carcinomas: Clinicopathologic Characteristics and Treatment Outcomes

Based on a single study.
ChemotherapyFDA off-label1 studyFull profile →
PaclitaxelHuman · observationalMixed results1 human

Human observational evidence only — no trials.

Largest credible effect: median age 66, n=24 PMID 30036218 · response rates 11–63 across 7 studies

Most authoritative study: Undifferentiated Endometrial Carcinomas: Clinicopathologic Characteristics and Treatment Outcomes

Based on a single study.
ChemotherapyFDA off-label1 studyFull profile →
Sacituzumab GovitecanAnimal onlyReported positive1 animal

Animal studies only — no human data.

Largest credible effect: Median IC50 in UCS PDOs 167.7 [51.4–3200], n=9 PMID 40344963 · effect sizes 90–167.7 across 2 studies

Most authoritative study: TROP2 expression and therapeutic targeting in uterine carcinosarcoma

No human studies yet · Based on a single study.
Targeted therapyFDA off-label1 studyFull profile →
CisplatinLab onlyMixed results1 lab

Lab / cell studies only — no human or animal data.

Most authoritative study: Impact of the glutathione synthesis pathway on sulfasalazine-treated endometrial cancer

No human studies yet · No numeric effect sizes reported · Based on a single study.
ChemotherapyFDA off-label1 studyFull profile →
Sulfasalazine †RxLab onlyMixed results1 lab

Lab / cell studies only — no human or animal data.

Most authoritative study: Impact of the glutathione synthesis pathway on sulfasalazine-treated endometrial cancer

No human studies yet · No numeric effect sizes reported · Based on a single study.
Repurposed drugs1 studyFull profile →
PembrolizumabInsufficient evidenceReported positive

No primary experimental studies yet.

Most authoritative study: New Approved Use for Keytruda

No human studies yet · No numeric effect sizes reported · Based on a single study.
ImmunotherapyFDA approved1 studyFull profile →

Supplements & natural agents · 1

Curcumin / TheracurminInsufficient evidenceReported positive

No primary experimental studies yet.

Most authoritative study: Curcumin and endometrial carcinoma: an old spice as a novel agent

No human studies yet · No numeric effect sizes reported · Based on a single study.
Supplements & natural agents1 studyFull profile →

What recent studies report in Endometrial Carcinoma

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

60 studies18 human3 animal2 lab⚠ Conflicting evidenceMechanism (42)Trial (1)

Tracking 60 published studies of Endometrial Carcinoma: 18 in humans, 3 in animals, 2 in the lab, 37 reviews/other.

Reported direction across studies: 19 positive, 16 mixed, 3 negative, 22 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 Carcinoma.

Compounds with studies mentioning Endometrial Carcinoma

Sacituzumab govitecan (1)Durvalumab (1)Pembrolizumab (1)Sulfasalazine (1)Cisplatin (1)Curcumin (1)
Case reportInconclusiveLimited evidenceTier 3 · early humann = 1

Ureteral Metastasis From Endometrial Carcinoma Mimicking Upper Tract Urothelial Carcinoma

IJU case reports · Jul 2026 · case report

endometrial carcinomaupper tract urothelial carcinoma (differential)

This is a single-patient case report of a 64-year-old woman whose ureteral mass and malignant urine cytology were initially suspected to be upper tract urothelial carcinoma. After nephroureterectomy, histopathology and PAX8 immunohistochemistry indicated the ureteral lesion was metastatic endometrial adenocarcinoma, and the patient was staged as IVB endometrial carcinoma.

Key findings
  • Contrast-enhanced CT showed hydronephrosis and a left ureteral mass suggestive of upper tract urothelial carcinoma (UTUC).
  • Urine cytology showed malignant cells, but ureteroscopy was inconclusive.
  • Simultaneous surgery including nephroureterectomy was performed because UTUC would affect management and prognosis.
  • Histopathology revealed ureteral adenocarcinoma morphologically similar to endometrial carcinoma.
  • Immunohistochemical staining was PAX8 positive, supporting the diagnosis of metastatic endometrial carcinoma.
  • Final diagnosis was stage IVB endometrial carcinoma.
Limitations: Single case report (n=1) limits generalizability.; No preoperative tissue diagnosis of the ureteral lesion was obtained (ureteroscopy inconclusive).; No follow-up outcomes or treatments after diagnosis are reported in the abstract.; No quantitative data or comparative analysis..

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

ReviewMechanismMixed resultsModerate evidenceTier 4 · clinical

Recent advances in characterizing the immune microenvironment and biomarkers of endometrial carcinoma

Frontiers in immunology · May 2026

endometrial carcinoma

This review used bioinformatics and cross-study analyses to screen immune-related biomarkers and prognostic models in the tumor microenvironment of endometrial carcinoma. The authors report five immune-related markers and two gene families that were repeatedly found across studies, validate their clinical prognostic significance, and summarize implicated oncogenic signaling pathways and functions of infiltrating immune cells.

Key findings
  • Performed a systematic bioinformatics cross-study screen of biomarkers and prognostic models related to immune infiltration in endometrial carcinoma.
  • Identified five immune-related markers and two gene families that were consistently reported across multiple studies.
  • Reported validation of the clinical prognostic significance of those markers (as stated in the abstract).
  • Summarized oncogenic signaling pathways in which the markers are involved.
  • Summarized functional implications of immune-infiltrating cells for tumor behavior to guide target identification and future immunopharmacological research.
Limitations: This is a review/synthesis and does not present new primary experimental data.; Methods and selection criteria for the bioinformatics screening and cross-study analysis are not detailed in the abstract, so risk of heterogeneity or selection bias across studies is possible.; Although the abstract states clinical prognostic validation, no sample sizes, cohorts, or validation methods are reported here.; Functional/mechanistic proposals appear to be inferred from existing studies and bioinformatics rather than demonstrated experimentally in this report..

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

Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 25

Stage IA3 endometrial cancer in the FIGO 2023 classification: a case of clarity or complexity?

International journal of gynecological cancer : official journal of the International Gynecological Cancer Society · Jan 2026 · case series with centralized pathology review

endometrial carcinomaovarian endometrioid carcinoma

The authors reviewed 25 patients with synchronous endometrial and ovarian endometrioid carcinomas and compared staging under the FIGO 2009 versus FIGO 2023 classifications with centralized pathology review. Applying FIGO 2023 (and ESGO risk stratification) changed stage in 5 patients (20%), with 2 downstaged and 3 upstaged; among 11 patients with disease limited to uterus and ovaries, 5 met stage IA3 and none recurred, including 2 managed with surgery alone. The authors conclude FIGO 2023 IA3 can improve risk stratification, particularly for low-grade, ER-positive tumors with favorable molecular profiles, but note issues about adequate staging surgery and ovarian grading criteria.

Reported effects: stage_shifts 20%, n=25 · downstaged_count 2, n=25 · +4 more

Key findings
  • Study cohort comprised 25 patients with concurrent endometrial and ovarian tumors.
  • Applying FIGO 2023 classification and ESGO risk stratification led to stage shifts in 5 patients (20%): 2 were downstaged and 3 were upstaged.
  • Among 11 patients whose disease was limited to the uterus and ovaries, 5 met criteria for stage IA3 and none experienced recurrence; this group included 2 patients managed with surgery alone.
  • FIGO 2023 stage IA3 classification enables more precise risk stratification, particularly in low-grade, estrogen receptor-positive tumors with favorable molecular profiles (POLE-mutated or p53 wild-type / non-specific molecular profile).
  • The new classification raises operational issues: the need for appropriate staging surgery and debate about the optimal grading system for ovarian endometrioid carcinoma.
Limitations: Small sample size (25 patients).; Observational case-series design with potential selection bias.; Follow-up duration and timing of recurrence assessment are not reported in the abstract.; Low event counts (no recurrences reported) limit strength of outcome conclusions.; Generalizability limited by small cohort and lack of multi-center data in the abstract..

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

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

Human · observationalMechanismMixed resultsLimited evidenceTier 3 · early human

Endometrial Carcinoma Molecular Classification and Barriers to Implementation, Possible Solutions, and the Implications for Ongoing Clinical Trials

Journal of obstetrics and gynaecology Canada : JOGC = Journal d'obstetrique et gynecologie du Canada : JOGC · Nov 2025 · digital survey of gynaecologic pathologists

endometrial carcinoma

The authors administered a digital survey to gynecologic pathologists at 13 Canadian academic pathology departments to assess use of molecular classification for endometrial carcinoma. They found variability in how molecular classification is applied and that respondents perceived resource restrictions and unclear management implications as barriers. The paper recommends focused research, knowledge translation, and guideline development to improve consistent implementation. The abstract also notes that ongoing clinical trials are investigating treatment paradigms and therapy de-escalation based on molecular classification.

Key findings
  • Molecular classification of endometrial carcinoma provides prognostic and predictive information.
  • Ongoing clinical trials are investigating different treatment paradigms and therapy de-escalation informed by molecular classification.
  • There is variability in the application of molecular classification worldwide, including in Canada.
  • A digital survey of gynecologic pathologists in 13 Canadian academic pathology departments identified areas of homogeneity and variability in practice.
  • Perceived barriers to universal application included resource restrictions and ambiguity of management implications.
  • Authors propose focused research, knowledge translation, and guideline development to facilitate more consistent implementation.
Limitations: Survey-based study with no respondent count or response rate reported in abstract (potential nonresponse/selection bias).; Limited to academic pathology departments in Canada (limited generalizability).; Findings based on perceptions/self-report rather than objective measures of practice or patient outcomes.; Abstract provides no quantitative results or statistical analysis..

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

Case reportMechanismInconclusiveLimited evidenceTier 3 · early humann = 3

High-grade endometrioid carcinomas with pilomatrix-like features lacking CTNNB1 Mutations: Clinicopathologic characteristics and novel molecular events

Human pathology · Oct 2025 · case series

endometrial carcinomaendometrioid carcinomapilomatrix-like high-grade endometrioid carcinoma (PiMHEC)

The authors report three human cases of high-grade endometrioid carcinoma with pilomatrix-like features (PiMHEC) that lacked CTNNB1 exon 3 mutations and nuclear β-catenin by IHC. All tumors had characteristic pilomatrix-like morphology, presented at advanced stage, showed aggressive clinical behavior (two recurrences within 12 months), and targeted NGS identified alternative likely oncogenic alterations including FGFR4 p.T259A, TSC2 mutations, KRAS p.G12D, and MYC amplification.

Reported effects: number_of_cases 3, n=3 · patients_presenting_with_advanced_stage_disease 3, n=3 · +6 more

Key findings
  • Three cases of high-grade endometrioid carcinoma with pilomatrix-like features were analyzed.
  • All tumors demonstrated two components: a high-grade basaloid component with solid sheets of atypical basaloid cells, geographic necrosis, and focal "ghost" cells, and an associated low-grade FIGO grade 1 endometrioid carcinoma component.
  • None of the three cases showed nuclear &#x3b2;-catenin expression by IHC, and all lacked CTNNB1 exon 3 mutations.
  • All the patients presented with advanced-stage disease (stages IIC-IVB).
  • Two patients had a recurrence within 12 months.
  • NGS revealed no CTNNB1 mutations, but identified alternative likely oncogenic alterations: one tumor harbored an FGFR4 p. T259A mutation, two tumors had pathogenic TSC2 mutations, one had a KRAS p.G12D mutation, and two showed MYC amplification.
Limitations: Very small sample size (n=3) and single case-series design.; Case reports are descriptive and cannot establish causal relationships between identified mutations and the PiMHEC phenotype.; No functional validation provided to show that the alternative oncogenic alterations drive the pilomatrix-like phenotype.; Limited follow-up data reported (recurrence noted within 12 months for two patients), limiting assessment of long-term outcomes and prognostic significance..

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

Animal studyReported positivePreclinical onlyTier 2 · animaln = 72

TROP2 expression and therapeutic targeting in uterine carcinosarcoma

Gynecologic oncology · Jun 2025 · archival tissue analysis plus patient-derived organoid and xenograft preclinical study

Sacituzumab-govitecanuterine carcinosarcomaendometrial carcinoma

This study looked at TROP2 levels in uterine carcinosarcoma samples and tested the TROP2-targeting antibody-drug conjugate sacituzumab govitecan in patient-derived organoid and xenograft models. Most tumors had detectable TROP2, and the organoid models responded to the drug in a dose-dependent way. In two xenograft models, tumor volume was lower with sacituzumab govitecan than without it.

Reported effects: TROP2 expression in primary UCSs 90%, n=72 · Higher TROP2 expression by histologic subtype, p p < 0.001 and p = 0.022, n=72 · +2 more

Key findings
  • TROP2 protein and mRNA were detected in at least 90% of primary uterine carcinosarcomas.
  • Tumors with a predominant carcinomatous component or homologous differentiation had higher TROP2 expression than those with predominant sarcomatous component or heterologous differentiation.
  • All 9 uterine carcinosarcoma organoid models responded in a dose-dependent manner to sacituzumab govitecan.
  • Both xenograft models showed significant reduction in tumor volume with sacituzumab govitecan.
Limitations: Preclinical study; findings are from archival tissues, organoids, and mouse xenografts, not patients.; Only 2 xenograft models were tested.; No clinical outcomes, safety data, or survival data in humans were reported.; The abstract does not provide dosing details or treatment duration..

Supports preclinical exploration of TROP2-targeted therapy in uterine carcinosarcoma.

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

ReviewMechanismInconclusiveLimited evidenceTier 4 · clinical

Aggressive Serous Carcinomas of the Female Reproductive Tract: Cancer-Prone Cell States and Genetic Drivers

Cancers · Feb 2025 · narrative review

high-grade serous ovarian carcinomaserous endometrial carcinomagynecological cancers

This narrative review summarizes current knowledge about cell states and genetic drivers associated with aggressive serous carcinomas of the female reproductive tract, focusing on high-grade serous ovarian carcinoma (HGSC) and serous endometrial carcinoma (SEC). The authors note common features such as frequent TP53 mutations, alterations in the RB1 pathway, marked cellular heterogeneity and poor differentiation at detection, and discuss how new transcriptomic and genetic tools applied to models might help identify targets for earlier detection and therapeutic intervention.

Key findings
  • HGSC and SEC commonly harbor TP53 mutations and alterations of the RB1 pathway.
  • Both carcinoma types are poorly differentiated and consist of highly heterogeneous cell populations at the time of detection.
  • Latent development and rapid progression of HGSC and SEC impede identification of definitive cells of origin and genetic drivers.
  • Emerging transcriptomic and genetic tools applied to contemporary model systems may facilitate identification of novel targets for detection and therapeutic intervention.
Limitations: Narrative review with no primary experimental or clinical data presented.; Not a systematic review or meta-analysis; methodology for literature selection is not specified in the abstract.; Does not identify definitive cells of origin or specific validated therapeutic targets based on new data..

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

Case reportMechanismInconclusiveLimited evidenceTier 3 · early humann = 2

High-grade corded and hyalinized endometrioid carcinoma of "no specific molecular profile": report of two cases

Pathologica · Feb 2025 · case report (two cases)

corded and hyalinized endometrioid carcinomaendometrioid carcinomaendometrial carcinoma

This paper reports two human cases of high-grade corded and hyalinized endometrioid carcinoma (CHEC) that showed a "no specific molecular profile" (NSMP). Both tumors had a markedly atypical, mitotically active corded component merging with FIGO G3 endometrioid carcinoma and squamous/morular differentiation, and both showed nuclear β-catenin accumulation, retained mismatch repair protein expression, wild-type p53 pattern, and no POLE mutations. The authors note heterogeneity in age and presentation (patients aged 25 and 81) and suggest these tumors be considered a variant of FIGO G3 endometrioid carcinoma.

Reported effects: number_of_cases 2 · tumor_size_case1 6 · +2 more

Key findings
  • Both cases demonstrated a markedly atypical and mitotically active corded component merging with a FIGO G3 endometrioid component and accompanied by squamous/morular differentiation.
  • Both tumors showed nuclear β-catenin accumulation, retained MMR protein expression, wild-type p53 pattern, and no POLE mutations.
  • Case #1 was a 6-cm endometrial mass in a 25-year-old woman, infiltrating the deep myometrium and cervical stroma, with diffuse lymphovascular space invasion.
  • Case #2 was an advanced, unresectable endometrial carcinoma involving the lower third of the vagina in an 81-year-old woman.
  • The corded component was absent in the hysterectomy specimen of case #1 and in the vaginal biopsy specimen of case #2.
  • Authors conclude these cases expand the clinical and molecular heterogeneity of high-grade CHEC and suggest considering them as a variant of FIGO G3 endometrioid carcinoma.
Limitations: Very small sample size (two cases) — case report-level evidence.; Descriptive pathology series without systematic follow-up or outcome data reported in the abstract.; No control or comparison group.; Methods for molecular testing (e.g., POLE testing) and detailed molecular data are not provided in the abstract.; Findings may not be generalizable..

Pathology case report that expands the morphological and molecular spectrum of high-grade corded and hyalinized endometrioid carcinoma (CHEC) by describing two human cases with NSMP.

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 = 669

Identifying mesonephric-like adenocarcinoma of the endometrium by combining SOX17 and PAX8 immunohistochemistry

Histopathology · Jan 2025 · retrospective observational immunohistochemistry study on archival tumour specimens and tissue microarrays

mesonephric-like adenocarcinomaendometrial carcinomaovarian carcinoma

The authors examined immunohistochemical expression of SOX17, PAX8 and other markers in 17 previously diagnosed mesonephric-like adenocarcinomas (MLAs) and screened tissue microarrays of 652 endometrial carcinomas. They found that MLAs were diffusely PAX8-positive, ER-negative, and showed either negative (10 cases) or focal weak/moderate (7 cases) SOX17 staining. Screening the 652 TMAs for PAX8-positive but SOX17-negative/focal cases identified 14 cases, of which 7 (50%) were reclassified as MLA after morphology and additional IHC (CD10, TTF1, GATA3). The authors conclude that strong PAX8 combined with negative SOX17 supports diagnosing MLA.

Reported effects: number of MLAs collected 17, n=17 · TMAs composed of endometrial carcinomas 652, n=652 · +7 more

Studied with: SOX17, PAX8.

Key findings
  • Seventeen previously diagnosed endometrial/ovarian MLAs were collected and multiple IHCs performed.
  • All 17 MLAs showed diffuse strong positive PAX8, negative ER and variable TTF1/GATA3 staining.
  • All MLAs showed negative (n = 10) or focal weak/moderate (n = 7) staining for SOX17.
  • TMAs composed of 652 endometrial carcinomas were screened with combined SOX17 and PAX8 IHCs.
  • Fourteen cases with positive PAX8 but negative/focal weak SOX17 were identified from the TMAs.
  • Of those 14 cases, seven (50%) were classified as MLAs after further morphology review and additional IHC (CD10, TTF1 and/or GATA3).
Limitations: Retrospective, pathology-based study of archival specimens; Small number of confirmed MLA cases (n = 17) limits generalisability; Validation of the marker approach yielded only 14 candidate cases, with 7 reclassified as MLAs (limited validation sample size); No clinical outcome or follow-up data reported to correlate IHC classification with prognosis; Potential subjectivity in IHC interpretation and morphological reassessment.

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 human

Epigenetic Signatures and Prognostic Biomarkers Analysis of Methylation-Driven Genes in Uterine Endometrial Carcinosarcoma

Critical reviews in eukaryotic gene expression · Jan 2025 · bioinformatic analysis of TCGA datasets integrating mRNA expression and DNA methylation (MethylMix) with Kaplan-Meier survival analysis

uterine endometrial carcinosarcomauterine corpus endometrial carcinoma (UCEC)

The authors analyzed TCGA transcriptomic and DNA methylation data for uterine endometrial carcinoma to identify methylation-driven genes. They report differential methylation and expression for six genes (TP53, PTEN, PTX3, TNK1, PPP2R1A, KLRG2) and found that higher expression of PTX3, TNK1, and KLRG1 was associated with poorer overall survival, while TP53, PTEN, and PPP2R1A were not significantly associated with survival. Pathway enrichment and protein interaction analyses indicated involvement of these genes in cancer-related pathways. The work is a bioinformatic/prognostic biomarker analysis and does not report experimental validation in this abstract.

Key findings
  • Integrated mRNA expression and DNA methylation analysis (MethylMix) identified differential methylation-driven expression patterns for six genes: TP53, PTEN, PTX3, TNK1, PPP2R1A, and KLRG2.
  • TP53, TNK1, PPP2R1A, and KLRG2 were reported as upregulated in tumors; PTX3 was downregulated in tumors; PTEN expression showed no significant change.
  • Kaplan-Meier survival analysis reported that higher expression of PTX3, TNK1, and KLRG1 was significantly associated with poorer overall survival in UCEC patients.
  • Expression of TP53, PTEN, and PPP2R1A did not show a significant impact on patient survival according to the abstract.
  • Pathway enrichment and protein-protein interaction network analyses suggested these genes participate in critical cancer pathways.
Limitations: Retrospective bioinformatic analysis of TCGA data only (no prospective or experimental validation reported in the abstract).; No sample size or cohort characteristics are provided in the abstract.; No independent validation cohort or functional (in vitro/in vivo) experiments are mentioned in the abstract.; Association-based findings cannot establish causation..

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

ReviewMechanismInconclusiveLimited evidenceTier 1 · lab

Advances in MiRNAs Involved in Endometrial Carcinoma

Combinatorial chemistry & high throughput screening · Jan 2025 · Review

endometrial carcinoma

This is a review article summarizing recent studies on microRNAs (miRNAs) in endometrial carcinoma. The authors report that evidence supports miRNAs as important regulators of gene expression via binding to 3'-UTR regions. The review aims to clarify the association between miRNAs and endometrial carcinoma and to serve as a reference for further research into miRNA-related therapies.

Key findings
  • Endometrial carcinoma may be associated with abnormal gene expression.
  • Evidence supports that miRNAs act as critical regulators of gene expression through binding to the 3'-untranslated region (3'-UTR).
  • The review summarizes recent studies focusing on miRNAs that influence endometrial carcinoma.
  • The authors intend the review to provide a reference for further studies on miRNA-related drugs in endometrial carcinoma.
Limitations: This is a review article and presents no new experimental data.; Abstract does not describe review methods, selection criteria, or whether the review was systematic.; Abstract does not specify which findings are from human clinical studies versus preclinical (in vitro/animal) studies.; The review does not establish clinical efficacy or safety of miRNA-related therapies in patients..

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

Browse all studies mentioning Endometrial Carcinoma →

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
Durvalumab11—1
Carboplatin1———
Paclitaxel1———
Cisplatin—1——
Curcumin / Theracurmin————
Pembrolizumab—1——
Sacituzumab Govitecan—1——
Sulfasalazine †Rx—1——

Study mix

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

30 Human4 Animal3 Lab72 Review/other
Reported directionReported positive35Mixed results28Reported negative3Inconclusive43

Compounds with reported-positive results in Endometrial Carcinoma

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.

Preclinical only: lab / animal (3)
Sacituzumab Govitecan1 positive1 animal
Limitations: Preclinical study; findings are from archival tissues, organoids, and mouse xenografts, not patients.; Only 2 xenograft models were tested.; No clinical outcomes, safety data, or survival data in humans were reported.; The abstract does not provide dosing details or treatment duration..
Cited positive studies (1)
Pembrolizumab1 positive
Limitations: This abstract is an approval announcement and does not present primary trial data.; No sample size, efficacy outcomes, safety/adverse event data, dosing, or follow-up duration are provided.; Underlying trial design, statistical significance, and comparator information are not reported here..
Cited positive studies (1)
Limitations: Review article; no original experimental data reported in the abstract.; Abstract does not specify which molecular pathways or mechanisms are involved.; No details on methods, study selection, or quantitative results are provided in the abstract..
Cited positive studies (1)

Evidence at a glance: compounds studied in Endometrial Carcinoma

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.

DurvalumabHuman trial / meta-analysisReported negative1 human

Includes human trial or meta-analysis evidence.

Largest credible effect: ORR Arm 2 5.3% [1.4–100], p one-sided 90% CI, n=38 PMID 36512912 · effect sizes 4–82 across 4 studies

Most authoritative study: Durvalumab with or without tremelimumab in patients with persistent or recurrent endometrial cancer or endometrial carcinosarcoma: A randomized open-label phase 2 study

Based on a single study.
CarboplatinHuman · observationalMixed results1 human

Human observational evidence only — no trials.

Largest credible effect: median age 66, n=24 PMID 30036218 · response rates 11–63 across 7 studies

Most authoritative study: Undifferentiated Endometrial Carcinomas: Clinicopathologic Characteristics and Treatment Outcomes

Based on a single study.
PaclitaxelHuman · observationalMixed results1 human

Human observational evidence only — no trials.

Largest credible effect: median age 66, n=24 PMID 30036218 · response rates 11–63 across 7 studies

Most authoritative study: Undifferentiated Endometrial Carcinomas: Clinicopathologic Characteristics and Treatment Outcomes

Based on a single study.
Sacituzumab GovitecanAnimal onlyReported positive1 animal

Animal studies only — no human data.

Largest credible effect: Median IC50 in UCS PDOs 167.7 [51.4–3200], n=9 PMID 40344963 · effect sizes 90–167.7 across 2 studies

Most authoritative study: TROP2 expression and therapeutic targeting in uterine carcinosarcoma

No human studies yet · Based on a single study.
CisplatinLab onlyMixed results1 lab

Lab / cell studies only — no human or animal data.

Most authoritative study: Impact of the glutathione synthesis pathway on sulfasalazine-treated endometrial cancer

No human studies yet · No numeric effect sizes reported · Based on a single study.
Sulfasalazine †RxLab onlyMixed results1 lab

Lab / cell studies only — no human or animal data.

Most authoritative study: Impact of the glutathione synthesis pathway on sulfasalazine-treated endometrial cancer

No human studies yet · No numeric effect sizes reported · Based on a single study.
Curcumin / TheracurminInsufficient evidenceReported positive

No primary experimental studies yet.

Most authoritative study: Curcumin and endometrial carcinoma: an old spice as a novel agent

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

No primary experimental studies yet.

Most authoritative study: New Approved Use for Keytruda

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

What the research shows for Endometrial Carcinoma

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

  • A guideline-review article updated prior ESGO/ESTRO/ESP consensus guidance to reflect a large and growing literature on management of endometrial carcinoma, indicating evolving standards and new topics for care.
  • Molecular reviews and an integrated genomic/proteomic study of 373 endometrial carcinomas reported that the disease comprises multiple molecular subtypes (POLE ultramutated, MSI hypermutated, copy-number low, and copy-number high) with distinct mutation patterns and prognoses.
  • An observational genomic/proteomic analysis reported mixed associations between some molecular biomarkers and clinical outcomes, indicating complexity and heterogeneity across tumors.
  • A preclinical study tested the TROP2-targeting antibody–drug conjugate sacituzumab govitecan in patient-derived organoids and xenograft models of uterine carcinosarcoma/endometrial carcinoma: most tumors expressed TROP2 and the laboratory models responded to the agent.
  • Overall, the collected studies are primarily molecular characterizations and preclinical laboratory work; direct clinical trial evidence for novel targeted agents in endometrial carcinoma was not provided in these reports.

Compounds studied in Endometrial Carcinoma

Sacituzumab Govitecan1 study
In the included preclinical study, sacituzumab govitecan (a TROP2-targeting antibody–drug conjugate) was tested in patient-derived organoid and xenograft models of uterine carcinosarcoma/endometrial carcinoma; most tumors had detectable TROP2 and the laboratory models showed anti-tumor responses — the main limitation is that the evidence is preclinical (organoids/xenografts) with no clinical trial data in patients reported in these studies.

Supportive & alternative options discussed

  • Exercise / prehabilitation: Also discussed as a supportive option for people with endometrial carcinoma to help maintain fitness, function, and quality of life.
  • Mind–body (MBSR / CBT): Also discussed as a supportive approach (e.g., stress reduction, counseling, relaxation techniques) to help with emotional well-being during and after cancer care.
  • Acupuncture: Also discussed as a supportive option for symptom management (for example, pain or nausea) in people with cancer.
  • Ketogenic / metabolic therapy: Also discussed by some as a dietary approach adjunctive to cancer care, but clinical evidence in endometrial carcinoma is not established in these studies.
  • Hyperthermia (heat): Also discussed in some contexts as an adjunctive modality combined with other treatments, though these studies do not provide clinical evidence supporting its use in endometrial carcinoma.

What we don’t know yet

  • Does sacituzumab govitecan have measurable clinical safety and anti-tumor activity in patients with endometrial carcinoma or uterine carcinosarcoma, and if so in which subtypes?
  • Which endometrial carcinoma molecular subtypes most commonly express TROP2, and can TROP2 reliably predict response to TROP2-targeted therapy?
  • What are the appropriate dosing, scheduling, and combination strategies for TROP2-directed therapies with existing standard treatments (surgery, radiation, chemotherapy, immunotherapy)?
  • Are the preclinical responses observed in organoid and xenograft models predictive of outcomes in human patients with endometrial carcinoma?
  • How should updated molecular classifications be integrated into routine clinical decision-making and clinical trial design for targeted therapies?
  • What are the long-term outcomes and potential toxicities of novel targeted approaches in this population?
The evidence presented in these studies is mainly molecular characterization and preclinical laboratory work; clinical effectiveness and safety in patients remain unestablished and require clinical trials.

Clinical trials in Endometrial Carcinoma

87 ongoing · 82 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
22 stopped (terminated / withdrawn / suspended)

Search all trials on ClinicalTrials.gov →

Getting care & support

Nonprofit / Gov

Practical, vetted help for Endometrial Carcinoma — 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.

Interactions & safety to check: Endometrial Carcinoma

This is not a complete interaction check. It only covers the compounds we track and the signals reported in studies. A drug or supplement not listed here is not therefore safe. Bring your full medication and supplement list to your pharmacist and oncologist before changing anything.

Potential interactions: highest-stakes first

Safety considerations

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