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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
62 published studies that name Endometrial Carcinoma9 human studies approved & graded (trial, observational, or meta-analysis)79 human clinical studies in the Endometrial Carcinoma corpus817 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
Studied, not standard - investigational
  • radiotherapy
  • lymphadenectomy
  • office endometrial biopsy
  • hysteroscopy
  • dilatation and curettage
  • fertility preservation
  • Robotic single-site hysterectomy (RSSH)
  • Minimally invasive surgery (MIS) for recurrent endometrial carcinoma
  • carboplatin plus paclitaxel
  • Hormone therapy
  • External-beam radiation therapy
  • Vaginal brachytherapy
  • Fertility-sparing treatment
  • Novel targeted therapies
  • Total hysterectomy with bilateral salpingo-oophorectomy and pelvic lymphadenectomy
  • levonorgestrel intrauterine system + oral progestins
  • oral progestins
  • adjuvant chemotherapy
  • pelvic and para‑aortic lymph node dissection
  • surgery
  • adjuvant therapy
  • Sacituzumab Govitecan

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.

23
Interventions
0
Standard of care
10
Tested in people
1
Lab / animal
11
Named in lit.
7
Classes
Standard of care (0) Guideline option (1) Tested in people (10) Lab / animal only (1) Named in the literature (11)

Tested in people, by trial phase: phase not reported ×10

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
—
—
2
—
—
Targeted therapy
—
—
—
1
1
Immunotherapy
—
1
—
—
—
Hormonal therapy
—
—
2
—
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 (1)
Immunotherapy
Durvalumab
FDA-approved for this cancer.
—Guideline option
Investigational & adjunct compounds — detail (22)
Meta-analysis (10)
adjuvant chemotherapy· Adjuvant (after surgery)carboplatin plus paclitaxelfertility preservationlevonorgestrel intrauterine system + oral progestinsMinimally invasive surgery (MIS) for recurrent endometrial carcinoma· Recurrent or later-lineoral progestinspelvic and para‑aortic lymph node dissectionradiotherapyRobotic single-site hysterectomy (RSSH)Total hysterectomy with bilateral salpingo-oophorectomy and pelvic lymphadenectomy
Named in the literature
lymphadenectomyoffice endometrial biopsyhysteroscopydilatation and 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: 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
58
Systematic review
16
Randomized trial
1
Clinical trial
8
Observational
1
Case report
116
Review
591
Preclinical
0
Other
9

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
  • ORR: 8.05% (5.3–10.8 across studies) · durvalumab + tremelimumab
    2 studies · 0% agree · heterogeneous36512912

Numbers pooled deterministically across 53 published studies that passed our figure-accuracy checks — a quick synthesis, not a formal meta-analysis. Updated 7/22/2026.

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—

Ranked across 2 compounds with published studies for this cancer. Updated 7/22/2026.

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 · 2

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 →
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 →

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 studies9 human1 animal1 lab⚠ Conflicting evidenceMechanism (48)Trial (1)

Tracking 60 published studies of Endometrial Carcinoma: 9 in humans, 1 in animals, 1 in the lab, 49 reviews/other.

Reported direction across studies: 13 positive, 17 mixed, 2 negative, 28 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)
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

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

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

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

Case reportMechanismInconclusiveLimited evidenceTier 3 · early humann = 2

POLE-mutated Endometrial "Carcinosarcoma"

International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists · Jan 2025 · Case report (2 cases)

Endometrial carcinomaCarcinosarcomaEndometrioid carcinoma

The authors report two cases that were morphologically suspicious for endometrial carcinosarcoma but did not meet essential diagnostic criteria. Molecular testing identified pathogenic POLE mutations in both cases, and the tumors were described as low-grade endometrioid carcinomas with a homologous sarcoma component. The report questions the existence of a true POLE-mutated carcinosarcoma entity.

Key findings
  • Two cases had morphologic suspicion for endometrial carcinosarcoma but lacked essential criteria for that diagnosis.
  • Pathogenic POLE mutations were detected on molecular testing in both cases.
  • A descriptive diagnosis rendered was endometrial endometrioid carcinomas, low-grade, with a homologous sarcoma component.
  • These observations challenge the existence of POLE-mutated 'carcinosarcoma.'
Limitations: Very small sample size (2 cases).; Case report design without a systematic series or controls.; No clinical follow-up, treatment, or outcome data reported in the abstract.; Abstract provides limited pathological and methodological detail..

AI summary of the abstract, human-reviewed · Jun 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

Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 18

Single-cell transcriptome profiles the heterogeneity of tumor cells and microenvironments for different pathological endometrial cancer and identifies specific sensitive drugs

Cell death & disease · Aug 2024 · Single-cell RNA sequencing of 18 human endometrial cancer samples across multiple pathological types, with patient-derived organoid drug testing and in vitro validation experiments

endometrial canceruterine clear cell carcinomaendometrioid endometrial carcinomauterine serous carcinoma

The authors performed single-cell RNA sequencing on 18 endometrial cancer samples across different pathological subtypes to map tumor-cell and microenvironment heterogeneity. They report pathology-specific tumor cell programs (immune-, proliferation-, or metabolism-modulating) and distinct microenvironment compositions, identified candidate drugs for each pathological group and confirmed drug activity in patient-derived organoids, and validated oncogenic effects of SOD2+ inflammatory cancer-associated fibroblasts in vitro. These findings provide descriptive molecular and cellular maps that may guide future, but not yet clinical, personalized approaches.

Reported effect: n_samples 18, n=18

Key findings
  • scRNA-seq was performed on 18 endometrial cancer samples from multiple pathological types.
  • Cancer cells showed pathology-associated hallmarks: immune-modulating in uterine clear cell carcinoma (UCCC), proliferation-modulating in well-differentiated endometrioid endometrial carcinoma (EEC-I), and metabolism-modulating in uterine serous carcinoma (USC).
  • Cancer cells from UCCC exhibited the greatest heterogeneity among the groups studied.
  • Potential effective drugs were predicted for each pathological group and their effectiveness was confirmed using patient-derived endometrial cancer organoids.
  • Tumor microenvironment differences: normal endometrium had prognostically favorable CD8+ cytotoxic T cells and NK cells, whereas tumors were dominated by CD4+ regulatory T cells, CD4+ exhausted T cells, and CD8+ exhausted T cells.
  • CXCL3+ macrophages with an M2 signature and angiogenesis association were found exclusively in tumors.
  • Epithelium-specific CAFs (eCAFs) predominated in EEC-I while SOD2+ inflammatory CAFs (iCAFs) predominated in UCCC.
  • The oncogenic effects of SOD2+ iCAFs were validated in vitro.
Limitations: Relatively small sample size (18 samples) limits generalizability.; Observational single-cell profiling: no prospective clinical outcome data or in vivo validation reported.; Drug effectiveness was confirmed in patient-derived organoids (ex vivo) but not in patients or animal models.; In vitro validation of SOD2+ iCAFs does not establish causality in vivo or clinical relevance.; Abstract does not report specific drug names, doses, or safety data..

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

Human · observationalMechanismMixed resultsLimited evidenceTier 3 · early humann = 96

Correlation between immunohistochemical staining and clinicopathological findings in endometrial carcinoma

Saudi medical journal · Jun 2024

endometrial carcinomaendometrioid carcinomapapillary serous carcinomaclear cell carcinomamixed Müllerian tumor

The authors analyzed immunohistochemical staining for mismatch repair (MMR) proteins and p53 in 96 endometrial carcinoma cases across multiple histologic subtypes. They found 36 cases were MMR-deficient (mostly endometrioid) and that a subset showed a p53 mutational staining pattern which was associated with a dismal prognosis. However, these stains did not predict synchronous or metachronous cancers in five patients. The authors conclude that MMR and p53 IHC are important for classification and prognosis of endometrial carcinoma.

Key findings
  • Total of 96 endometrial carcinoma cases analyzed (72 endometrioid, 14 papillary serous, 5 clear cell, 5 mixed Müllerian).
  • 36 cases were MMR deficient, with the majority being of endometrioid subtype.
  • p53 immunostain showed a mutational pattern in a subset of cases, which was associated with a documented dismal prognosis.
  • MMR and p53 immunohistochemical stains failed to predict synchronous or metachronous cancers in 5 patients.
  • Authors highlight the importance of MMR and p53 IHC in classification and prognosis of endometrial carcinoma.
Limitations: Observational immunohistochemical study without details of study design in abstract (e.g., retrospective vs prospective).; Small numbers in several histologic subgroups (e.g., clear cell and mixed Müllerian tumor, n=5 each).; Abstract reports no statistical measures, effect sizes, confidence intervals, or p-values to quantify associations.; No follow-up duration or method for determining 'dismal prognosis' reported in the abstract — prognosis definition and timing unclear.; IHC associations cannot establish causality and prognostic performance (sensitivity/specificity) is not reported..

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

Case reportReported positiveLimited evidenceTier 3 · early humann = 1

Endometrioid carcinomas with sex cord-like formations and hyalinization: spontaneous pregnancy after conservative treatment

BMC pregnancy and childbirth · Jan 2024 · case report

corded and hyalinized endometrioid adenocarcinoma (CHEC)endometrial carcinomaendometrioid carcinoma

This single-case report describes a 23-year-old woman with presumed stage IA corded and hyalinized endometrioid adenocarcinoma (CHEC) who received fertility-sparing conservative treatment and achieved a complete response after 10 months. She subsequently conceived spontaneously and delivered a healthy male infant, with no signs of recurrence during 37 months of follow-up after complete response.

Reported effects: time_to_complete_response 10 mo, n=1 · recurrence_free_followup 37 mo, n=1

Key findings
  • A 23-year-old nulliparous patient with presumed stage IA CHEC received fertility-sparing treatment and achieved complete response (CR) after 10 months of conservative treatment.
  • The patient subsequently became pregnant spontaneously, successfully conceived, and gave birth to a healthy male neonate.
  • There were no signs of recurrence during 37 months follow-up after CR.
  • CHEC is a rare variant not currently included in fertility-sparing guidelines; this case suggests fertility-sparing treatment may be an option for highly selected patients, with continuous follow-up required.
Limitations: Single-patient case report limits generalizability.; Abstract does not specify the exact conservative treatment regimen or detailed management protocol.; No control or comparison group.; Long-term outcomes beyond the reported 37 months are unknown..

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

ReviewMechanismInconclusiveLimited evidenceTier 4 · clinical

Roles of estrogen receptor α in endometrial carcinoma (Review)

Oncology letters · Oct 2023 · review

endometrial carcinoma

This narrative review summarizes the structure and multi-dimensional regulation of estrogen receptor α (ERα) and its relation to endometrial carcinoma. It describes the classical estradiol/ERα signaling pathway and the crosstalk between ERα and other regulators, and explains how ERα interactions influence proliferation, metastasis, invasion and inhibition of apoptosis in endometrial cancer. The authors also discuss therapeutic targeting of ERα as a potential future direction.

Key findings
  • The occurrence and development of endometrial carcinoma is closely associated with the interaction between estrogen (estradiol, E2) and estrogen receptors, particularly ERα.
  • ERα is described as a carcinogenic factor in endometrial carcinoma.
  • Interactions of ERα with upstream and downstream effectors and co-regulators have important implications for proliferation, metastasis, invasion and inhibition of apoptosis in endometrial carcinoma.
  • The review outlines the structure of ERα and its regulation in multiple dimensions, the classical E2/ERα signaling pathway, and crosstalk between ERα and other endometrial carcinoma regulators.
  • Therapeutic targeting of ERα is discussed as a potential new direction for clinical applications.
Limitations: Review article with no original experimental or clinical data presented.; Appears to be a narrative review; no methods or systematic review/meta-analysis approach are described 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

ReviewMechanismMixed resultsModerate evidenceTier 4 · clinical

HER2 in uterine serous carcinoma: Current state and clinical perspectives

American journal of clinical pathology · Oct 2023 · PubMed literature review

uterine serous carcinomaendometrial carcinomaendometrial canceruterine cancer

This PubMed literature review summarizes evidence about HER2 in uterine serous carcinoma (USC). The authors report that HER2 overexpression and gene amplification are important prognostic and therapeutic biomarkers in USC but that testing is complicated by intratumoral heterogeneity, atypical lateral/basolateral membranous staining, and discordance between IHC and in situ hybridization. They state a universal HER2 testing and scoring system suited to endometrial cancer is needed and is under investigation.

Key findings
  • HER2 has been established as an important biomarker with prognostic and therapeutic implications in USC.
  • Intratumoral heterogeneity and lateral/basolateral membranous staining of HER2 are more common in USC than in breast carcinoma.
  • High discordance between HER2 immunohistochemistry and in situ hybridization is more common in USC.
  • A universal HER2 testing and scoring system more suitable to endometrial cancer is needed and is currently under investigation.
  • The review discusses resistance mechanisms of HER2-targeted therapy and likely areas for future investigation.
Limitations: This is a literature review, not primary experimental or clinical trial data.; Methods beyond a PubMed literature search are not detailed in the abstract (potential for selection bias).; No new quantitative or patient-level results are reported in this abstract.; Heterogeneity of HER2 assays and scoring across studies may limit generalizability of conclusions..

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
Sacituzumab Govitecan—1——

Study mix

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

9 Human1 Animal1 Lab51 Review/other
Reported directionReported positive13Mixed results18Reported negative2Inconclusive29

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 (1)
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)

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.
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.

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

38 ongoing · 37 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
6 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

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