Endometrial / Uterine Cancer Clinical Trials

About Endometrial / Uterine Cancer trials

Endometrial cancer trials are increasingly organized around the four molecular classes defined by TCGA: POLE-ultramutated, MMR-deficient (MSI-high), TP53 abnormal (serous-like), and no specific molecular profile (NSMP). POLE pathogenic mutations identify a small but distinctive subgroup with excellent prognosis and trials studying treatment de-escalation. MMR (mismatch repair) status and the underlying genes (MSH6, PMS2, plus EPCAM for Lynch syndrome screening) define eligibility for immunotherapy trials, which now have a major frontline role in MMR-deficient disease. TP53 status defines the high-risk serous-like group, where HER2 (ERBB2) amplification overlaps in roughly 30% of serous carcinomas and gates anti-HER2 ADC trials. PTEN, PIK3CA, and ARID1A are common in endometrioid endometrial cancer and gate PI3K / AKT pathway trials. ESR1 represents hormone receptor status and informs endocrine therapy trials. BRCA2 is tested for emerging PARP inhibitor strategies. PD-L1 (CD274) gates a subset of immunotherapy trials.

Active trials in endometrial cancer split by molecular class, recurrence status, and target. Front-line trials for advanced or recurrent disease test combinations of carboplatin / paclitaxel chemotherapy with immunotherapy (following RUBY and NRG-GY018, dostarlimab and pembrolizumab are approved for this setting regardless of MMR/MSI status, with the strongest benefit established in dMMR/MSI-H disease) and additions of anti-HER2 ADCs, PARP inhibitors, or targeted agents. Adjuvant trials are increasingly molecularly stratified, with dedicated arms for each TCGA class testing escalation for high-risk subgroups (TP53 abnormal) and de-escalation for low-risk (POLE-mutated). Recurrent MMR-deficient trials are heavily IO-focused, often with combinations to extend or rescue IO response. Recurrent MMR-proficient trials are an active space, with ADCs targeting HER2 or TROP2 and novel mechanisms competing across lines. HER2-amplified serous carcinoma trials test anti-HER2 ADCs as monotherapy or in combination. Hormone receptor-positive endometrioid trials test endocrine therapy with CDK4/6 inhibitors and other combinations. Lynch syndrome patients have separate prevention and screening trials.

Most endometrial cancer trials screen on histology, molecular class, and prior chemotherapy and IO exposure. Histology subtype (endometrioid grade 1-3, serous, clear cell, carcinosarcoma, mixed) determines which trials apply. TCGA molecular classification (POLE-mutated, MMR-deficient, TP53 abnormal, NSMP) is increasingly required for adjuvant trials and is a stratification factor for many recurrent-disease trials. Prior platinum and taxane chemotherapy lines matter for line-specific trials. Prior immunotherapy exposure is becoming a defining filter as IO enters earlier lines. Prior anti-HER2 exposure for HER2-targeted trials. ECOG of 0 or 1 is standard. Adequate organ function and recovery from any prior surgery for adjuvant trial timing. Lynch syndrome status from germline testing affects eligibility for some trials.

Biomarkers tested in Endometrial / Uterine Cancer trials

These are the molecular markers most commonly required or evaluated in Endometrial / Uterine Cancer eligibility criteria. OncoMatch extracts them from each trial's protocol and matches them against your test results.