| Treatment Modality | Specific Agents / Approaches | Indications | Efficacy Data (if available) | Molecular Stratification |
|---|---|---|---|---|
| Surgery | Primary cytoreductive surgery; total hysterectomy with bilateral salpingo-oophorectomy; omentectomy; peritoneal staging/biopsies; lymph node assessment in selected early-stage cases | Standard initial management for most resectable OEC; also used for diagnosis, staging, and tumor debulking | OEC is often diagnosed at earlier stage than high-grade serous carcinoma and generally has a more favorable prognosis, supporting surgery-centered management in localized disease (pqac-00000000, pqac-00000006) | Not molecularly restricted, but stage, grade, and histotype remain key determinants; p53-abnormal/high-grade tumors may warrant more aggressive multimodality treatment (pqac-00000001, pqac-00000003) |
| Adjuvant / First-line chemotherapy | Carboplatin + paclitaxel | Standard systemic therapy after surgery for advanced-stage disease and many high-risk early-stage cases | Standard ovarian cancer backbone regimen; in mixed epithelial ovarian cohorts remains the default comparator and routine regimen. OEC generally has better outcomes than HGSC, but high-grade/p53-abnormal OEC behaves more aggressively (pqac-00000000, pqac-00000006) | Used across molecular subtypes; potential relative de-escalation interest in POLE-mutated tumors and intensification interest in p53-abnormal tumors are emerging concepts rather than established standards (pqac-00000001, pqac-00000003) |
| Neoadjuvant chemotherapy | Carboplatin + paclitaxel followed by interval debulking surgery | Patients with bulky, unresectable, or medically high-risk advanced disease | No OEC-specific trial data in available contexts; approach extrapolated from epithelial ovarian cancer practice (pqac-00000000) | Not subtype-specific; tumor burden and surgical feasibility drive use |
| Immunotherapy + chemotherapy | Pembrolizumab + carboplatin/paclitaxel, followed by pembrolizumab maintenance | Advanced or recurrent MMR-deficient/dMMR tumors; increasingly relevant where OEC shows MMRd enrichment | In NRG-GY018 endometrial cancer, 12-month PFS in dMMR disease was 74% with pembrolizumab-chemotherapy vs 38% with placebo-chemotherapy; in pMMR disease median PFS was 13.1 vs 8.7 months (pqac-00000003) | Most compelling in MMRd/MSI-H OEC; OEC is enriched for Lynch-associated/MMRd tumors, supporting biomarker-driven use of checkpoint inhibitors (pqac-00000001, pqac-00000003) |
| Immune checkpoint inhibitor monotherapy | Pembrolizumab; dostarlimab | Recurrent/metastatic MMRd/MSI-H disease after prior therapy, or when chemotherapy is unsuitable | Robust tumor-agnostic and endometrial-cancer evidence supports activity in MMRd/MSI-H gynecologic tumors; OEC-specific efficacy data were not reported in the available contexts (pqac-00000001, pqac-00000003) | Best suited to MMRd/MSI-H tumors, including Lynch syndrome-associated OEC (pqac-00000001) |
| Hormonal therapy | Progestins; other endocrine therapy approaches used by analogy to endometrioid gynecologic tumors | Selected low-grade, hormone receptor-positive, indolent, recurrent, or fertility-/toxicity-sensitive settings | Direct OEC efficacy data not provided in the available contexts; biologic rationale exists because endometrioid tumors may retain hormone receptor expression (pqac-00000003, pqac-00000006) | Most plausible in ER/PR-positive, low-grade, NSMP-type tumors rather than p53-abnormal tumors |
| Targeted therapy: PI3K/AKT/mTOR axis | Investigational PI3K, AKT, or mTOR inhibitors | Recurrent or refractory tumors with PIK3CA activation and/or PTEN loss | Pathway is a major driver in OEC and endometriosis-associated ovarian cancer; clinical benefit remains investigational in available sources (pqac-00000006) | Best rationalized for PIK3CA-mutant and PTEN-deficient tumors; often overlaps with NSMP tumors (pqac-00000001, pqac-00000006) |
| Targeted therapy: ARID1A-directed synthetic lethality | ATR inhibitors; epigenetic/synthetic-lethal strategies under investigation | Recurrent ARID1A-deficient tumors in trials or precision-oncology settings | Preclinical and translational rationale is strong, but no definitive OEC-specific efficacy data were reported in the available contexts (pqac-00000006) | ARID1A-loss tumors, often with coexisting PI3K-pathway alterations (pqac-00000006) |
| Targeted therapy: PARP inhibitors | Olaparib and related PARP inhibitors | Selected tumors with homologous recombination deficiency or pathogenic BRCA alterations; less established in typical OEC than in HGSC | In ovarian cancer organoid models, a BRCA1-mutant endometrioid organoid showed increased olaparib sensitivity relative to non-BRCA models (pqac-00000003) | Most relevant to BRCA1/2-mutant or HRD tumors; likely a minority of OECs compared with HGSC |
| Molecularly adapted management | POLE/MMRd/NSMP/p53-abnormal classification integrated with histology and stage | Risk stratification, prognosis, trial selection, and tailoring of adjuvant/systemic therapy | POLE-mutated and MMRd subsets generally show excellent outcomes, while p53-abnormal/high-grade tumors have poorer prognosis and may merit intensified management (pqac-00000001, pqac-00000003) | POLE-mutated: favorable prognosis; MMRd: immunotherapy-sensitive; p53-abnormal: highest-risk biology; NSMP: heterogeneous, often enriched for PI3K/Wnt alterations (pqac-00000001, pqac-00000003) |
| Precision preclinical testing | Patient-derived organoids (drug screening with platinum, taxane, olaparib); xenografts | Research use; potential future patient-specific therapy selection | Ovarian cancer organoids preserved histopathology/genomics and showed drug-response patterns correlating with clinical course in small series (pqac-00000003) | Enables individualized testing across BRCA-mutant, platinum-sensitive/resistant, and pathway-defined tumors |


*Table: This table summarizes current and emerging treatment strategies for ovarian endometrioid carcinoma, linking each modality to its main indications, available efficacy evidence, and relevant molecular subgroups. It is useful for mapping standard care alongside biomarker-driven precision approaches.*