Recent Developments in Studies on the Relation Between Endometriosis and Ovarian Cancer: Phenotype-Specific Risk, Molecular Convergence and Clinical Risk Stratification

Klaudia Gutowska, A Urbán, Cezary Wojtyła, Sławomir Ławicki, Piotr Laudański
In: Cancers · 2026 · vol. 18(19) , pp. 3241 · doi:10.3390/cancers18193241 · W7221019515
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This narrative review synthesizes recent evidence linking endometriosis phenotypes, particularly clear-cell and endometrioid ovarian carcinoma, to molecular alterations while recommending individualized risk assessment over routine surveillance due to low absolute incidence.

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Abstract

Purpose: We aim to synthesize recent clinical and translational evidence on the relationship between endometriosis and ovarian cancer, with emphasis on publications from 2024 to 2026 and on clinically conservative risk stratification. Materials and methods: This state-of-the-art narrative review prioritizes major peer-reviewed publications from July 2024 to June 2026. Older landmark publications were used only where necessary to contextualize recent findings. Results: Recent evidence supports a selective, phenotype-dependent association instead of a generalized malignant potential of endometriosis. The strongest and most reproducible signal concerns epithelial ovarian cancer, especially clear-cell and endometrioid ovarian carcinoma, with the highest relative risks reported for ovarian endometrioma and/or deep endometriosis. The ENDOCANCER meta-analysis found increased ovarian cancer risk across odds ratio, hazard ratio and standardized incidence ratio estimates but confirmed low absolute incidence and substantial heterogeneity. Contemporary reviews, including Leone Roberti Maggiore et al. and Bogani et al., emphasize low absolute lifetime risk and the absence of evidence supporting universal oncologic surveillance. Newer clinicopathological studies distinguish endometriosis-correlated tumors supported by transitional lesions indicative of malignant transformation from incidental coexistence. Molecular data support biological plausibility through ARID1A, PIK3CA, KRAS, PTEN, mismatch repair deficiency, POLE-mutated disease and p53-abnormal phenotypes, but these markers are not ready for routine prediction in endometriosis care. Conclusions: The immediate clinical implication is individualized risk assessment in place of routine cancer screening or prophylactic surgery based solely on the increased cancer risk associated with endometriosis. Counseling should integrate endometriosis phenotype, age, menopausal status, lesion dynamics, imaging atypia, hereditary cancer risk, reproductive goals and surgical consequences.

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