Ovarian cancer in endometriosis: an update on the clinical and molecular aspects

Rachel Ruderman, Rachel S. Ruderman, Mary Ellen Pavone
Minerva ginecologica · 2017 · vol. 69(3) , pp. 286–294 · doi:10.23736/s0026-4784.17.04042-4 · PMID:28271698 · W2734722120
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

This review synthesizes current clinical and molecular knowledge regarding the link between endometriosis, particularly endometriomas, and the development of endometrioid and clear cell ovarian cancers through shared pathways and genetic mutations.

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Abstract

While endometriosis is a benign condition, the presence of endometriosis has been associated with the development of several types of cancers, including ovarian. Endometriomas, or ovarian endometriotic cysts, are found in 17-44% of patients with endometriosis, and may be a common precursor lesions to ovarian cancer. Endometriosis associated ovarian cancer is especially prominent in endometrioid and clear cell ovarian tumor histological subtypes. Several common pathways linking endometriosis and ovarian cancer have been elucidated, including the dominance of certain cytokines, oxidative stress, and a hyper-estrogenic hormonal milieu, which propagate both endometriosis and endometriosis associated ovarian cancer. Additionally, genetic mutations including PTEN, PIK3CA, ARID1A, Wnt/β-catenin, microsatellite instability, Src, and KRAS have been shown to be critical in the pathogenesis of endometriosis associated ovarian cancers. Research continues to develop and provide insights into various prevention, screening, and treatment modalities. In this article, we present a comprehensive review of our current knowledge on this topic in both a clinical and molecular context.

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Condition tags

mesh:D004715endometriosis

MeSH descriptors

Endometriosis Ovarian Neoplasms Animals Cytokines Cytokines Endometriosis Endometriosis Female Humans Mass Screening Mass Screening Mutation Ovarian Neoplasms Ovarian Neoplasms Ovarian Neoplasms Oxidative Stress

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

Cited by (32)

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