Endometriosis-Associated Ovarian Cancer: The Role of Oxidative Stress

Yoriko Yamashita, Shinya Toyokuni
In: Endometriosis - Basic Concepts and Current Research Trends · 2012 · doi:10.5772/30541 · W1556747636
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

Oxidative stress from recurrent hemorrhage in endometrial cysts causes genomic mutations, contributing to endometriosis-associated ovarian clear cell and endometrioid cancers by affecting genes like ARID1A and p53.

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Abstract

Recent studies indicated that oxidative stress has a causal role in the carcinogenesis of mainly two histological subtypes of ovarian cancer, namely, clear cell carcinoma and endometrioid adenocarcinoma. Because of recurrent hemorrhage in endometrial cysts, excess of reactive oxygen species are produced due to iron deposition, which results in direct genomic mutation of the epithelial cells and exaggeration of oxidative stress by stromal cells such as macrophages. In endometriosis-associated ovarian cancer, genomic mutations in specific genes such as ARID1A, p53, K-ras, PTEN, PI3CA and Met have been reported. Mechanism of carcinogenesis, especially focusing on the precise role of oxidative stress, remains to be clarified. Development of novel drugs and methods for therapy or prevention of endometriosis-associated ovarian cancer is necessary.

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endometriosis

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