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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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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This chapter examines the mechanistic link between endometriosis and ovarian cancer, focusing on how chronic oxidative stress contributes to malignant transformation. It details how retrograde menstruation in endometriosis leads to iron accumulation from red blood cell breakdown, which generates reactive oxygen species that damage DNA and promote inflammation within the peritoneal cavity. The text highlights that this persistent oxidative environment creates a pro-carcinogenic milieu that facilitates the development of specific ovarian cancer subtypes, particularly clear cell and endometrioid carcinomas. This paper is centrally about endometriosis — specifically its role as a precursor condition for certain types of ovarian cancer through oxidative stress mechanisms.

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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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Open access Submitted: 19 March 2011 Published: 09 May 2012 DOI: 10.5772/30541 From the Edited Volume Edited by Koel Chaudhury and Baidyanath Chakravarty Submitted: 19 March 2011 Published: 09 May 2012 © 2012 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution 3.0 License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Discover 2026 Nobel Laureate Francis Halzen’s chapter on IntechOpen >

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