Molecular Mechanisms Linking Endometriosis Under Oxidative Stress With Ovarian Tumorigenesis and Therapeutic Modalities

Hiroshi Shigetomi, Taihei Tsunemi, Shoji Haruta, Hirotaka Kajihara, Yoriko Yoshizawa, Yasuhito Tanase, Naoto Furukawa, Shozo Yoshida, Toshiyuki Sado, Hiroshi Kobayashi
Cancer investigation · 2012 · vol. 30(6) , pp. 473–480 · doi:10.3109/07357907.2012.681821 · PMID:22530740 · W2119771882
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

This paper investigates how oxidative stress in endometriosis promotes ovarian tumorigenesis through genomic instability and gene mutations, and discusses potential therapeutic targets.

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Abstract

Inflammation plays a role in the pathogenesis of endometriosis. Endometriosis-associated ovarian carcinogenesis might be promoted through oxidative stress-induced increased genomic instability, aberrant methylation, and aberrant chromatin remodeling, as well as mutations of tumor suppressor genes. Aberrant expression of ARID1A, PIK3CA, and NF-kB genes has been recognized as the major target genes involved in oxidative stress-induced carcinogenesis. HNF-1beta appears to play a key role in anti-oxidative defense mechanisms. We discuss the pathophysiologic roles of oxidative stress as somatic mutations as well as highly specific agents that effectively modulate these targets.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Endometriosis Ovarian Neoplasms Adenocarcinoma, Clear Cell Adenocarcinoma, Clear Cell Adenocarcinoma, Clear Cell Antioxidants Antioxidants Endometriosis Endometriosis Female Humans Inflammation Inflammation Ovarian Neoplasms Ovarian Neoplasms Ovarian Neoplasms Oxidative Stress Oxidative Stress 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.

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Cited by (17)

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