Molecular mechanisms linking endometriosis under oxidative stress with ovarian tumorigenesis and therapeutic modalities.

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.

journal_name

Cancer Invest

journal_title

Cancer investigation

authors

Shigetomi H,Tsunemi T,Haruta S,Kajihara H,Yoshizawa Y,Tanase Y,Furukawa N,Yoshida S,Sado T,Kobayashi H

doi

10.3109/07357907.2012.681821

subject

Has Abstract

pub_date

2012-07-01 00:00:00

pages

473-80

issue

6

eissn

0735-7907

issn

1532-4192

journal_volume

30

pub_type

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