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在氧化应激下将子宫内膜异位症与卵巢肿瘤发生联系起来的分子机制和治疗方式。

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

机构信息

Department of Obstetrics and Gynecology, Nara Medical University, Nara, Japan.

出版信息

Cancer Invest. 2012 Jul;30(6):473-80. doi: 10.3109/07357907.2012.681821. Epub 2012 Apr 25.

DOI:10.3109/07357907.2012.681821
PMID:22530740
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.

摘要

炎症在子宫内膜异位症的发病机制中起作用。子宫内膜异位症相关的卵巢癌发生可能通过氧化应激诱导的增加的基因组不稳定性、异常甲基化和异常染色质重塑以及肿瘤抑制基因的突变而促进。ARID1A、PIK3CA 和 NF-kB 基因的异常表达已被认为是涉及氧化应激诱导的致癌作用的主要靶基因。HNF-1beta 似乎在抗氧化防御机制中发挥关键作用。我们讨论了氧化应激作为体细胞突变以及有效调节这些靶标的高度特异性药物的病理生理作用。

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