Genotoxicity of steroidal estrogens

被引：62

作者：

Russo, J ^{[1
]}

Russo, IH ^{[1
]}

机构：

[1] Fox Chase Canc Ctr, Philadelphia, PA 19111 USA

来源：

TRENDS IN ENDOCRINOLOGY AND METABOLISM | 2004年 / 15卷 / 05期

关键词：

D O I：

10.1016/j.tem.2004.05.007

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

The molecular mechanisms underlying the development of breast cancer in general, and estrogen-associated breast carcinogenesis in particular, are not completely understood. There are three mechanisms considered responsible for the carcinogenicity of estrogens in the human breast: (i) receptor-mediated hormonal activity, which stimulates cellular proliferation, resulting in more opportunities for accumulation of the genetic damage that leads to carcinogenesis; (ii) a cytochrome P450-mediated metabolic activation, which elicits direct genotoxic effects by increasing mutation rates; and (iii) the induction of aneuploidy by estrogen. In this article, we concentrate on discussing the role of estrogen receptors and the metabolic activation of 17beta-estradiol (E-2) as mechanisms of breast cancer initiation.

引用

页码：211 / 214

页数：4

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