Defective DNA repair systems and the development of breast and prostate cancer (Review)

被引:16
作者
Kitagishi, Yasuko [1 ]
Kobayashi, Mayumi [1 ]
Matsuda, Satoru [1 ]
机构
[1] Nara Womens Univ, Dept Environm Hlth Sci, Nara 6308506, Japan
关键词
DNA repair; estrogen; androgen; p53; BRCA1; carcinogenesis; VITAMIN-D; P53; ESTROGEN; RECEPTOR; BRCA1; MECHANISMS; GENES; RISK; CHEMOPREVENTION; OVEREXPRESSION;
D O I
10.3892/ijo.2012.1696
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Genetic defects in DNA repair and DNA damage response genes often lead to an increase in cancer incidence. The role of defects is also associated with the modulation of hormone signaling pathways. A number of studies have suggested a role for estrogen in the regulation of DNA repair activity. Furthermore, mutations or epigenetic silencing in DNA repair genes have been associated with the sensitivity of cancers to hormonal therapy. The molecular basis for the progression of cancers from hormone-dependent to hormone-independent remains a critical issue in the management of these types of cancer. In the present review, we aimed to summarize the function of DNA repair molecules from the viewpoint of carcinogenesis and hormone-related cell modulation, providing a comprehensive view of the molecular mechanisms by which hormones may exert their effects on the regulation of tumor progression.
引用
收藏
页码:29 / 34
页数:6
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