The accumulation of DNA repair defects is the molecular origin of carcinogenesis

被引:23
|
作者
Cha, Hyuk-Jin [1 ]
Yim, Hyungshin [2 ]
机构
[1] Sogang Univ, Dept Life Sci, Seoul 120742, South Korea
[2] Hanyang Univ, Coll Pharm, Inst Pharmaceut Sci & Technol, Dept Pharm, Ansan 426791, Kyeonggi Do, South Korea
基金
新加坡国家研究基金会;
关键词
Genomic instability; DNA damage; DNA repair; Cancer; Aging; STRAND BREAK REPAIR; DEPENDENT PROTEIN-KINASE; BASE EXCISION-REPAIR; DAMAGE RESPONSE; GENOMIC INSTABILITY; ATM ACTIVATION; ATAXIA-TELANGIECTASIA; CHECKPOINT ACTIVATION; MISMATCH-REPAIR; END RESECTION;
D O I
10.1007/s13277-013-1038-y
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Genomic instability has been considered to be one of the prominent factors for carcinogenesis and the development of a number of degenerative disorders, predominantly related to the aging. The cellular machineries involved in the maintenance of genomic integrity such as DNA repair and DNA damage responses are extensively characterized by a large number of studies. The failure of proper actions of such cellular machineries may lead to the devastating effects mostly inducing cancer or premature aging, even with no acute exogenous DNA damage stimuli. In this review, we especially focus on the pathophysiological aspects of the defective DNA damage responses in carcinogenesis and premature aging. Clear understanding the causes of carcinogenesis and age-related degenerative diseases will provide novel and efficient approaches for prevention and rational treatment of cancer and premature aging.
引用
收藏
页码:3293 / 3302
页数:10
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