Defective homologous recombination in human cancers

被引:56
作者
Cerbinskaite, A. [1 ]
Mukhopadhyay, A. [1 ,2 ]
Plummer, E. R. [1 ]
Curtin, N. J. [1 ]
Edmondson, R. J. [1 ,2 ]
机构
[1] Newcastle Univ, NICR, Newcastle Upon Tyne NE2 4HH, Tyne & Wear, England
[2] Queen Elizabeth Hosp, No Gynaecol Oncol Ctr, Gateshead, England
关键词
Homologous recombination; DNA repair; BRCA; ATM; ATR; MRE11; RAD50; NSB1; RAD51; FANC; DNA-DAMAGE-RESPONSE; FANCONI-ANEMIA PATHWAY; STRAND BREAK REPAIR; NONPOLYPOSIS COLORECTAL-CANCER; SINGLE-NUCLEOTIDE POLYMORPHISM; ATM-DEPENDENT PHOSPHORYLATION; BRCA1 185DELAG MUTATION; POPULATION-BASED SAMPLE; ASHKENAZI JEWISH WOMEN; ATAXIA-TELANGIECTASIA;
D O I
10.1016/j.ctrv.2011.04.015
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Homologous recombination (HR) is a process by which DNA double strand breaks are repaired through the alignment of homologous sequences of DNA. Interest continues to increase in HR pathway function due to the development of new therapeutic agents which selectively exploit DNA damage repair pathways. Currently the most promising of these new agents are inhibitors of poly(ADP ribose) polymerase (PARP). The response of cancers known to be deficient in HR, due to BRCA1 or 2 mutations has been demonstrated, and a wider use of PARP inhibitors in cancers with mutations of other HR pathway genes has been suggested. With ongoing clinical studies into the use of PARP inhibitors, further understanding of the HR pathway, to allow patient selection by cancer biology, is now essential. Numerous studies have investigated individual aberrations of genes involved in the HR pathway. Here we collate this evidence to give an overview of the role of the HR pathway in human cancer. (C) 2011 Elsevier Ltd. All rights reserved.
引用
收藏
页码:89 / 100
页数:12
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