Cellular response to DNA damage

被引:24
|
作者
Kao, Johnny
Rosenstein, Barry S.
Peters, Seila
Milano, Michael T.
Kron, Stephen J.
机构
[1] Univ Chicago, Ctr Mol Oncol, Chicago, IL 60637 USA
[2] Mt Sinai Sch Med, Dept Radiat Oncol, New York, NY 10029 USA
[3] NYU, Sch Med, Dept Radiat Oncol, New York, NY 10016 USA
[4] Univ Rochester, Dept Radiat Oncol, Rochester, NY 14627 USA
关键词
DNA damage; DNA repair; radiation; non-homologous end-joining; homologous recombination;
D O I
10.1196/annals.1363.012
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Eukaryotic cells, from yeast to man, possess evolutionarily conserved mechanisms to accurately and efficiently repair the overwhelming majority of DNA damage, thereby ensuring genomic integrity. Important repair pathways include base excision repair, nucleotide excision repair, mismatch repair, non-homologous end-joining, and homologous recombination. Defects in DNA repair processes generally result in susceptibility to cancer and, often, abnormalities in multiple organ systems. While signal transduction pathways have been intensely studied, epigenetic changes occurring in response to DNA damage are rapidly increasing in importance. Effective radiation and chemotherapy sensitization could result from selective inhibition of DNA repair in tumor cells. DNA damage repair is a dynamic field of research where the fruits of basic research often have important clinical implications.
引用
收藏
页码:243 / 258
页数:16
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