期刊
BIOCHEMICAL SOCIETY TRANSACTIONS
卷 37, 期 -, 页码 483-494出版社
PORTLAND PRESS LTD
DOI: 10.1042/BST0370483
关键词
cancer; cancer therapy; cell cycle; DNA damage; DNA repair
资金
- Biotechnology and Biological Sciences Research Council Funding Source: Medline
- Cancer Research UK [A5290] Funding Source: Medline
- Medical Research Council Funding Source: Medline
- Wellcome Trust Funding Source: Medline
The DNA of all cells is continually under assault from a wide range of DNA-damaging agents. To counter this threat to their genetic integrity, cells possess systems, collectively known as the DDR (DNA-damage response), to detect DNA damage, signal its presence and mediate its repair. In the present article, I provide an overview of the DDIR and then describe how work in my laboratory and elsewhere has identified some of the key protein players that mediate cellular responses to the most cytotoxic form of DNA damage: the DNA DSB (double-strand break). I also discuss some of my laboratory's recent work, which has revealed that the way cells respond to DSBs is modulated in a cell-cycle-dependent manner to ensure that the cell uses the DSB repair system that is most suited to its cell-cycle stage. Finally, I explain how our increasing knowledge of the DDR is suggesting new avenues for treating cancer and provide an example of a DDR-inhibitory drug that is showing promise in clinical trials.
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