解旋酶
DNA
DNA修复
DNA复制
生物
DNA损伤
药品
遗传学
癌症研究
化学
基因
药理学
核糖核酸
作者
Andrew J. Deans,Stephen C. West
出处
期刊:Nature Reviews Cancer
[Springer Nature]
日期:2011-06-24
卷期号:11 (7): 467-480
被引量:864
摘要
Interstrand crosslinks (ICLs) are highly toxic DNA lesions that prevent transcription and replication by inhibiting DNA strand separation. Agents that induce ICLs were one of the earliest, and are still the most widely used, forms of chemotherapeutic drug. Only recently, however, have we begun to understand how cells repair these lesions. Important insights have come from studies of individuals with Fanconi anaemia (FA), a rare genetic disorder that leads to ICL sensitivity. Understanding how the FA pathway links nucleases, helicases and other DNA-processing enzymes should lead to more targeted uses of ICL-inducing agents in cancer treatment and could provide novel insights into drug resistance.
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