DNA Double-strand Break Repair in a Cellular Context

被引：118

作者：

Shibata, A. ^{[1
]}

Jeggo, P. A. ^{[2
]}

机构：

[1] Gunma Univ, Adv Sci Res Leaders Dev Unit, Maebashi, Gunma 371, Japan

[2] Life Sci Univ Sussex, Genome Damage & Stabil Ctr, Brighton, E Sussex, England

来源：

CLINICAL ONCOLOGY | 2014年 / 26卷 / 05期

基金：

英国医学研究理事会;

关键词：

DNA damage response signalling; DNA non-homologous end-joining; DSB repair; homologous recombination; radiation; radiotherapy; HOMOLOGOUS RECOMBINATION; CRYSTAL-STRUCTURE; 53BP1; ATM; PATHWAY; BRCA1; TRANSCRIPTION; RECOGNITION; COOPERATION; MECHANISM;

D O I：

10.1016/j.clon.2014.02.004

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Substantial insight into the mechanisms responding to DNA double-strand breaks has been gained from molecular, biochemical and structural approaches. Attention is now focusing on understanding the interplay between the pathways, how they interface through the cell cycle and the communication with other DNA transactions, such as replication and transcription. Understanding these aspects will facilitate an assessment of how cancer cells have modified these processes to achieve unlimited proliferative capacity and adaptability, and pave the way to identify targets suitable for therapy. Here, we briefly overview the processes responding to double-strand breaks and discuss our current understanding of their interplay in a cellular context. (C) 2014 The Royal College of Radiologists. Published by Elsevier Ltd. All rights reserved.

引用

页码：243 / 249

页数：7

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