共济失调毛细血管扩张
癌症
癌症研究
突变
体细胞
DNA修复
生殖系
生物
种系突变
基因组不稳定性
DNA损伤
基因
遗传学
医学
DNA
作者
Michael J. Choi,Thomas J. Kipps,Razelle Kurzrock
出处
期刊:Molecular Cancer Therapeutics
[American Association for Cancer Research]
日期:2016-08-01
卷期号:15 (8): 1781-1791
被引量:308
标识
DOI:10.1158/1535-7163.mct-15-0945
摘要
Abstract Activation of checkpoint arrest and homologous DNA repair are necessary for maintenance of genomic integrity during DNA replication. Germ-line mutations of the ataxia telangiectasia mutated (ATM) gene result in the well-characterized ataxia telangiectasia syndrome, which manifests with an increased cancer predisposition, including a 20% to 30% lifetime risk of lymphoid, gastric, breast, central nervous system, skin, and other cancers. Somatic ATM mutations or deletions are commonly found in lymphoid malignancies, as well as a variety of solid tumors. Such mutations may result in chemotherapy resistance and adverse prognosis, but may also be exploited by existing or emerging targeted therapies that produce synthetic lethal states. Mol Cancer Ther; 15(8); 1781–91. ©2016 AACR.
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