Studies of genomic copy number changes in human cancers reveal signatures of DNA replication stress

被引：59

作者：

Dereli-Oez, Ayguel ^{[1
]}

Versini, Gwennaelle ^{[1
]}

Halazonetis, Thanos D. ^{[1
,2
]}

机构：

[1] Univ Geneva, Dept Mol Biol, CH-1205 Geneva, Switzerland

[2] Univ Geneva, Dept Biochem, CH-1205 Geneva, Switzerland

来源：

MOLECULAR ONCOLOGY | 2011年 / 5卷 / 04期

关键词：

Genomic deletions; Copy number changes; DNA replication stress; Common fragile sites; Large genes; TUMOR-SUPPRESSOR GENE; COMMON FRAGILE SITES; ONCOGENE-INDUCED SENESCENCE; COLORECTAL CANCERS; DAMAGE RESPONSE; INSTABILITY; MICE; MUTATIONS; TUMORIGENESIS; CHROMOSOMES;

D O I：

10.1016/j.molonc.2011.05.002

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Human cancers are characterized by the presence of genomic instability. Recently, two studies have catalogued the presence of a specific class of genomic aberrations, large deletions and insertions, in a few thousand human cancers and reported that most of the prevalent recurrent focal deletions targeted common fragile sites and large genes. In various experimental systems, deletions in common fragile sites and large genes have been linked to the presence of DNA replication stress. Thus, taken together, these results suggest the presence of DNA replication stress in human cancers, consistent with the recently proposed oncogene-induced DNA damage model for cancer development. (C) 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

引用

页码：308 / 314

页数：7