DNA replication stress: a source of APOBEC3B expression in breast cancer

被引：12

作者：

Cescon, David W. ^{[1
,2
,3
]}

Haibe-Kains, Benjamin ^{[1
,4
,5
,6
]}

机构：

[1] Univ Hlth Network, Princess Margaret Canc Ctr, Toronto, ON, Canada

[2] Campbell Family Inst Breast Canc Res, Toronto, ON, Canada

[3] Univ Toronto, Dept Med, Div Med Oncol & Hematol, Toronto, ON, Canada

[4] Univ Toronto, Dept Med Biophys, Toronto, ON, Canada

[5] Univ Toronto, Dept Comp Sci, Toronto, ON, Canada

[6] Ontario Inst Canc Res, Toronto, ON, Canada

来源：

GENOME BIOLOGY | 2016年 / 17卷

关键词：

MUTATIONAL PROCESSES; POLYMORPHISM; MUTAGENESIS; DELETION;

D O I：

10.1186/s13059-016-1069-y

中图分类号：

Q81 [生物工程学（生物技术）]; Q93 [微生物学];

学科分类号：

071005 ; 0836 ; 090102 ; 100705 ;

摘要：

APOBEC cytidine deaminases have been implicated as major contributors to the mutation burden in many cancers on the basis of their mutational signature. A new experimental study sheds light on the inciting factors, linking APOBEC3B expression to oncogene-and drug-induced replication stress.

引用

页数：3

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