APOBEC Enzymes: Mutagenic Fuel for Cancer Evolution and Heterogeneity

被引：367

作者：

Swanton, Charles ^{[1
,2
]}

McGranahan, Nicholas ^{[1
,3
]}

Starrett, Gabriel J. ^{[4
,5
]}

Harris, Reuben S. ^{[4
,5
]}

机构：

[1] Francis Crick Inst, London WC2A 3LY, England

[2] CRUK Lung Canc Ctr Excellence, UCL Canc Inst, London, England

[3] UCL, Ctr Math & Phys Life Sci & Expt Biol CoMPLEX, London, England

[4] Univ Minnesota, Inst Mol Virol, Dept Biochem Mol Biol & Biophys, Minneapolis, MN USA

[5] Univ Minnesota, Masonic Canc Ctr, Minneapolis, MN USA

来源：

CANCER DISCOVERY | 2015年 / 5卷 / 07期

基金：

美国国家科学基金会; 欧洲研究理事会;

关键词：

CHRONIC LYMPHOCYTIC-LEUKEMIA; 21 BREAST CANCERS; CHROMOSOMAL INSTABILITY; INTRATUMOR HETEROGENEITY; RESTRICTION FACTORS; LUNG-CANCER; GENETIC-HETEROGENEITY; CYTOSINE DEAMINATION; MUTATIONAL PROCESSES; CLINICAL RESISTANCE;

D O I：

10.1158/2159-8290.CD-15-0344

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Deep sequencing technologies are revealing the complexities of cancer evolution, casting light on mutational processes fueling tumor adaptation, immune escape, and treatment resistance. Understanding mechanisms driving cancer diversity is a critical step toward developing strategies to attenuate tumor evolution and adaptation. One emerging mechanism fueling tumor diversity and subclonal evolution is genomic DNA cytosine deamination catalyzed by APOBEC3B and at least one other APOBEC family member. Deregulation of APOBEC3 enzymes causes a general mutator phenotype that manifests as diverse and heterogeneous tumor subclones. Here, we summarize knowledge of the APOBEC DNA deaminase family in cancer, and their role as driving forces for heterogeneity and a therapeutic target to limit tumor adaptation. Significance: APOBEC mutational signatures may be enriched in tumor subclones, suggesting APOBEC cytosine deaminases fuel subclonal expansions and intratumor heterogeneity. APOBEC family members might represent a new class of drug target aimed at limiting tumor evolution, adaptation, and drug resistance. (C) 2015 AACR.

引用

页码：704 / 712

页数：9

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