Journal
CANCER DISCOVERY
Volume 5, Issue 7, Pages 704-712Publisher
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/2159-8290.CD-15-0344
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Funding
- CRUK
- Rosetrees Trust
- EU [259303]
- Prostate Cancer Foundation
- European Research Council (Theseus)
- Breast Cancer Research Foundation
- National Institute for Health Research University College London Hospitals Biomedical Research Centre
- Department of Defense Breast Cancer Research Program [BC121347]
- Jimmy V Foundation for Cancer Research
- Norwegian Centennial Chair Program
- Minnesota Partnership for Biotechnology and Medical Genomics
- Randy Shaver Cancer Research and Community Fund
- U.S. National Science Foundation [DGE 13488264]
- Cancer Research UK [17786, 19310] Funding Source: researchfish
- Rosetrees Trust [M179, M391] Funding Source: researchfish
- The Francis Crick Institute [10172, 10303, 10174, 10170, 10359, 10169] Funding Source: researchfish
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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.
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