Journal
DNA REPAIR
Volume 94, Issue -, Pages -Publisher
ELSEVIER
DOI: 10.1016/j.dnarep.2020.102905
Keywords
APOBEC mutations; Cancer mutagenesis; Mutational signature; Kataegis; Chromothripsis; Cancer cell lines
Categories
Funding
- NCI [R00CA212290]
- Pew Charitable Trusts
- V Foundation
- Starr Cancer Consortium
- Emerald Foundation
- Geoffrey Beene Center at MSKCC
- NIH/NCI Cancer Center Support Grant [P30 CA008748]
- European Molecular Biology Organization (EMBO) LongTerm Fellowship [ALTF 760-2019]
- Ludwig Center at MSKCC
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The APOBEC family of cytidine deaminases has been proposed to represent a major enzymatic source of mutations in cancer. Here, we summarize available evidence that links APOBEC deaminases to cancer mutagenesis. We also highlight newly identified human cell models of APOBEC mutagenesis, including cancer cell lines with suspected endogenous APOBEC activity and a cell system of telomere crisis-associated mutations. Finally, we draw on recent data to propose potential causes of APOBEC misregulation in cancer, including the instigating factors, the relevant mutator(s), and the mechanisms underlying generation of the genome-dispersed and clustered APOBEC-induced mutations.
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