An APOBEC3A hypermutation signature is distinguishable from the signature of background mutagenesis by APOBEC3B in human cancers
Open accessAbstract
Elucidation of mutagenic processes shaping cancer genomes is a fundamental problem whose solution promises insights into new treatment, diagnostic and prevention strategies. Single-strand DNA-specific APOBEC cytidine deaminase(s) are major source(s) of mutation in several cancer types. Previous indirect evidence implicated APOBEC3B as the more likely major mutator deaminase, whereas the role of APOBEC3A is not established. Using yeast models enabling the controlled generation of long single-strand genomic DNA substrates, we show that the mutation signatures of APOBEC3A and APOBEC3B are statistically distinguishable. We then apply three complementary approaches to identify cancer samples with mutation signatures resembling either APOBEC. Strikingly, APOBEC3A-like samples have over tenfold more APOBEC-signature mutations than APOBEC3B-like samples. We propose that APOBEC3A-mediated mutagenesis is much more frequent because APOBEC3A itself is highly proficient at generating DNA breaks, whose repair can trigger the formation of single-strand hypermutation substrates.
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DNA polymerase η is thought to scan a limited length of DNA to mutate nucleotides in a preferred motif.
“pol h is thought to scan a limited length of DNA to mutate nucleotides in a preferred motif 36,54 .”
From DNA polymerase <b>η</b> mutational signatures are found in a variety of different types of cancer (2018) · cites this paper as [54]
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- Authors
- Chan, K., Roberts, S. A., Klimczak, L. J., Sterling, J. F., Saini, N., Malc, E. P., Kim, J., Kwiatkowski, D. J., Fargo, D. C., Mieczkowski, P. A., Getz, G., & Gordenin, D. A.
- Affiliations
- National Institutes of Health (US)
- University of North Carolina at Chapel Hill (US)
- Broad Institute (US)
- Corresponding author
- Gordenin, Dmitry A
- ORCID
- Venue
- Nature Genetics
- Published
- 2015-08-10
- Volume
- 47
- Issue
- 9
- Pages
- 1067-1072
- ISSN
- 1061-4036 (ISSN-L)
- 1546-1718
- PMC
- PMC4594173
- OpenAlex
- W2204392137
- Cited by
- 414
- References
- 52
- Citations by year
- 2026: 21 · 2025: 24 · 2024: 31 · 2023: 49 · 2022: 37 · 2021: 46 · 2020: 48 · 2019: 46 · 2018: 30 · 2017: 46 · 2016: 31 · 2015: 5
- FWCI
- 12.35
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nature Genetics (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- Funders
- National Institutes of Health (Z99-ES999999)
- U.S. Public Health Service (Z1AES103266)
- National Cancer Institute (U24CA143845, P01CA120964)
- National Institute of General Medical Sciences (R01GM052319)
- National Institute of Environmental Health Sciences (K99ES024424, R00ES022633, ZIAES103266)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Carcinogens and Genotoxicity Assessment
- Keywords
- APOBEC3A, APOBEC3B, cytosine deaminase, mutational signatures, hypermutation, single-stranded DNA, DNA strand breaks, DNA repair, cancer genomics, mutagenesis
- MeSH terms
- Base Sequence, Cytidine Deaminase, DNA Mutational Analysis, Humans, Mutation, Neoplasms, Proteins, Minor Histocompatibility Antigens, Mutagenesis, DNA Breaks, Double-Stranded
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