Abstract
Although BRAF V600 mutations in melanocytic tumors are not UV-signature mutations, it is plausible that they could still arise from error-prone replication of UV-damaged DNA. We propose a mechanism for their origin, taking into consideration melanocytic-specific BRAF tandem mutations, nearby potential pyrimidine dimer sites, the properties of specialized DNA polymerases, and biological selection.
Publication types
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Comment
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Research Support, N.I.H., Extramural
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Review
MeSH terms
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DNA Damage*
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Humans
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Melanoma / epidemiology
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Melanoma / genetics*
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Neoplasms, Radiation-Induced / epidemiology
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Neoplasms, Radiation-Induced / genetics*
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Proto-Oncogene Proteins B-raf / genetics*
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Risk Factors
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Skin Neoplasms / epidemiology
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Skin Neoplasms / genetics*
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Ultraviolet Rays
Substances
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BRAF protein, human
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Proto-Oncogene Proteins B-raf