Douglas E Brash
教授
Department of Therapeutic Radiology
School of Medicine, Yale University;Yale Comprehensive Cancer Center;Department of Genetics, School of Medicine, Yale University;Department of Dermatology, School of Medicine, Yale University;Yale Comprehensive Cancer Center, Yale University
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his lab used the distinctive UV mutation pattern to identify genes mutated by sunlight in causing skin cancer: p53 in squamous cell carcinoma and its actinic keratosis precursor, and p53 and PTCH in basal cell carcinoma. They then showed p53 to be a key element of UV-induced apoptosis, preventing damaged cells from becoming mutants. Because the multiple-genetic-hit model of cancer predicts that our bodies harbor cells mutated in just one or another of the genes needed for cancer, the lab then sought p53-mutant cells in normal skin. These cells were not only present but were already proliferating as clones and were astonishingly common – many people carry 60,000 clones, occupying almost 5% of their epidermis. Switching to mice revealed that clonal expansion is driven by physiology, not by adding mutations. One mechanism is the mutant's resistance to UV-induced apoptosis. Another is UV's ability to tilt a clone's balance of progenitor cells and differentiating cells toward self-renewal of the progenitors. Recently the lab discovered that chemical excitation of electrons, "chemiexcitation", is a new mode of disease that uses the pigment melanin to create UV-like carcinogenic lesions even after UV exposure has ended. These results contribute to what is perhaps the best picture available of how a human carcinogen works. Another current project is identifying UV-hypersensitive genome regions for use as "genomic dosimeters" to assess a person's past sun exposure and future skin cancer risk.
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Proceedings of the National Academy of Sciences of the United States of Americano. 44 (2023)
Proceedings of the National Academy of Sciences of the United States of Americano. 20 (2023)
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Vijay Menon,Douglas E Brash
Mutation research. Reviews in mutation research (2023): 108471-108471
Cancer Prevention Researchno. 7_Supplement (2020): PR01-PR01
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Sanjay Premi, Lynn Han,Sameet Mehta,James Knight, Dejian Zhao,Antonella Bacchiocchi,Ruth Halaban,Meg A. Palmatier,Karl Kornacker,Douglas E. Brash
CANCER PREVENTION RESEARCHno. SUP7 (2020): 25-25
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