title: Slow repair of pyrimidine dimers at p53 mutation hotspots in skin cancer.
abstract: Ultraviolet light has been linked with the development of human skin cancers. Such cancers often exhibit mutations in the p53 tumor suppressor gene. Ligation-mediated polymerase chain reaction was used to analyze at nucleotide resolution the repair of cyclobutane pyrimidine dimers along the p53 gene in ultraviolet-irradiated human fibroblasts. Repair rates at individual nucleotides were highly variable and sequence-dependent. Slow repair was seen at seven of eight positions frequently mutated in skin cancer, suggesting that repair efficiency may strongly contribute to the mutation spectrum in a cancer-associated gene.
authors.affiliation: Beckman Rsearch Institute of the City of Hope, Department of Biology, Duarte, CA 91010.
authors.forename: S
authors.initials: S
authors.lastname: Tornaletti
authors.forename: G P
authors.initials: GP
authors.lastname: Pfeifer
mesh_terms: D002478:Cells, Cultured; D004260:DNA Repair; D005091:Exons; D016158:Genes, p53; D006367:HeLa Cells; D006801:Humans; D009154:Mutation; D010735:Phosphoglycerate Kinase / Q000235:genetics; D016133:Polymerase Chain Reaction; D011740:Pyrimidine Dimers / Q000378:metabolism*; D012867:Skin / Q000378:metabolism / Q000528:radiation effects*; D012878:Skin Neoplasms / Q000235:genetics* / Q000378:metabolism; D014466:Ultraviolet Rays
chemical_list: D011740:Pyrimidine Dimers; D010735:Phosphoglycerate Kinase