SLOW REPAIR OF PYRIMIDINE DIMERS AT P53 MUTATION HOTSPOTS IN SKIN-CANCER

Ultraviolet light has been linked with the development of human skin c ancers. Such cancers often exhibit mutations in the p53 tumor suppress or gene. Ligation-mediated polymerase chain reaction was used to analy ze at nucleotide resolution the repair of cyclobutane pyrimidine dimer s along the p53 gene in ultraviolet-irradiated human fibroblasts. Repa ir rates at individual nucleotides were highly variable and sequence-d ependent. 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.