Slow repair of pyrimidine dimers at p53 mutation hotspots in skin cancer

See allHide authors and affiliations

Science  11 Mar 1994:
Vol. 263, Issue 5152, pp. 1436-1438
DOI: 10.1126/science.8128225


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.

Stay Connected to Science