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

Science. 1994 Mar 11;263(5152):1436-8. 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.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Cells, Cultured
  • DNA Repair*
  • Exons
  • Genes, p53*
  • HeLa Cells
  • Humans
  • Mutation
  • Phosphoglycerate Kinase / genetics
  • Polymerase Chain Reaction
  • Pyrimidine Dimers / metabolism*
  • Skin / metabolism
  • Skin / radiation effects*
  • Skin Neoplasms / genetics*
  • Skin Neoplasms / metabolism
  • Ultraviolet Rays


  • Pyrimidine Dimers
  • Phosphoglycerate Kinase