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Science 11 March 1994:
Vol. 263. no. 5152, pp. 1436 - 1438
DOI: 10.1126/science.8128225
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Articles

Science, Vol 263, Issue 5152, 1436-1438
Copyright © 1994 by American Association for the Advancement of Science

articles

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

S Tornaletti and GP Pfeifer

Beckman Rsearch Institute of the City of Hope, Department of Biology, Duarte, CA 91010.

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.


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The Multilayered Organization of Engineered Human Skin Does Not Influence the Formation of Sunlight-induced Cyclobutane Pyrimidine Dimers in Cellular DNA.
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A p53-independent damage-sensing mechanism that functions as a checkpoint at the G1/S transition in Chinese hamster ovary cells.
H. Lee, J. M. Larner, and J. L. Hamlin (1997)
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Effects of Aminofluorene and Acetylaminofluorene DNA Adducts on Transcriptional Elongation by RNA Polymerase II.
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DNA repair rates mapped along the human PGK1 gene at nucleotide resolution.
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Science 263, 1438-1440
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