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Low Incidence of p53 Mutations in UVA (365-nm)-induced Skin Tumors in Hairless Mice¹

Laboratories of Health Effects Research [H. J. v. K., A. d. V., C. F. v. K.] and Pathology [P. W. W.], National Institute of Public Health and the Environment, P. O. Box 1, 3720 BA Bilthoven, and Department of Dermatology, University Hospital Utrecht [A. d. L., R. J. W. B., F. R. d. G.], the Netherlands

Mutations with clear "UVB fingerprints" have been observed in the p53 gene of human nonmelanoma skin tumors and of experimentally UVB-induced murine skin tumors. Although UVA (315–400 nm) radiation is also a complete carcinogen, its contribution to sunlight-induced mutagenesis remains poorly characterized. There is experimental evidence that the production of reactive oxygen species plays a more dominant role with long-wave UVA than with UVB radiation. We have induced skin tumors (n = 42) in hairless SKH:HR1 mice (n = 14) by daily exposure to long-wave UVA (365-nm) radiation. The incidence of p53 alterations in these tumors is low compared to UVB-induced tumors; positive staining for the p53 protein was observed in only 50% of the tumors, and less than 15% of the tumors showed a mutation in one of the exons 5, 7, or 8 of the p53 gene. The pattern of p53 staining was more irregular and less dense compared to UVB, and the mutations (all CT) were mainly (six of seven) located at codon 267. Besides a general p53 hotspot, this codon is also the main hotspot for UVB-induced skin tumors in these mice. No mutations specific for UVA, i.e., mutations specific for reactive oxygen species, could be detected.

¹ Partially financed by grant ENV4-CT96-0172 of the European Union.

² To whom requests for reprints should be addressed.

Received 12/11/96. Accepted 2/14/97.

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