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Photocarcinogenesis: UVA vs. UVB Radiation

de Gruijl F.R.

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Department of Dermatology, Leiden University Medical Center/LUMC, Leiden, Netherlands

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Skin Pharmacol Appl Skin Physiol 2002;15:316–320

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Article / Publication Details

First-Page Preview
Abstract of Paper

Published online: September 16, 2002
Issue release date: September – October

Number of Print Pages: 5
Number of Figures: 0
Number of Tables: 0

ISSN: 1660-5527 (Print)
eISSN: 1660-5535 (Online)

For additional information: https://www.karger.com/SPP

Abstract

Recent research is revealing combinations of disturbed oncogenic and tumor-suppressive signaling pathways by altered or missing genes in skin cancers: mutated PTCH (in the mitogenic Sonic Hedgehog pathway) and mutated p53 tumor suppressor gene in basal cell carcinomas (BCC), possibly an activated mitogenic RAS pathway and mutated p53 in squamous cell carcinomas (SCC), and possibly an activated MET/RAS pathway and inactive p16INK4a tumor suppressor in cutaneous melanomas. UV radiation damages DNA and can give rise to genomic alterations, varying from point mutations to crude chromosomal dislocations. UVB radiation (wavelength band 280–315 nm) is more carcinogenic than UVA radiation (315–400 nm) in experimental induction of SCC. The impact of UVB radiation can be clearly inferred from the characteristic point mutations in p53 found in human SCC and BCC. In contrast to UVB radiation, much of the mutagenic and carcinogenic action of UVA radiation appears to be mediated through reactive oxygen species (ROS). Experiments have shown that UVA1 (340–400 nm) exposure induces SCC largely without the characteristic point mutations in p53. Both UVB and UVA radiation can give rise to ROS-related point mutations (e.g. G to T) and crude genomic alterations (e.g. deletions) which may not be recognized as caused by UV radiation.

© 2002 S. Karger AG, Basel


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Article / Publication Details

First-Page Preview
Abstract of Paper

Published online: September 16, 2002
Issue release date: September – October

Number of Print Pages: 5
Number of Figures: 0
Number of Tables: 0

ISSN: 1660-5527 (Print)
eISSN: 1660-5535 (Online)

For additional information: https://www.karger.com/SPP


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