Photocarcinogenesis: UVA vs. UVB Radiationde Gruijl F.R.
Department of Dermatology, Leiden University Medical Center/LUMC, Leiden, Netherlands
Do you have an account?
- Rent for 48h to view
- Buy Cloud Access for unlimited viewing via different devices
- Synchronizing in the ReadCube Cloud
- Printing and saving restrictions apply
Rental: USD 8.50
Cloud: USD 20.00
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
Jagger J: Introduction to Research in Ultraviolet Radiation Photobiology. Englewood Cliffs, Prentice-Hall, 1967, pp 54–59, 102–110.
- Peak JG, Peak MJ, Carnes BA: Induction of direct and indirect single-strand breaks in human cell DNA by far- and near-ultraviolet radiations: Action spectrum and mechanisms. Photochem Photobiol 1987;45:381–387.
- Serrano M, Lin WA, McCurrach ME, Beach D, Lowe SW: Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a. Cell 1997;88:593–602.
- Dahmane N, Lee J, Robins P, Heller P, Ruiz i Altaba A: Activation of the transcription factor Gli1 and the sonic hedgehog signalling pathway in skin tumours. Nature 1997;389:876–881.
- Ziegler A, Leffell DJ, Kunala S, Sharma HW, Gailani M, Simon JA, Halperin AJ, Baden HP, Shapiro PE, Bale AE, Brash DE: Mutation hotspots due to sunlight in the p53 gene of nonmelanoma skin cancers. Proc Natl Acad Sci USA 1993;90:4216–4220.
- Brash DE, Rudolph JA, Simon JA, Lin A, McKenna GJ, Baden HP, Halperin AJ, Ponten J: A role for sunlight in skin cancer: UV-induced p53 mutations in squamous cell carcinomas. Proc Natl Acad Sci USA 1991;88:10124–10128.
- van ‘t Veer LJ, Burgering BMT, Versteeg R, Boot AJM, Ruiter DJ, Osanto S, Schrier PI, Bos JL: N-ras mutations in human cutaneous melanoma from sun-exposed body sites. Mol Cell Biol 1989;9:3114–3116.
- Otsuka T, Takayama H, Sharp R, Celli G, LaRochelle WJ, Bottaro D, Ellmore N, Vieira W, Owens JW, Anver M, Merlino G: c-Met autocrine activation induced development of malignant melanoma and acquisition of the metastatic phenotype. Cancer Res 1998;58:5157–5167.
- Noonan FP, Recio JA, Takayama H, Duray P, Anver MR, Rush WL, De Fabo EC, Merlino G: Neonatal sunburn and melanoma in mice. Nature 2001;413:271–271.
- Kamb A, Gruis NA, Weaver-Feldhaus J, Liu Q, Harshman K, Tavtigian SV, Stockert E, Day RS 3rd, Johnson BE, Skolnick MH: A cell cycle regulator potentially involved in genesis of many tumor types. Science 1994;264:436–440.
- Funk JO, Schiller PI, Barrett MT, Wong DJ, Kind P, Sander CA: p16INK4a expression is frequently decreased and associated with 9p21 loss of heterozygosity in sporadic melanoma. J Cutan Pathol 1998;25:291–296.
- Dumaz N, van Kranen HJ, de Vries A, Berg RJW, Wester PW, van Kreijl CF, Sarasin A, Daya-Grosjean L, de Gruijl FR: The role of UVB light in skin carcinomas through the analysis of p53 mutations in squamous cell carcinomas of hairless mice. Carcinogenesis 1997;18:897–904.
- Kielbassa C, Roza L, Epe B: Wavelength dependence of oxidative DNA damage induced by UV and visible light. Carcinogenesis 1997;18:811–816.
- Shibutani S, Takeshita M, Grollman AP: Insertion of specific bases during DNA synthesis past the oxidation-damaged base 8-oxo-G. Nature 1991;349:431–434.
- van Kranen HJ, de Laat JMT, van de Ven J, Wester PW, de Vries A, Berg RJW, van Kreijl, CF, de Gruijl FR: Low incidence of p53 mutations in UVA (365 nm)-induced skin tumors in hairless mice. Cancer Res 1997;57:1238–1240.
- Kelfkens G, de Gruijl FR, van der Leun JC: Tumorigenesis by short-wave ultraviolet A: Papillomas versus squamous cell carcinomas. Carcinogenesis 1991;12:1377–1382.
de Laat JMT, de Gruijl FR: The role of UVA in the aetiology of non-melanoma skin cancer; in Leigh IM, Newton Bishop JA, Kripke ML (eds): Cancer Survey: Skin Cancer, vol 26. New York, Cold Spring Harbor Laboratory Press, 1996, pp 173–191.
Article / Publication Details
Copyright / Drug Dosage / DisclaimerCopyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.
Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.