Medizinische Universität Graz - Research portal
Selected Publication:
SHR Neuro Cancer Cardio Lipid Metab Microb
Wolf, P; Kreimer-Erlacher, H; Seidl, H; Bäck, B; Soyer, HP; Kerl, H.
The ultraviolet fingerprint dominates the mutational spectrum of the p53 and Ha-ras genes in psoralen + ultraviolet A keratoses from psoriasis patients.
J Invest Dermatol. 2004; 122(1):190-200
Doi: 10.1046/j.0022-202X.2004.22118.x
[OPEN ACCESS]
Web of Science
PubMed
FullText
FullText_MUG
Google Scholar
- Leading authors Med Uni Graz
- Wolf Peter
- Co-authors Med Uni Graz
- Kerl Helmut
- Seidl Hannes
- Soyer Hans Peter
- Altmetrics:
- Dimensions Citations:
- Plum Analytics:
- Scite (citation analytics):
- Abstract:
- Psoriasis patients exposed to high cumulative doses of psoralen + ultraviolet A frequently exhibit so-called "psoralen + ultraviolet A keratoses" (i.e., hyperkeratotic lesions with varying degrees of histologic atypia). The exact causes and molecular mechanisms of psoralen + ultraviolet A keratoses however, are not clear. We therefore performed DNA mutational analysis of the tumor suppressor gene p53 (exons in psoralen + ultraviolet A keratoses from 10 long-term psoralen + ultraviolet A-treated psoriasis patients. We detected 39 p53 mutations in 16 of 28 psoralen + ultraviolet A keratoses (57%) and 18 Ha-ras mutations in 11 of 25 psoralen + ultraviolet A keratoses (44%). Of the 39 p53 mutations and 18 Ha-ras mutations, 22 (56%) and 13 (72%), respectively, were of the ultraviolet fingerprint type (C-->T or CC-->TT transitions at dipyrimidine sites); 13 (33%) and two (11%), respectively, occurred at potential psoralen-binding sites (5'-TpA, 5'-TpG, or 5'-TpT DNA sequences) and were potentially psoralen + ultraviolet A induced; two (5%) and three (17%), respectively, were of ambiguous origin (ultraviolet and/or psoralen + ultraviolet A); and two (5%) and none (0%), respectively, were of the "other" type, respectively. We conclude that (1) the frequent mutation of p53 and Ha-ras may play a key part in the formation of at least some psoralen + ultraviolet A keratoses; (2) environmental and/or therapeutic ultraviolet exposure may be a major cause of psoralen + ultraviolet A keratosis as most Ha-ras and p53 mutations are induced by ultraviolet light; and (3) psoralen + ultraviolet A itself plays a smaller, though direct, role in causing these mutations.
- Find related publications in this database (using NLM MeSH Indexing)
- Adult -
- Carcinoma, Squamous Cell - epidemiology
- Female -
- Ficusin - adverse effects
- Genes, p53 - genetics
- Genes, ras - genetics
- Humans -
- Keratosis - drug therapy
- Male -
- Middle Aged -
- Mutation, Missense -
- Neoplasms, Radiation-Induced - epidemiology
- PUVA Therapy - adverse effects
- Psoriasis - drug therapy
- Radiation-Sensitizing Agents - adverse effects
- Risk Factors -
- Skin Neoplasms - epidemiology
- Ultraviolet Rays -
- Find related publications in this database (Keywords)
- carcinogenesis
- mutagenesis
- psoralen
- skin cancer
- ultraviolet radiation