[Photocarcinogenesis. Molecular mechanisms and preventive strategies].
Ultraviolet (UV) radiation is the main carcinogen in the development of epithelial skin cancer. A variety of biological and molecular effects in the skin have been described. In order to avoid malignant transformation, various protective mechanisms have developed in the skin, whereby p53 plays a central role. UV signature mutations in p53, Ras and INK4a/ARF as well as UV-induced NFkappaB and cyclooxygenase 2 are principally involved in photocarcinogenesis. Chemoprevention has gained increasing importance for primary prevention. Numerous natural or synthetic substances can be antiinflammatory, antioxidative, proapoptotic or antiproliferative and suppress photocarcinogenesis. Extensive clinical data exist for the use of retinoids systemically or DNA repair enzymes topically. However, clinical trials are lacking, for example for green tea, which has been shown repeatedly to be chemoprotective in vitro and in mouse models after topical or oral application.
Berking
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Klinik und Poliklinik für Dermatologie und Allergologie, Ludwig-Maximilians-Universität München, 80337, München. Carola.Berking@med.uni-muenchen.de.
D002280:Basal Cell Carcinoma / Q000235:genetics* / Q000517:prevention & control; D002294:Carcinoma, Squamous Cell / Q000235:genetics* / Q000517:prevention & control; D002471:Cell Transformation, Neoplastic / Q000235:genetics*; D004249:DNA Damage / Q000235:genetics; D004252:DNA Mutational Analysis; D004260:DNA Repair / Q000235:genetics; D006801:Humans; D009381:Neoplasms, Radiation-Induced / Q000235:genetics* / Q000517:prevention & control; D012307:Risk Factors; D012878:Skin Neoplasms / Q000235:genetics* / Q000517:prevention & control; D014466:Ultraviolet Rays / Q000009:adverse effects*