The scientific basis of skin cancer.
BACKGROUND
Mutations in tumor suppressor gene p53 are very common in many human cancers. They are present in more than 90% of squamous cell carcinomas (SCCs) and are usually found in actinic keratoses (AKs). Data demonstrate a strong relationship between the early effects of ultraviolet radiation (UVR) on p53 in skin and the development of AK and SCC.


OBJECTIVE
The purpose of this article is to review specific data about the p53 tumor suppressor gene, UVR, and their interaction to cause AKs.


METHODS
The published, peer-reviewed literature is reviewed and a published proposal for the mechanism for UVR-induced carcinogenesis is explained.


RESULTS
The specific effect of UVR on the p53 tumor suppressor gene, including its impact on apoptosis, in humans, and in animals, suggests a cause-effect relationship between UVR and the earliest mutations seen in AKs.


CONCLUSIONS
AKs result from UVR in a process by which UVR mutates a known tumor suppressor gene (p53). It is likely that the mutated cells expand preferentially in a clonal fashion at the expense of the normal surrounding keratinocytes to develop into a clinical lesion of AK.
Leffell
D J
DJ
Department of Dermatology, Section of Dermatologic Surgery and Cutaneous Oncology, and the Department of Surgery, Yale School of Medicine, CT, USA.
D017209:Apoptosis; D002294:Carcinoma, Squamous Cell / Q000235:genetics*; D016158:Genes, p53 / Q000235:genetics*; D006801:Humans; D007642:Keratosis / Q000235:genetics*; D009154:Mutation; D010787:Photosensitivity Disorders / Q000235:genetics*; D012878:Skin Neoplasms / Q000235:genetics*; D014466:Ultraviolet Rays / Q000009:adverse effects