The scientific basis of skin cancer - 05/09/11
Reprint requests: David J. Leffell, MD, 800 Howard Ave, Room 481, New Haven, CT 06520.Résumé |
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.
Method |
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.
Conclusion 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.
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Vol 42 - N° 1S1
P. S18-S22 - janvier 2000 Retour au numéro
Article précédent
- Histopathology of incipient intraepidermal squamous cell carcinoma (“actinic keratosis”)
- Clay J. Cockerell
- The risk of progression to invasive disease
- Richard G. Glogau
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