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.
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.