The scientific basis of skin cancer

J Am Acad Dermatol. 2000 Jan;42(1 Pt 2):18-22. doi: 10.1067/mjd.2000.103340.


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.

Publication types

  • Review

MeSH terms

  • Apoptosis
  • Carcinoma, Squamous Cell / genetics*
  • Genes, p53 / genetics*
  • Humans
  • Keratosis / genetics*
  • Mutation
  • Photosensitivity Disorders / genetics*
  • Skin Neoplasms / genetics*
  • Ultraviolet Rays / adverse effects