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J Am Acad Dermatol. 2000 Jan;42(1 Pt 2):18-22.

The scientific basis of skin cancer.

Author information

1
Department of Dermatology, Section of Dermatologic Surgery and Cutaneous Oncology, and the Department of Surgery, Yale School of Medicine, CT, USA.

Abstract

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.

PMID:
10607352
[Indexed for MEDLINE]

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