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Correspondence
December 1999

Analysis of the TP53 Gene in Normal Skin and Hair Follicle Samples From Sun-Exposed and Non–Sun-Exposed Sites on Normal and Albino Individuals Living in Southeast Brazil

Author Affiliations
 

Copyright 1999 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.1999

Arch Dermatol. 1999;135(12):1559-1560. doi:10-1001/pubs.Arch Dermatol.-ISSN-0003-987x-135-12-dlt1299

Nonmelanoma skin cancers (NMSCs) are the most common malignant neoplasms in white populations. Epidemiological studies have revealed a positive correlation between the incidence of NMSCs and UV exposure, as well as an inverse relationship with the degree of skin pigmentation.1 The early role of sunlight in cutaneous carcinogenesis is supported by the finding of UV-induced mutations in the TP53 tumor suppressor gene in precancerous lesions and in chronically sun-exposed epidermis. TP53 mutations may accumulate in normal skin, with a frequency that directly reflects an individual's skin type and sun exposure and serves as an initial step that starts the cells on a path toward cancer.2TP53-mutated clones have been detected in normal interfollicular epidermis as well as in hair follicles, which are the locations of the presumed stem cells in skin and appear to be the source of tumors in experimental animals.3

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