Ultraviolet radiation induced signature mutations in photocarcinogenesis

N. Wikonkál, Douglas E. Brash

Research output: Contribution to journalArticle

138 Citations (Scopus)

Abstract

The photons of sunlight begin a series of genetic events in skin leading to cancer. UV signature mutations provide an alternative to inherited mutations as a way of identifying genes that are involved in cancer development. They augment epidemiologic and clinical data by serving as molecular evidence for the role of UV radiation in skin carcinogenesis. Signature mutations are present in TP53 and PTCH, two tumor suppressor genes responsible for non-melanoma skin cancer. We review evidence that clones of TP53-mutated cells are present in normal human and murine epidermis exposed to UVB and conclude that, in addition to being a tumorigenic mutagen, sunlight acts as a tumor promoter by favoring the clonal expansion of TP53 mutated cells. These combined actions of sunlight result in normal individuals' carrying a substantial burden of keratinocytes predisposed to cancer. Thus cancer involves both a single-cell problem and a multi-cell problem; in skin cancer, sunlight appears to drive both.

Original languageEnglish
Pages (from-to)6-10
Number of pages5
JournalJournal of Investigative Dermatology Symposium Proceedings
Volume4
Issue number1
Publication statusPublished - 1999

Fingerprint

Sunlight
Radiation
Mutation
Skin Neoplasms
Neoplasms
Skin
Mutagens
Tumor Suppressor Genes
Keratinocytes
Photons
Epidermis
Carcinogens
Carcinogenesis
Clone Cells
Genes

Keywords

  • Basal cell cancer
  • P53
  • PTCH
  • Squamous cell cancer

ASJC Scopus subject areas

  • Dermatology

Cite this

Ultraviolet radiation induced signature mutations in photocarcinogenesis. / Wikonkál, N.; Brash, Douglas E.

In: Journal of Investigative Dermatology Symposium Proceedings, Vol. 4, No. 1, 1999, p. 6-10.

Research output: Contribution to journalArticle

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