Ultraviolet radiation and cutaneous malignant melanoma

Oncogene. 2003 May 19;22(20):3099-112. doi: 10.1038/sj.onc.1206450.

Abstract

Recent years have seen a steady rise in the incidence of cutaneous malignant melanoma worldwide. Although it is now appreciated that the key to understanding the process by which melanocytes are transformed into malignant melanoma lies in the interplay between genetic factors and the ultraviolet (UV) spectrum of sunlight, the nature of this relation has remained obscure. Recently, prospects for elucidating the molecular mechanisms underlying such gene-environment interactions have brightened considerably through the development of UV-responsive experimental animal models of melanoma. Genetically engineered mice and human skin xenografts constitute novel platforms upon which to build studies designed to elucidate the pathogenesis of UV-induced melanomagenesis. The future refinement of these in vivo models should provide a wealth of information on the cellular and genetic targets of UV, the pathways responsible for the repair of UV-induced DNA damage, and the molecular interactions between melanocytes and other skin cells in response to UV. It is anticipated that exploitation of these model systems will contribute significantly toward the development of effective approaches to the prevention and treatment of melanoma.

Publication types

  • Review

MeSH terms

  • Animals
  • Apoptosis / radiation effects
  • Cell Cycle / physiology
  • Cell Cycle / radiation effects
  • Cyprinodontiformes / genetics
  • DNA Damage / physiology
  • DNA Repair / physiology
  • Disease Models, Animal*
  • Hepatocyte Growth Factor / genetics
  • Humans
  • Melanoma / epidemiology
  • Melanoma / etiology*
  • Melanoma / pathology
  • Mice
  • Mice, Transgenic
  • Opossums / genetics
  • Skin Neoplasms / epidemiology
  • Skin Neoplasms / etiology*
  • Skin Neoplasms / pathology
  • Skin Transplantation / methods
  • Sunlight / adverse effects
  • Transplantation, Heterologous
  • Ultraviolet Rays / adverse effects*

Substances

  • Hepatocyte Growth Factor