UV wavelength-dependent DNA damage and human non-melanoma and melanoma skin cancer

Abstract

Ultraviolet (UV) irradiation from the sun has been epidemiologically and mechanistically linked to skin cancer, a spectrum of diseases of rising incidence in many human populations. Both non-melanoma and melanoma skin cancers are associated with sunlight exposure. In this review, we discuss the UV wavelength-dependent formation of the major UV-induced DNA damage products, their repair and mutagenicity and their potential involvement in sunlight-associated skin cancers. We emphasize the major role played by the cyclobutane pyrimidine dimers (CPDs) in skin cancer mutations relative to that of (6-4) photoproducts and oxidative DNA damage. Collectively, the data implicate the CPD as the DNA lesion most strongly involved in human cancers induced by sunlight.

Figure 1. The major UVB- and UVA-induced DNA photoproducts are induced at different wavelengths

The diagram shows the subdivision of the solar UV spectrum. Shorter UV wavelengths are blocked by oxygen and ozone (stop signs). Terrestrial sunlight contains UVA and UVB components at wavelengths of ~300 nm and longer. The specific DNA lesions produced by UVA and UVB in this range of wavelengths are indicated by arrows.