¹Department of Dermatology, Boston University School of Medicine, Boston, Massachusetts, USA

Correspondence: Dr Thomas Rünger, Department of Dermatology, Boston University School of Medicine, 609 Albany Street, Boston, Massachusetts 02118, USA. E-mail: truenger@bu.edu

Abstract

The carcinogenic properties of ultraviolet (UV) light are mediated by its ability to generate DNA damage. Cellular responses to UV-induced DNA damage profoundly modulate the carcinogenic effects of UV exposures, and these responses are wavelength dependent. However, the exact contributions of different wavelengths of UV light to DNA damage, cellular damage responses, mutation, and skin carcinogenesis are incompletely understood. Given that UV-induced apoptosis is a protective cellular response to UV that prevents survival of damaged cells, inhibition of UVB-induced apoptosis by adding UVA, as reported by Ibuki et al. in this issue, may be a mechanism by which UVA augments UVB-mediated mutation and skin cancer formation.