Int. J. Mol. Sci. 2013, 14(6), 12222-12248; doi:10.3390/ijms140612222
John D'Orazio 1,* , Stuart Jarrett 2, Alexandra Amaro-Ortiz 3 and Timothy Scott 3
1 Graduate Center for Toxicology and the Departments of Pediatrics, Biomedical and Molecular Pharmacology and Physiology, Markey Cancer Center, University of Kentucky College of Medicine, 800 Rose Street, Lexington, KY 40536, USA 2 Markey Cancer Center, University of Kentucky College of Medicine, 800 Rose Street, Lexington, KY 40536, USA 3 Graduate Center for Toxicology, University of Kentucky College of Medicine, 800 Rose Street, Lexington, KY 40536, USA
*jdorazio@uky.edu.
Received: 25 April 2013; in revised form: 18 May 2013 / Accepted: 24 May 2013 / Published: 7 June 2013
(This article belongs to the Special Issue Radiation Toxicity in Cells)
UV radiation (UV) is classified as a “complete carcinogen” because it is both a mutagen and a non-specific damaging agent and has properties of both a tumor initiator and a tumor promoter. In environmental abundance, UV is the most important modifiable risk factor for skin cancer and many other environmentally-influenced skin disorders. However, UV also benefits human health by mediating natural synthesis of vitamin D and endorphins in the skin, therefore UV has complex and mixed effects on human health. Nonetheless, excessive exposure to UV carries profound health risks, including atrophy, pigmentary changes, wrinkling and malignancy. UV is epidemiologically and molecularly linked to the three most common types of skin cancer, basal cell carcinoma, squamous cell carcinoma and malignant melanoma, which together affect more than a million Americans annually. Genetic factors also influence risk of UV-mediated skin disease. Polymorphisms of the melanocortin 1 receptor (MC1R) gene, in particular, correlate with fairness of skin, UV sensitivity, and enhanced cancer risk. We are interested in developing UV-protective approaches based on a detailed understanding of molecular events that occur after UV exposure, focusing particularly on epidermal melanization and the role of the MC1R in genome maintenance.
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Made statement: 5 sunburns doubles the risk of skin cancer