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.