title: Vitamin D receptor, UVR, and skin cancer: a potential protective mechanism.
abstract: More than 1 million skin cancers occur annually in the United States--of which 80% are basal-cell carcinoma (BCC), 16% are squamous-cell carcinoma (SCC), and 4% are melanomas--making skin cancer by far the most common cancer (Greenlee et al., 2001). UVR is the major etiologic agent. UV wavelengths shorter than 280 nm (UVC) are absorbed by the ozone layer and do not reach the earth. UV wavelengths longer than 320 nm (UVA) have limited ability to induce the characteristic mutations in DNA seen in epidermal cancers. Thus, UVB, with a spectrum between 280 and 320 nm, is the major cause of these cancers (Freeman et al., 1989), but this is the same spectrum required for vitamin D production in the skin. Is there a link?
authors.affiliation: Department of Medicine, University of California San Francisco/VA Medical Center, San Francisco, California 94121, USA. daniel.bikle@ucsf.edu
authors.forename: Daniel D
authors.initials: DD
authors.lastname: Bikle
mesh_terms: D000818:Animals; D006801:Humans; D009381:Neoplasms, Radiation-Induced / Q000517:prevention & control*; D018167:Receptors, Calcitriol / Q000378:metabolism*; D012867:Skin / Q000378:metabolism; D012878:Skin Neoplasms / Q000209:etiology* / Q000517:prevention & control*; D025521:Tumor Suppressor Proteins / Q000378:metabolism; D014466:Ultraviolet Rays / Q000009:adverse effects*; D014807:Vitamin D / Q000378:metabolism
chemical_list: D018167:Receptors, Calcitriol; D025521:Tumor Suppressor Proteins; D014807:Vitamin D
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