Vitamin D receptor, UVR, and skin cancer: a potential protective mechanism
- PMID: 18787544
- PMCID: PMC9017605
- DOI: 10.1038/jid.2008.249
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?
Conflict of interest statement
CONFLICT OF INTEREST
The author states no conflict of interest.
Comment on
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Inactivation of the vitamin D receptor enhances susceptibility of murine skin to UV-induced tumorigenesis.J Invest Dermatol. 2008 Oct;128(10):2508-17. doi: 10.1038/jid.2008.131. Epub 2008 May 29. J Invest Dermatol. 2008. PMID: 18509362 Free PMC article.
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