{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T04:26:04Z","timestamp":1790915164780,"version":"4.1.0"},"reference-count":34,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2004,2,22]],"date-time":"2004-02-22T00:00:00Z","timestamp":1077408000000},"content-version":"vor","delay-in-days":52,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Environ and Mol Mutagen"],"published-print":{"date-parts":[[2004,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Ultraviolet radiation (UVR) exposure may protect against prostate cancer development via a mechanism involving vitamin D. The vitamin D receptor (<jats:italic>VDR<\/jats:italic>) gene is therefore a candidate susceptibility factor for prostate cancer. This possibility has been previously investigated with conflicting results. We examined the association of <jats:italic>VDR<\/jats:italic> genotypes (variants at the <jats:italic>CDX\u20102<\/jats:italic>, <jats:italic>Fok<\/jats:italic>1, and <jats:italic>Taq<\/jats:italic>1 sites), haplotypes, and genotype combinations with risk by studying 368 prostate cancer and 243 benign prostatic hypertrophy (BPH) patients. <jats:italic>CDX\u20102<\/jats:italic>, <jats:italic>Fok<\/jats:italic>1, and <jats:italic>Taq<\/jats:italic>1 genotype and haplotype frequencies were not significantly different in cancer and BPH patients. As the impact of <jats:italic>VDR<\/jats:italic> polymorphisms may depend on UVR exposure, we studied associations of variants with risk in men stratified into low (below median) and high (above median) cumulative exposure\/year groups. In men with UVR exposure above the median (1,100 hr\/year), <jats:italic>CDX\u20102<\/jats:italic> GA and AA (odds ratios [OR] = 2.11 and 2.02, respectively) and <jats:italic>Fok<\/jats:italic>1 ff (OR = 2.91) were associated with increased prostate cancer risk. No associations were observed for <jats:italic>Taq<\/jats:italic>1 genotypes. Of the genotype combinations, relative to all other <jats:italic>CDX\u20102<\/jats:italic> and <jats:italic>Taq<\/jats:italic>1 and combinations, GGTT (<jats:italic>P<\/jats:italic> = 0.022, OR = 0.30), and relative to all other <jats:italic>Fok<\/jats:italic>1 and <jats:italic>Taq<\/jats:italic>1 combinations, FFTT (<jats:italic>P<\/jats:italic> = 0.026, OR = 0.35) were associated with reduced prostate cancer risk in the presence of the main effects. None of the other two\u2010 or three\u2010genotype combinations was associated with risk. These data indicate that <jats:italic>VDR<\/jats:italic> variants influence prostate cancer risk and that this association is dependent on the extent of UVR exposure. Environ. Mol. Mutagen. 43:121\u2013127, 2004. \u00a9 2004 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/em.20000","type":"journal-article","created":{"date-parts":[[2004,2,26]],"date-time":"2004-02-26T20:37:34Z","timestamp":1077827854000},"page":"121-127","source":"Crossref","is-referenced-by-count":59,"title":["Polymorphisms in the vitamin D receptor gene, ultraviolet radiation, and susceptibility to prostate cancer"],"prefix":"10.1002","volume":"43","author":[{"given":"Dhaval","family":"Bodiwala","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christopher J.","family":"Luscombe","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael E.","family":"French","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Samson","family":"Liu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark 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