1. ¹Department of Epidemiology, The University of Texas M.D. Anderson Cancer Center, Houston, Texas, USA
2. ²Department of Surgical Oncology, The University of Texas M.D. Anderson Cancer Center, Houston, Texas, USA
3. ³Department of Pathology, The University of Texas M.D. Anderson Cancer Center, Houston, Texas, USA
4. ⁴Department of Dermatology, The University of Texas M.D. Anderson Cancer Center, Houston, Texas, USA
5. ⁵Department of Experimental Therapeutics, The University of Texas M.D. Anderson Cancer Center, Houston, Texas, USA

Correspondence: Dr Qingyi Wei, Department of Epidemiology, Unit 1365, The University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030, USA. E-mail: qwei@mdanderson.org

Received 25 April 2006; Revised 26 July 2006; Accepted 31 July 2006; Published online 21 September 2006.

Abstract

Sunlight causes DNA damage but also induces production of vitamin D whose metabolite 1,25-(OH)₂D₃ has antiproliferative and pro-differentiative effects in both melanocytes and cutaneous melanoma (CM) cells mediated through the vitamin D receptor (VDR). We hypothesized that genetic polymorphisms of VDR are associated with risk of CM. In a hospital-based case–control study of 602 non-Hispanic white CM patients and 603 cancer-free control subjects frequency matched by age and sex, we genotyped two VDR polymorphisms (TaqI and FokI) and assessed their association with CM risk. We found that a significantly decreased risk was associated with VDR-TaqI Tt (adjusted odds ratio (OR), 0.70; 95% confidence interval (CI), 0.54–0.90) and Tt+tt (OR=0.70; 95% CI, 0.55–0.89) genotypes, compared with the VDR-TaqI TT genotype, whereas an increased risk was associated with VDR-FokI Ff genotype (OR=1.32; 95% CI, 1.03–1.68), and a borderline significantly increased risk was associated with Ff+ff (OR=1.26; 95% CI, 1.00–1.59) genotypes, compared with the VDR-FokI FF genotype. In conclusion, genetic variants (i.e., TaqI t protective allele and FokI f risk allele) in VDR may alter risk of CM.