Vitamin D receptor gene polymorphisms and prostate cancer risk

被引:52
作者
Cheteri, MBK
Stanford, JL
Friedrichsen, DM
Peters, MA
Iwasaki, L
Langlois, MC
Feng, ZD
Ostrander, EA
机构
[1] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98109 USA
[2] Univ Washington, Sch Publ Hlth & Community Med, Dept Epidemiol, Seattle, WA 98195 USA
[3] Univ Washington, Dept Microbiol, Seattle, WA 98195 USA
[4] Fred Hutchinson Canc Res Ctr, Dept Microbiol, Seattle, WA 98104 USA
[5] Fred Hutchinson Canc Res Ctr, Div Clin Res, Seattle, WA 98104 USA
[6] Fred Hutchinson Canc Res Ctr, Div Human Biol, Seattle, WA 98104 USA
关键词
BsmI; FokI; Poly-A; VDR; polymorphism; prostate cancer; genotype; relative risk; vitamin D; epidemiology;
D O I
10.1002/pros.20001
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
BACKGROUND. Vitamin D is a steroid hormone that is thought to play a role in the etiology and progression of Prostate cancer. Hormone activity requires binding to the vitamin D receptor (VDR), which contains several genetic polymorphisms that have been associated with risk of prostate cancer. To further evaluate this relationship, we conducted a population-based case-control study of the VDR BsmI, FokI, and Poly-A polymorphisms, and prostate cancer. METHODS. Germline DNA samples and survey data from incident prostate cancer cases (n = 559) and controls (n = 523) of similar age (40-64 years) without a history of the disease who resided in King County, Washington were analyzed. RESULTS. The frequency of the BsmI, FokI, and Poly-A genotypes were similar in cases and controls, and no overall association between any variants and prostate cancer risk were noted. Stratification by clinical features of disease revealed that among men with localized stage disease, the BsmI bb genotype was associated with a modest increase in risk (OR, 1.49; 95% CI, 1.02 - 2.17; P = 0.04) compared to the BB genotype. CONCLUSIONS. These results suggest that polymorphisms in the VDR gene are not strong predictors of prostate cancer risk among Caucasian men in the U.S. (C) 2003 Wiley-Liss, Inc.
引用
收藏
页码:409 / 418
页数:10
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