Association of the G289S single nucleotide polymorphism in the HSD17B3 gene with prostate cancer in Italian men

被引:42
作者
Margiotti, K
Kim, E
Pearce, CL
Spera, E
Novelli, G
Reichardt, JKV
机构
[1] Univ So Calif, Keck Sch Med, Inst Med Genet, Los Angeles, CA 90089 USA
[2] Univ So Calif, Keck Sch Med, Dept Biochem & Mol Biol, Los Angeles, CA 90089 USA
[3] Univ Roma Tor Vergata, Dipartimento Biopatol & Diagnost Imagini, Rome, Italy
[4] Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90089 USA
关键词
androgen metabolism; 17 beta-hydroxysteroid dehydrogenase; SNP;
D O I
10.1002/pros.10134
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
BACKGROUND. Prostate cancer is a significant public health problem in this country. Substantial data support a plausible role for androgens in the etiology of this disease. The human HSD17B3 gene encodes the testicular (or type III) 17beta-hydroxysteroid dehydrogenase enzyme, which catalyzes testosterone biosynthesis in men. METHODS. We have investigated the G289S (glycine at codon 289 replaced by serine) polymorphism at the HSD17B3 locus as a candidate single nucleotide polymorphism (SNP) for prostate cancer risk in constitutional DNA from 103 Italian prostate cancer patients and 109 Italian disease-free centenarians to assess the role of this SNP in susceptibility to prostate cancer. RESULTS. The G289S polymorphism confers a significant increase in risk for prostate cancer (odds ratio = 2.5; 95% confidence interval, 1.03-6.07) in our study population. CONCLUSION. Our data are consistent with a plausible role of the G289S SNP in prostate cancer susceptibility. Therefore, the HSD17B3 gene may be a plausible candidate gene for prostate cancer risk. (C) 2002 Wiley-Liss, Inc.
引用
收藏
页码:65 / 68
页数:4
相关论文
共 12 条
[1]  
Bernstein L, 1991, CANC LOS ANGELES COU
[2]  
Cheng Earl, 1993, P57
[3]   MALE PSEUDOHERMAPHRODITISM CAUSED BY MUTATIONS OF TESTICULAR 17-BETA-HYDROXYSTEROID DEHYDROGENASE-3 [J].
GEISSLER, WM ;
DAVIS, DL ;
WU, L ;
BRADSHAW, KD ;
PATEL, S ;
MENDONCA, BB ;
ELLISTON, KO ;
WILSON, JD ;
RUSSELL, DW ;
ANDERSSON, S .
NATURE GENETICS, 1994, 7 (01) :34-39
[4]   Cancer statistics, 2000 [J].
Greenlee, RT ;
Murray, T ;
Bolden, S ;
Wingo, PA .
CA-A CANCER JOURNAL FOR CLINICIANS, 2000, 50 (01) :7-33
[5]   Hormones and prostate cancer: What's next? [J].
Hsing, AW .
EPIDEMIOLOGIC REVIEWS, 2001, 23 (01) :42-58
[6]   Association of mis-sense substitution in SRD5A2 gene with prostate cancer in African-American and Hispanic men in Los Angeles, USA [J].
Makridakis, NM ;
Ross, RK ;
Pike, MC ;
Crocitto, LE ;
Kolonel, LN ;
Pearce, CL ;
Henderson, BE ;
Reichardt, JKV .
LANCET, 1999, 354 (9183) :975-978
[7]   Multiplex automated primer extension analysis: Simultaneous genotyping of several polymorphisms [J].
Makridakis, NM ;
Reichardt, JKV .
BIOTECHNIQUES, 2001, 31 (06) :1374-1380
[8]   Evidence for an association between the SRD5A2 (type II steroid 5α-reductase) locus and prostate cancer in Italian patients [J].
Margiotti, K ;
Sangiuolo, F ;
De Luca, A ;
Froio, F ;
Pearce, CL ;
Ricci-Barbini, V ;
Micali, F ;
Bonafè, M ;
Franceschi, C ;
Dallapiccola, B ;
Novelli, G ;
Reichardt, JKV .
DISEASE MARKERS, 2000, 16 (3-4) :147-150
[9]   Deleterious missense mutations and silent polymorphism in the human 17β-hydroxysteroid dehydrogenase 3 gene (HSD17B3) [J].
Moghrabi, N ;
Hughes, IA ;
Dunaif, A ;
Andersson, S .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1998, 83 (08) :2855-2860
[10]  
NOBLE RL, 1977, CANCER RES, V37, P1929