The Common Variant rs1447295 on Chromosome 8q24 and Prostate Cancer Risk: Results from an Australian Population-Based Case-Control Study
- Gianluca Severi1,2,
- Vanessa M. Hayes4,5,
- Emma J.D. Padilla4,
- Dallas R. English1,2,
- Melissa C. Southey3,6,
- Robert L. Sutherland4,5,
- John L. Hopper2 and
- Graham G. Giles1,2
- 1Cancer Epidemiology Centre, The Cancer Council Victoria, 2Centre for Molecular, Environmental, Genetic, and Analytic Epidemiology, and 3Department of Pathology, University of Melbourne, Melbourne, Victoria, Australia; 4Cancer Research Program, Garvan Institute of Medical Research, St. Vincent's Hospital, Darlinghurst, New South Wales, Australia; 5Faculty of Medicine, University of New South Wales, Sydney, New South Wales, Australia; and 6International Agency for Research on Cancer, Lyons, France
- Requests for reprints:
Gianluca Severi, Cancer Epidemiology Centre, The Cancer Council Victoria, 1 Rathdowne Street, Carlton, Victoria 3053, Australia. Phone: 61-39635-5412; Fax: 61-39635-5330. E-mail: gianluca.severi{at}cancervic.org.au
Abstract
A recent study from deCode reported an association between common variants in the region 8q24 and prostate cancer risk. The strongest association was found with the single nucleotide polymorphism rs1447295. We genotyped 821 prostate cancer cases and 732 population controls for rs1447295 to test the association between this common variant and prostate cancer risk, and examine whether this association depends on Gleason score. Our case-control study confirmed the association between rs1447295 and prostate cancer risk (P = 0.0005). The odds ratio (OR) for prostate cancer was 1.52 [95% confidence interval (CI), 1.20-1.93] for carriers of any A allele compared with noncarriers. The OR for Gleason score 5 to 6 prostate cancer (1.48; 95% CI, 1.13-1.95) was similar to the OR for Gleason score 7 to 10 prostate cancer (1.58; 95% CI, 1.18-2.11, P for heterogeneity = 0.7). We conclude that the A allele of rs1447295 is associated with a higher risk of prostate cancer regardless of tumor aggressiveness, suggesting that such a variant, or a variant in linkage disequilibrium with it, plays a role early in prostate carcinogenesis. (Cancer Epidemiol Biomarkers Prev 2007;16(3):610–2)
Footnotes
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Grant support: National Health and Medical Research Council (251533, 940394, 991129, 299955, 396407), the Cancer Institute of New South Wales, and Australian Cancer Research Foundation. Also supported by grants from Tattersall's, The Whitten Foundation, Armati Family Fellowship, BNP Paribas, Australia, and by infrastructure provided by The Cancer Council Victoria. V.M. Hayes is a Cancer Institute of New South Wales Fellow.
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The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
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Note: G. Severi and V.M. Hayes contributed equally to the study.
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- Accepted December 19, 2006.
- Received October 14, 2006.
- Revision received December 11, 2006.
