AMACR polymorphisms, dietary intake of red meat and dairy and prostate cancer risk

Authors

  • Jonathan L. Wright,

    Corresponding author
    1. Department of Urology, University of Washington School of Medicine, Seattle, Washington
    2. Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington
    • Department of Urology, University of Washington Medical Center, Health Sciences Building, 1959 NE Pacific, BB-1115, Box 356510, Seattle, WA 98195.
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  • Marian L. Neuhouser,

    1. Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington
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  • Daniel W. Lin,

    1. Department of Urology, University of Washington School of Medicine, Seattle, Washington
    2. Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington
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  • Erika M. Kwon,

    1. Cancer Genetics Branch, National Human Genome Research Institute, Bethesda, Maryland
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  • Ziding Feng,

    1. Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington
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  • Elaine A. Ostrander,

    1. Cancer Genetics Branch, National Human Genome Research Institute, Bethesda, Maryland
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  • Janet L. Stanford

    1. Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington
    2. Department of Epidemiology, School of Public Health, University of Washington, Seattle, Washington
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Abstract

BACKGROUND

Alpha-methylacyl CoA racemase (AMACR) is an enzyme involved in fatty acids metabolism. One of AMACRs primary substrates, phytanic acid, is principally obtained from dietary red meat/dairy, which are associated with prostate cancer (PCa) risk. AMACR is also a tumor tissue biomarker over-expressed in PCa. In this study, we explored the potential relationship between AMACR polymorphisms, red meat/dairy intake, and PCa risk.

METHODS

Caucasian participants from two population-based PCa case–control studies were included. AMACR single nucleotide polymorphisms (SNPs) were selected to capture variation across the gene and regulatory regions. Red meat and dairy intake was determined from food frequency questionnaires. The odds ratio (OR) of PCa (overall and by disease aggressiveness) was estimated by logistic and polytomous regression. Potential interactions between genotypes and dietary exposures were evaluated.

RESULTS

Data from 1,309 cases and 1,267 controls were analyzed. Carriers of the variant T allele (rs2287939) had an OR of 0.81 (95% CI 0.68–0.97) for less aggressive PCa, but no alteration in risk for more aggressive PCa. Red meat consumption was positively associated with PCa risk, and the association was stronger for more aggressive disease (lowest vs. highest tertile OR = 1.55, 95% CI 1.10–2.20). No effect modification of AMACR polymorphisms by either dietary red meat or dairy intake on PCa risk was observed.

CONCLUSIONS

PCa risk varied by level of red meat intake and by one AMACR SNP, but there was no evidence for gene–environment interaction. These findings suggest that the effects of AMACR polymorphisms and red meat and dairy on PCa risk are independent. Prostate 77:498–506, 2011. © 2010 Wiley-Liss, Inc.

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