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Case–control study of oral and oropharyngeal cancer in whites and genetic variation in eight metabolic enzymes

Authors

  • Shama C. Buch PhD,

    1. Department of Medicine, University of Pittsburgh, University of Pittsburgh Medical Center, and University of Pittsburgh Cancer Institute, Pittsburgh, Pennsylvania
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  • Valle Nazar-Stewart PhD,

    1. Center for Research on Occupational and Environmental Toxicology, Oregon Health and Science University, Portland, Oregon
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  • Joel L. Weissfeld MD, MPH,

    1. Department of Epidemiology, University of Pittsburgh, University of Pittsburgh Medical Center, and University of Pittsburgh Cancer Institute, Pittsburgh, Pennsylvania
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  • Marjorie Romkes PhD

    Corresponding author
    1. Department of Medicine, University of Pittsburgh, University of Pittsburgh Medical Center, and University of Pittsburgh Cancer Institute, Pittsburgh, Pennsylvania
    • Department of Medicine, University of Pittsburgh, University of Pittsburgh Medical Center, and University of Pittsburgh Cancer Institute, Pittsburgh, Pennsylvania
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Abstract

Background.

Genetic variation in xenobiotic metabolizing enzymes may explain differing susceptibilities to the cancer causing effects of tobacco and alcohol.

Methods.

We compared 203 oral squamous cell carcinoma cases and 416 controls for single nucleotide polymorphisms (SNPs) in 8 genes (CYP1A1, CYP2E1, MPO, mEH, GSTM1, GSTT1, GSTP1, and NAT2). Except for NAT2, genotype frequencies were similar in the 2 groups. We classified subjects as fast or slow NAT2 acetylators genotyping 13 NAT2 SNPs.

Results.

Fast acetylators were overrepresented in cases (53.7%) compared with controls (43.9%; odds ratio (OR) 1.55, 95% confidence interval (CI) 1.08–2.20; p value = .03). Gene–gene interaction testing suggested several cancer-NAT2 associations, with association strongest among persons without a CYP1A1 variant (*2C or *4) allele (OR 1.77, 95% CI 1.20–2.60, p value = .03) or with a variant MPO (463A) allele (OR 2.38, 95% CI 1.34–4.21, p value = .05).

Conclusion.

These results implicate fast NAT2 acetylation as a risk factor for oral cancer. © 2008 Wiley Periodicals, Inc. Head Neck 2008

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