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Departments of 1 Epidemiology and 2 Biostatistics, College of Public Health, 3 Department of Pathology, Carver College of Medicine, 4 Holden Comprehensive Cancer Center, University of Iowa, 5 Veterans Affairs Medical Center, Iowa City, Iowa
Requests for reprints: Elaine Smith, College of Public Health, University of Iowa, Iowa City, IA 52242. Phone: 319-384-5014; Fax: 319-384-5031. E-mail: esmith{at}mail.public-health.uiowa.edu
In order to examine the association between alcohol dehydrogenase 3 (ADH3) genotypes and risk of head and neck squamous cell carcinomas (HNSCC), we conducted a hospital based case-control study including 348 cases and 330 controls. DNA isolated from exfoliated cells from the oral cavity were genotyped for ADH3 polymorphisms using PCR followed by SspI digestion. Odds ratios (OR) and hazards ratios (HR) were done by unconditional logistic regression and Cox regression. Relative to ADH32-2 carriers, ADH31-1 [OR, 0.7; 95% confidence interval (CI), 0.4-1.1] and ADH31-2 (OR, 0.8; 95% CI, 0.5-1.2) had a nonsignificant reduced risk of HNSCC. ADH1-2 smokers of >30 pack-years were at decreased risk of oral cavity squamous cell carcinomas compared with ADH32-2 (OR, 0.3, 0.1-0.9), whereas ADH31-1 smokers were not. After adjustment, those with ADH31-2 had significantly worse overall survival compared with ADH31-1 (HR, 0.3, 0.2-0.6) or ADH32-2 (HR, 0.4, 0.2-0.9) and increased recurrence (ADH31-1, 0.2, 0.1-0.6; ADH32-2, 0.6, 0.2-1.3). Our data did not show that ADH3 genotypes had a significantly independent effect on the risk of HNSCC, nor did they modify the risks increased by alcohol or tobacco consumption and high-risk human papillomavirus infection. However, participants with ADH31-2 genotype were associated with poorer survival compared with those who had the other two ADH3 genotypes and a higher rate of recurrence than participants with ADH31-1 genotype.
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