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CASP3 Polymorphisms and Risk of Squamous Cell Carcinoma of the Head and Neck

Authors' Affiliations: ¹ Department of Epidemiology, Tianjin Cancer Institute and Hospital, Tianjin Medical University, Tianjin, China; ² Department of Epidemiology and Biostatistics, Cancer Research Center of Nanjing Medical University, Nanjing, China; and Departments of ³ Epidemiology, ⁴ Pathology, and ⁵ Head and Neck Surgery, The University of Texas M. D. Anderson Cancer Center, Houston, Texas

Requests for reprints: Qingyi Wei, Department of Epidemiology, Unit 1365, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030. Phone: 713-792-3020; Fax: 713-563-0999; E-mail: qwei{at}mdanderson.org.

Abstract

Purpose: Caspase-3 plays a central role in executing cell apoptosis and thus in carcinogenesis, but little is known about the role of CASP3 variants in susceptibility to SCCHN.

Experimental Design: Genotype and haplotypes of the first intron (rs4647601:G>T and rs4647602:C>A) and 5'-untranslated region (UTR; rs4647603:G>A) of CASP3 (NT_022792.17) were determined for 930 SCCHN patients and 993 cancer-free controls in a U.S. non-Hispanic white population. Odds ratio (OR) and 95% confidence interval (95% CI) were calculated in multivariate logistic regression analysis.

Results: We found that the CASP3 rs4647601:TT variant genotype was associated with an increased risk of SCCHN (adjusted OR, 1.32; 95% CI, 1.00-1.73) compared with the GG genotype. This risk was more evident in the subgroups of younger (56 years) subjects, males, and never smokers with a significant trend for increased risk with increased number of variant T allele (P < 0.05 for all). However, these risks were not found for other two SNPs. Furthermore, individuals with two copies of haplotypes TCG or GCA were found to have a significant increased risk of SCCHN (OR, 1.31; 95% CI, 1.07-1.61) compared with the other haplotypes, and this risk was more evident in less advanced diseases (OR, 1.45; 95% CI, 1.11-1.89) than in the advanced diseases (OR, 1.22; 95% CI, 0.96-1.54).

Conclusions: These results suggested that genetic variation in CASP3 may contribute to SCCHN risk. Larger studies are needed to confirm our findings.