Abstract
Introduction: Oral cancer is a public health problem worldwide, being tobacco and alcohol consumption their main risk factors. Sulfotransferase (SULT) 1A1 (encoded by SULT1A1) is involved in procarcinogens metabolism, such as polycyclic aromatic hydrocarbons (PAHs) present in tobacco smoke. Objective: The aim of this study was to explore the magnitude of association between SULT1A1 gene Arg213His polymorphism and oral cancer, and to explore the interaction between such polymorphism and smoking. Methods: A hospital-based case-control study was carried out in Rio de Janeiro, Brazil, during 1999–2002. Epidemiological data and biological samples were obtained from 202 oral cancer patients and 196 sex and age-frequency matched controls without cancer antecedents. Results: No association was observed between Arg213His SULT1A1 polymorphism and oral cancer risk in overall analysis (OR = 1.06, 95% CI = 0.71–1.57). The magnitude of association between cigarette smoking and oral cancer was higher in individuals with a SULT1A1*1 isoform (wild type, genotype Arg/Arg) (OR = 10.19, 95% CI = 3.90–26.61) than in those with at least one SULT1A1*2 allele (genotypes Arg/His + His/His) (OR = 4.50, 95% CI =2.09–9.69). Conclusion: Our results suggest that Arg213His SULT1A1 polymorphism may modulate the association between smoking and oral cancer. However, this association needs to be replicated in other studies: due to modest number of cases and controls, the role of chance in the observed association cannot be ruled out.
Highlights
Oral cancer is a public health problem worldwide, being tobacco and alcohol consumption their main risk factors
The distribution of oral cancer cases and controls according to sex, age, skin color, smoking, alcohol consumption, and Arg213His SULT1A1 genotype are presented at Table 1
Data analysis did not show an association between the presence of at least one SULT1A1*2 allele and oral cancer (OR = 1.06, 95% confidence intervals (95% CI) 0.71–1.57)
Summary
Oral cancer is a public health problem worldwide, being tobacco and alcohol consumption their main risk factors. Results: No association was observed between Arg213His SULT1A1 polymorphism and oral cancer risk in overall analysis (OR = 1.06, 95% CI = 0.71–1.57). Conclusion: Our results suggest that Arg213His SULT1A1 polymorphism may modulate the association between smoking and oral cancer. This association needs to be replicated in other studies: due to modest number of cases and controls, the role of chance in the observed association cannot be ruled out. Some authors have described an association between xenobiotic metabolizing enzymes polymorphisms and the development of oral cancer (Jefferies et al, 1999; Tripathy and Roy, 2006). The basis of this genetic susceptibility is not well understood (Ram et al, 2011)
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