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SULT1A1 genetic polymorphisms and the association between smoking and oral cancer in a case-control study in Brazil

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. Objectiv...

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Autores principales: Santos, Sabrina S., Koifman, Rosalina J., Ferreira, Rafaela M., Diniz, Lilian F., Brennan, Paul, Boffetta, Paolo, Koifman, Sergio
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3524504/
https://www.ncbi.nlm.nih.gov/pubmed/23264952
http://dx.doi.org/10.3389/fonc.2012.00183
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author Santos, Sabrina S.
Koifman, Rosalina J.
Ferreira, Rafaela M.
Diniz, Lilian F.
Brennan, Paul
Boffetta, Paolo
Koifman, Sergio
author_facet Santos, Sabrina S.
Koifman, Rosalina J.
Ferreira, Rafaela M.
Diniz, Lilian F.
Brennan, Paul
Boffetta, Paolo
Koifman, Sergio
author_sort Santos, Sabrina S.
collection PubMed
description 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 Arg(213)His 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 Arg(213)His 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 Arg(213)His 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.
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spelling pubmed-35245042012-12-21 SULT1A1 genetic polymorphisms and the association between smoking and oral cancer in a case-control study in Brazil Santos, Sabrina S. Koifman, Rosalina J. Ferreira, Rafaela M. Diniz, Lilian F. Brennan, Paul Boffetta, Paolo Koifman, Sergio Front Oncol Oncology 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 Arg(213)His 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 Arg(213)His 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 Arg(213)His 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. Frontiers Media S.A. 2012-12-18 /pmc/articles/PMC3524504/ /pubmed/23264952 http://dx.doi.org/10.3389/fonc.2012.00183 Text en Copyright © 2012 Santos, Koifman, Ferreira, Diniz, Brennan, Boffetta and Koifman. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in other forums, provided the original authors and source are credited and subject to any copyright notices concerning any third-party graphics etc.
spellingShingle Oncology
Santos, Sabrina S.
Koifman, Rosalina J.
Ferreira, Rafaela M.
Diniz, Lilian F.
Brennan, Paul
Boffetta, Paolo
Koifman, Sergio
SULT1A1 genetic polymorphisms and the association between smoking and oral cancer in a case-control study in Brazil
title SULT1A1 genetic polymorphisms and the association between smoking and oral cancer in a case-control study in Brazil
title_full SULT1A1 genetic polymorphisms and the association between smoking and oral cancer in a case-control study in Brazil
title_fullStr SULT1A1 genetic polymorphisms and the association between smoking and oral cancer in a case-control study in Brazil
title_full_unstemmed SULT1A1 genetic polymorphisms and the association between smoking and oral cancer in a case-control study in Brazil
title_short SULT1A1 genetic polymorphisms and the association between smoking and oral cancer in a case-control study in Brazil
title_sort sult1a1 genetic polymorphisms and the association between smoking and oral cancer in a case-control study in brazil
topic Oncology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3524504/
https://www.ncbi.nlm.nih.gov/pubmed/23264952
http://dx.doi.org/10.3389/fonc.2012.00183
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