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Carcinogenesis Advance Access published online on November 4, 2005
Carcinogenesis, doi:10.1093/carcin/bgi257
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© The Author 2005. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org
Received July 26, 2005
Revised October 24, 2005
Accepted October 26, 2005

MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION

Gene-environment interaction: the role of SULT1A1 and CYP3A5 polymorphisms as risk modifiers for squamous cell carcinoma of the esophagus

Collet Dandara 1, Dong-Ping Li 1, Gabi Walther 2, and M. Iqbal Parker 1*

1 UCT/MRC-Oesophageal Cancer Research Group, Division of Medical Biochemistry, Institute of Infectious Disease and Molecular Medicine (IIDMM), Faculty of Health Sciences, University of Cape Town, South Africa
2 Section of Thoracic Surgery, Chris Barnard Division of Cardio-Thoracic Surgery, Groote Schuur Hospital, Faculty of Health Sciences, University of Cape Town, South Africa

* To whom correspondence should be addressed.
M. Iqbal Parker, E-mail: mparker{at}curie.uct.ac.za


  Abstract

An imbalance in the activities of enzymes involved in the metabolism, conjugation and transport of xenobiotics may account for the variability in susceptibility to the development of complex diseases such as cancer between different population groups. In this study we investigated a functional polymorphism in the SULT1A1 gene in 245 patients and 288 controls. Previous studies have shown that the 638G>A polymorphism that results in the substitution of arginine by histidine at codon 213 (SULT1A1*2) results in decreased SULT1A1 activity. The same group of samples used in this study had been previously genotyped for CYP3A5 genetic polymorphisms. Among Black subjects the burning of wood or charcoal for cooking and keeping warm was significantly associated with increased risk for oesophageal cancer (AOR, 15.2; p=0.001) as was the consumption of home-brewed beer (AOR, 6.97; p=0.0001). Among the Mixed Ancestry group, tobacco smoking combined with alcohol consumption were significantly associated with higher risk for oesophageal cancer (AOR, 5.18; p=0.0005). In both Blacks and Mixed Ancestry subjects, starting to smoke below the age of 20 years was associated with significantly increased risk for oesophageal cancer (AOR, 3.5 among the Blacks and AOR, 12 among the Mixed Ancestry). The homozygous SULT1A1*2/*2 genotype was associated with increased risk for oesophageal cancer among smokers. The SULT1A1*2/*2 genotype in combination with the CYP3A5 heterozygous genotypes was associated with significantly increased risk for oesophageal cancer (AOR, 3.60; p=0.001) with the risk being even higher among smokers compared to non-smokers. The above findings confirm the association between alcohol consumption and tobacco smoking with increased risk for oesophageal cancer. The genotype results show that SULT1A1*2/*2 genotype is associated with increased risk for oesophageal cancer among subjects exposed to tobacco smoke-related carcinogens.


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[Abstract] [Full Text] [PDF]


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