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Genetic and environmental interactions on oral cancer in Southern Thailand

✍ Scribed by Suparp Kietthubthew; Hutcha Sriplung; William W. Au


Publisher
John Wiley and Sons
Year
2001
Tongue
English
Weight
52 KB
Volume
37
Category
Article
ISSN
0893-6692

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✦ Synopsis


Abstract

Many countries are interested in understanding the relationship between genetic susceptibility and their prevalent environmental cancers for disease prevention. In Thailand we conducted a population‐based case‐control study of 53 matched pairs to assess the risk of oral cancer in relation to genetic polymorphism of the glutathione‐S‐transferase genes (GSTM1 and GSTT1) in cigarette smokers, alcohol drinkers, and betel quid chewers. Interaction of the genes with other potential risk factors such as local bean consumption were also elucidated. Homozygous deletion of GSTM1 has a frequency of 56.6% (n = 30 over 53) among the patients and 30.2% (16/53) among the controls. This gene is associated with a 2.6‐fold higher risk for development of oral cancer (95% CI 1.04–6.5). Among the null GSTM1 individuals, those who smoke, consume alcohol, and/or chew betel quid have a significantly increased risk for oral cancer with an odd ratio (OR) = 4.0 (95% CI = 1.2–13.7), OR = 7.2 (95% CI = 1.5–33.8), and OR = 4.4 (95% CI = 1.1–17.8), respectively. Interactions between any two of the lifestyle habits for oral cancer risk, however, are not found. The frequency of the GSTT1 null genotype is 34.0% (18/53) among the patients and 47.2% (25/53) among our controls. There is no association between the GSTT1 null allele and oral cancer risk. In conclusion, our study provides data to indicate that individuals who have homozygous deletion of the GSTM1 gene have increased risk for oral cancer. The risk increases further when these individuals are exposed to environmental toxicants such as chemicals in cigarette smoke, alcohol, and betel quid. These baseline data can be applied to a larger population‐based study, both to verify the observation and to conduct mechanistic investigations. Environ. Mol. Mutagen. 37:111–116, 2001 © 2001 Wiley‐Liss, Inc.


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