 | |  | |  | |  | |  | |  | |  | |  |
| IJCEM Copyright © 2008-All rights reserved. Published by e-Century Publishing Corporation, Madison, WI 53711 |
Int J Clin Exp Med 2(1):68-75,2009
Original Article
GSTM1 and GSTT1 null polymorphisms and risk of salivary gland carcinoma
Sayaka Kondo, Erich M. Sturgis, Fanglin Li, Qingyi Wei, Guojun Li
Departments of Head and Neck Surgery and Departments of Epidemiology, The University of Texas M. D. Anderson Cancer Center,
Houston, Texas, USA; The University of Texas Dental Branch, Houston, Texas, USA; Department of Hematology, Qilu Hospital,
Shandong University, Jinan, P.R. China, 250012
Received January 22, 2009; accepted February 23, 2009; available online February 25, 2009
Abstract: Glutathione S-transferase (GST) genes detoxify and metabolize carcinogens, including oxygen free radicals which may
contribute to salivary gland carcinogenesis. This cancer center-based case-control association study included 166 patients with
incident salivary gland carcinoma (SGC) and 511 cancer-free controls. We performed multiplex polymerase chain reaction-based
polymorphism genotyping assays for GSTM1 and GSTT1 null genotypes. Odds ratios (ORs) and 95% confidence intervals (CIs) were
calculated with multivariable logistic regression analyses adjusted for age, sex, ethnicity, tobacco use, family history of cancer, alcohol
use and radiation exposure. In our results, 27.7% of the SGC cases and 20.6% of the controls were null for the GSTT1 (P = 0.054), and
53.0% of the SGC cases and 50.9% of the controls were null for the gene for GSTM1 (P = 0.633). The results of the adjusted
multivariaale regression analysis suggested that having GSTT1 null genotype was associated with a significantly increased risk for
SGC (odds ratio 1.5, 95% confidence interval 1.0-2.3). Additionally, 13.9% of the SGC cases but only 8.4% of the controls were null for
both genes and the results of the adjusted multivariable regression analysis suggested that having both null genotypes was
significantly associated with an approximately 2-fold increased risk for SGC (odds ratio 1.9, 95% confidence interval 1.0-3.5). The
presence of GSTT1 null genotype and the simultaneous presence of GSTM1 and GSTT1 null genotypes appear associated with
significantly increased SGC risk. These findings warrant further study with larger sample sizes. (IJCEM901003).
Key Words: Glutathione S-transferase (GST); single nucleotide polymorphism; salivary gland carcinoma (SGC); genetic susceptibility;
molecular epidemiology
Full Text PDF
Address all correspondence to:
Guojun Li, MD, PhD
Department of Head and Neck Surgery
The University of Texas M.D. Anderson Cancer Center
1515 Holcombe Boulevard, Unit 1445
Houston, Texas 77030-4009
Tel: 713-792-0227. Fax: 713-794-4662
E-mail: gli@mdanderson.org
Original Article
GSTM1 and GSTT1 null polymorphisms and risk of salivary gland carcinoma
Sayaka Kondo, Erich M. Sturgis, Fanglin Li, Qingyi Wei, Guojun Li
Departments of Head and Neck Surgery and Departments of Epidemiology, The University of Texas M. D. Anderson Cancer Center,
Houston, Texas, USA; The University of Texas Dental Branch, Houston, Texas, USA; Department of Hematology, Qilu Hospital,
Shandong University, Jinan, P.R. China, 250012
Received January 22, 2009; accepted February 23, 2009; available online February 25, 2009
Abstract: Glutathione S-transferase (GST) genes detoxify and metabolize carcinogens, including oxygen free radicals which may
contribute to salivary gland carcinogenesis. This cancer center-based case-control association study included 166 patients with
incident salivary gland carcinoma (SGC) and 511 cancer-free controls. We performed multiplex polymerase chain reaction-based
polymorphism genotyping assays for GSTM1 and GSTT1 null genotypes. Odds ratios (ORs) and 95% confidence intervals (CIs) were
calculated with multivariable logistic regression analyses adjusted for age, sex, ethnicity, tobacco use, family history of cancer, alcohol
use and radiation exposure. In our results, 27.7% of the SGC cases and 20.6% of the controls were null for the GSTT1 (P = 0.054), and
53.0% of the SGC cases and 50.9% of the controls were null for the gene for GSTM1 (P = 0.633). The results of the adjusted
multivariaale regression analysis suggested that having GSTT1 null genotype was associated with a significantly increased risk for
SGC (odds ratio 1.5, 95% confidence interval 1.0-2.3). Additionally, 13.9% of the SGC cases but only 8.4% of the controls were null for
both genes and the results of the adjusted multivariable regression analysis suggested that having both null genotypes was
significantly associated with an approximately 2-fold increased risk for SGC (odds ratio 1.9, 95% confidence interval 1.0-3.5). The
presence of GSTT1 null genotype and the simultaneous presence of GSTM1 and GSTT1 null genotypes appear associated with
significantly increased SGC risk. These findings warrant further study with larger sample sizes. (IJCEM901003).
Key Words: Glutathione S-transferase (GST); single nucleotide polymorphism; salivary gland carcinoma (SGC); genetic susceptibility;
molecular epidemiology
Full Text PDF
Address all correspondence to:
Guojun Li, MD, PhD
Department of Head and Neck Surgery
The University of Texas M.D. Anderson Cancer Center
1515 Holcombe Boulevard, Unit 1445
Houston, Texas 77030-4009
Tel: 713-792-0227. Fax: 713-794-4662
E-mail: gli@mdanderson.org
