Role of GSTM3 Polymorphism in the Risk of Developing Esophageal Cancer
- Departments of 1Medical Genetics, 2Radiotherapy, and 3Gastroenterology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow, India
- Requests for reprints:
Balraj Mittal, Department of Medical Genetics, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Raebareilly Road, Lucknow 226014, India. Phone: 91-522-2668973, ext. 2322; Fax: 91-522-2668017/2668074. E-mail: balraj{at}sgpgi.ac.in or bml_pgi{at}yahoo.com
Abstract
GSTM3 is involved in detoxification of carcinogens and may be important in modulating cancer susceptibility. GSTM3 genotype frequencies were determined in peripheral blood DNA of 149 esophageal cancer patients and 200 nonmalignant controls using the PCR followed by PAGE. Patients who were heterozygous carriers of GSTM3 AB genotype had an enhanced risk for developing esophageal cancer [odds ratio (OR), 2.1; 95% confidence interval (95% CI), 1.1-3.7; P = 0.01]. In males, the risk due to GSTM3 AB genotype increased further (OR, 3.4; 95% CI, 1.7-6.8; P = 0.000). Interaction of GSTM3 AB + BB and GSTM1 null genotypes marginally modulated risk (OR, 2.3; 95% CI, 1.1-3.7; P = 0.01). Association with histology (adenocarcinoma: OR, 3.4; 95% CI, 1.1-10.9; P = 0.03) and tumor site (middle third location: OR, 2.2; 95% CI, 1.1-4.4; P = 0.01; lower third location: OR, 2.6; 95% CI, 1.2-5.6; P = 0.01) was also documented. Our results suggest that GSTM3 polymorphism may influence esophageal cancer susceptibility, in particular modulating the risk for adenocarcinoma histology and tumors of the mid and lower third region. (Cancer Epidemiol Biomarkers Prev 2007;16(1):178–81)
Footnotes
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Grant support: ICMR, DST, UGC Senior Research Fellowship (M. Jain).
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The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
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- Accepted November 1, 2006.
- Received July 7, 2006.
- Revision received September 21, 2006.
