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BioMed Research International
Volume 2017 (2017), Article ID 7365080, 9 pages
Research Article

The Interaction between GSTT1, GSTM1, and GSTP1 Ile105Val Gene Polymorphisms and Environmental Risk Factors in Premalignant Gastric Lesions Risk

1University of Medicine and Pharmacy, Tirgu Mureș, Gheorghe Marinescu 38, 540139 Mures, Romania
2University of Medicine and Pharmacy “Iuliu Hațieganu” Cluj-Napoca, 8 Victor Babeş, 400012 Cluj-Napoca, Romania
3Emergency County Hospital, Tirgu Mureș, Gheorghe Marinescu 50, 540136 Mures, Romania
4Center for Advanced Medical and Pharmaceutical Research, University of Medicine and Pharmacy, Tirgu Mureș, Gheorghe Marinescu 38, 540139 Mures, Romania

Correspondence should be addressed to Mihaela Iancu

Received 4 October 2016; Revised 16 November 2016; Accepted 20 November 2016; Published 15 January 2017

Academic Editor: Janusz Blasiak

Copyright © 2017 Anca Negovan et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The study investigated the possible influence of GSTM1, GSTT1, and GSTP1 gene polymorphisms as predisposing factors for premalignant gastric lesions as well as their interaction with H. pylori infection, gastrotoxic drugs, smoking, and alcohol consumption. In this study, 270 patients with a complet set of gastric biopsies and successfully genotyped were finally included. The GSTM1 gene polymorphism had significant contribution in mild/severe endoscopic lesions () as well as in premalignant lesions (). The GSTM1 null genotype increased the risk for mucosal defects in H. pylori-negative patients (OR = 2.27, 95% CI: 1.20–4.37) and the risk for premalignant lesions in patients with no alcohol consumption (OR = 2.13, 95% CI: 1.19–3.83). The GSTT1 deleted polymorphism did not significantly increase the risk for premalignant lesions in the absence of gastrotoxic drugs (OR = 1.82, 95% CI: 0.72–4.74). The combined GSTT1T1 and GSTM1 null polymorphisms were borderline correlated with an increased risk for premalignant lesions (OR = 1.72, 95% CI: 1.00–2.97). The wild-type GSTP1 Ile/Ile genotype versus the variant genotypes Ile/Val + Val/Val was significantly associated with a decreased risk of gastric atrophy/intestinal metaplasia (OR = 0.60, 95% CI: 0.37–0.98). In conclusion, the GSTM1 and GSTT1 null genotypes increased the risk for premalignant and endoscopic gastric lesions, modulated by H. pylori, alcohol, or gastrotoxic drug consumption, while the presence of the GSTP1Val allele seemed to reduce the risk for premalignant lesions.