Cohol (? superficial gastritis/gastric cancer OR (95 CI) (+) superficial gastritis/gastric cancer OR (95 CI) 170/74 1.000 62/49 1.816(1.142?.886) 86/32 0.855(0.524?.394) 48/28 1.34 (0.781?.3)P = 0.8/9 2.584(0.96?.96) 1/7 16.081(1.944?33.038)P = 0.94/41 1.002(0.634?.583) 49/35 1.641(0.983?.739)P = 0.P values were adjusted for age and sex. doi:10.1371/journal.pone.0047178.tP = 0.P = 0.Genetic Susceptibility to Gastric Carcinogenesisthe GSTP1 Ile/Val polymorphism could affect the stage of gastric carcinogenesis, the extent of atrophic gastritis as a precancerous lesion. Compared with other studies, we found that the allele Val frequencies of GSTP1 (21.1 ) were significantly 
different from those in western people, such as European mericans (33 ) and African mericans (42 ) [25,37]. This suggests the possibility of GSTP1-genotype-associated ethnic differences. The fact that, in our study, genotype frequencies among the population fitted the Hardy einberg law 22948146 further supports this view. The mechanism of the association between GSTP1 gene polymorphism and gastric cancer was 15481974 not clear in our study. However, it can be supposed that GSTP1 is a major GST isoform expressed in human gastrointestinal epithelium, which can eliminate DNA oxidative products of thymidine or uracil propenal. After induction by PS 1145 price cytochrome P450, some tumor-related carcinogens, such as benzo[a]pyrene diol epoxide and acrolein, can also be eliminated by GSTP1. The IleRVal substitution may be associated with a higher level of DNA adducts, thus increasing the susceptibility to gastric cancer induction. Furthermore, stratified analyses revealed that subgroups of smoking or alcohol consumption were more likely to have been diagnosed with gastric cancer. Our analysis supports there being an elevated risk of gastric cancer among individuals with H. Nafarelin pylori infection, smoking, or alcohol consumption, and the GSTP1 Val/ Val genotype. H. pylori has been assigned as a classs I carcinogen by the World Health Organization, and acts as the initiating agent [38]. Serological H. pylori IgG testing was a useful noninvasive strategy for testing for H. pylori. It was particularly useful in areas where the prevalence of H. pylori was high. We investigated the interaction between GSTP1 genotype and H. pylori infection in gastric cancer and its precancerous conditions. Association of the GSTP1 Val/ Val genotype with H. pylori infection significantly increased gastric cancer and atrophic gastritis risk. This important finding suggests that GSTP1 genotyping and H. pylori IgG seropositivity could be used to identify individuals with a high risk of gastric cancer and its precancerous conditions. The mechanism of action might be that the H. pylori infection resulting in gastric cancer and its precancerous conditions depends on genetic polymorphismsinfluencing the virulence of the organism. GSTP1 Ile/Ile has a higher catalytic efficiency than GSTP1 Ile/Val or Val/Val for most environmental carcinogens, including cytokines produced by H. pylori infection. These cytokines that could not be detoxified by GSTP1 could directly induce gastric mucosal damage and eventually lead to development of atrophic gastritis and even gastric cancer. The exact molecular biology mechanisms need further exploration. Tobacco smoking and alcohol consumption are the main known etiological factors of some cancers. In this study, we observed that higher ratios of people in the gastric cancer group had consumed tobacco and alcoh.Cohol (? superficial gastritis/gastric cancer OR (95 CI) (+) superficial gastritis/gastric cancer OR (95 CI) 170/74 1.000 62/49 1.816(1.142?.886) 86/32 0.855(0.524?.394) 
48/28 1.34 (0.781?.3)P = 0.8/9 2.584(0.96?.96) 1/7 16.081(1.944?33.038)P = 0.94/41 1.002(0.634?.583) 49/35 1.641(0.983?.739)P = 0.P values were adjusted for age and sex. doi:10.1371/journal.pone.0047178.tP = 0.P = 0.Genetic Susceptibility to Gastric Carcinogenesisthe GSTP1 Ile/Val polymorphism could affect the stage of gastric carcinogenesis, the extent of atrophic gastritis as a precancerous lesion. Compared with other studies, we found that the allele Val frequencies of GSTP1 (21.1 ) were significantly different from those in western people, such as European mericans (33 ) and African mericans (42 ) [25,37]. This suggests the possibility of GSTP1-genotype-associated ethnic differences. The fact that, in our study, genotype frequencies among the population fitted the Hardy einberg law 22948146 further supports this view. The mechanism of the association between GSTP1 gene polymorphism and gastric cancer was 15481974 not clear in our study. However, it can be supposed that GSTP1 is a major GST isoform expressed in human gastrointestinal epithelium, which can eliminate DNA oxidative products of thymidine or uracil propenal. After induction by cytochrome P450, some tumor-related carcinogens, such as benzo[a]pyrene diol epoxide and acrolein, can also be eliminated by GSTP1. The IleRVal substitution may be associated with a higher level of DNA adducts, thus increasing the susceptibility to gastric cancer induction. Furthermore, stratified analyses revealed that subgroups of smoking or alcohol consumption were more likely to have been diagnosed with gastric cancer. Our analysis supports there being an elevated risk of gastric cancer among individuals with H. pylori infection, smoking, or alcohol consumption, and the GSTP1 Val/ Val genotype. H. pylori has been assigned as a classs I carcinogen by the World Health Organization, and acts as the initiating agent [38]. Serological H. pylori IgG testing was a useful noninvasive strategy for testing for H. pylori. It was particularly useful in areas where the prevalence of H. pylori was high. We investigated the interaction between GSTP1 genotype and H. pylori infection in gastric cancer and its precancerous conditions. Association of the GSTP1 Val/ Val genotype with H. pylori infection significantly increased gastric cancer and atrophic gastritis risk. This important finding suggests that GSTP1 genotyping and H. pylori IgG seropositivity could be used to identify individuals with a high risk of gastric cancer and its precancerous conditions. The mechanism of action might be that the H. pylori infection resulting in gastric cancer and its precancerous conditions depends on genetic polymorphismsinfluencing the virulence of the organism. GSTP1 Ile/Ile has a higher catalytic efficiency than GSTP1 Ile/Val or Val/Val for most environmental carcinogens, including cytokines produced by H. pylori infection. These cytokines that could not be detoxified by GSTP1 could directly induce gastric mucosal damage and eventually lead to development of atrophic gastritis and even gastric cancer. The exact molecular biology mechanisms need further exploration. Tobacco smoking and alcohol consumption are the main known etiological factors of some cancers. In this study, we observed that higher ratios of people in the gastric cancer group had consumed tobacco and alcoh.
