Abstract
ObjectiveBoth variations in the interleukin-10 (IL10) gene and environmental factors are thought to influence inflammation and gastric carcinogenesis. Therefore, we investigated the associations between IL10 polymorphisms, Helicobacter pylori (H. pylori) infection, and smoking in noncardia gastric carcinogenesis in Koreans.MethodsWe genotyped three promoter polymorphisms (-1082A>G, -819T>C, and -592 A>C) of IL10 in a case-control study of 495 noncardia gastric cancer patients and 495 sex- and age-matched healthy controls. Multiple logistic regression models were used to detect the effects of IL10 polymorphisms, H. pylori infection, and smoking on the risk of gastric cancer, which was stratified by the histological type of gastric cancer.ResultsThe IL10-819C and -592C alleles were found to have complete linkage disequilibrium, and all three IL10 polymorphisms were associated with an increased risk of intestinal-type noncardia gastric cancer. These associations were observed only in H. pylori-positive subjects and current smokers. A statistically significant interaction between the IL10-592 genotype and H. pylori infection on the risk of intestinal-type gastric cancer was observed (P for interaction = 0.047). In addition, H. pylori-positive smokers who were carriers of either the IL10-1082G (OR [95% CI] = 17.76 [6.17−51.06]) or the -592C (OR [95% CI] = 8.37 [2.79−25.16]) allele had an increased risk of intestinal-type gastric cancer compared to H. pylori-negative nonsmokers homozygous for IL10-1082A and -592A, respectively. The interaction between the IL10-1082 polymorphism and the combined effects of H. pylori infection and smoking tended towards significance (P for interaction = 0.080).ConclusionsInflammation-related genetic variants may interact with H. pylori infection and smoking to increase the risk of noncardia gastric cancer, particularly the intestinal-type. These findings may be helpful in identifying individuals at an increased risk for developing noncardia gastric cancer.
Highlights
Gastric cancer is the second most common cause of cancer mortality globally and the prevalence of gastric cancer is higher in Asians than in Western populations [1]
Histologically-confirmed adenocarcinoma patients were included in this study, and other types of neoplasms found in the stomach (e.g., MALT lymphomas, other types of primary gastric lymphoma, gastrointestinal stromal tumors, carcinoid tumors, or adenomas) were excluded
We examined the association between IL10 genetic variants and the risk of gastric cancer after stratifying noncardia gastric cancer by stage
Summary
Gastric cancer is the second most common cause of cancer mortality globally and the prevalence of gastric cancer is higher in Asians than in Western populations [1]. H. pylori is a strong risk factor for gastric cancer, likely due to the extensive inflammation in the stomach mucosa caused by this bacteria [4]. It has been reported that these variants of IL10 are associated with increased IL10 production [11,12,13] and an elevated risk of gastric cancer [14,15]. Environmental factors, such as cigarette smoking, may alter cytokine expression in a manner more favorable for the development of gastric inflammation and carcinogenesis [16]. Inflammation-related polymorphisms may interact with environmental factors in the development of gastric cancer
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