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AIM: To explore potential interactions among Helicobacter pylori(H. pylori), CagA status, interleukin(IL)-1B-31 genotypes, and non-cardiac gastric cancer(GC) risk.METHODS: A case-control study of non-cardia GCwas performed at 3 hospitals located in Xi’an, China, between September 2008 and July 2010. We included 171 patients with histologically diagnosed primary noncardia GC and 367 population based controls(matched by sex, age and city of residence). A standardized questionnaire was used to obtain information regarding potential risk factors, including pork consumption. H. pylori CagA status was assessed by enzyme-linked immunosorbent assay, and IL-1B-31 genotypes were determined by polymerase chain reaction-restriction fragment length polymorphism. Multivariate unconditional logistic regression was used to explore potential interactions among the factors.RESULTS: The CagA appeared to confer an increased risk of GC(OR = 1.81, 95%CI: 1.25-2.61). The main associations with IL-1B-31C allele here were 0.98(95%CI: 0.59-1.63) for CC vs TT and 0.99(95%CI: 0.64-1.51) for C Carriers vs TT. However, no associations were observed for CagA or IL-1B-31 genotype status among subjects who reported low pork consumption(P for interaction = 0.11). In contrast, high pork consumption and IL-1B-31C genotypes appeared to synergistically increase GC risk(P for interaction = 0.048) after adjusting for confounding factors, particularly among subjects with CagA(OR = 3.07, 95%CI: 1.17-10.79). We did not observe effect modification of pork consumption by H. pylori CagA status, or between H. pylori CagA status and IL-1B-31 genotypes after adjustment for pork consumption and other factors.CONCLUSION: These interaction relationships among CagA, IL-1B-31 and pork consumption may have implications for development of the preventive strategies for the early detection of non-cardiac GC.
AIM: To explore potential interactions among Helicobacter pylori (H. pylori), CagA status, interleukin (IL) -1B-31 genotypes, and non-cardiac gastric cancer GCwas performed at 3 hospitals located in Xi’an, China, between September 2008 and July 2010. We included 171 patients with histologically diagnosed primary noncardia GC and 367 population based controls (matched by sex, age and city of residence). A standardized questionnaire was used to obtain information regarding potential risk factors, including pork consumption. H. pylori CagA status was assessed by enzyme-linked immunosorbent assay, and IL-1B-31 genotypes were determined by polymerase chain reaction- restriction fragment length polymorphism. Multivariate unconditional logistic regression was used to explore potential interactions among the factors .RESULTS: The CagA has been shown to confer an increased risk of GC (OR = 1.81, 95% CI: 1.25-2.61). The main associations with IL-1B-31C alle For a comparison of genotype status for C Carriers vs TT. However, no associations were observed for CagA or IL-1B-31 genotype status (95% CI: 0.59-1.63) for CC vs TT and 0.99 (95% CI: 0.64-1.51) Among subjects who reported low pork consumption (P for interaction = 0.11). In contrast, high pork consumption and IL-1B-31C genotypes had to synergistically increase GC risk (P for interaction = 0.048) after adjusting for confounding factors, particularly among subjects with CagA (OR = 3.07, 95% CI: 1.17-10.79). We did not observe effect modification of pork consumption by H. pylori CagA status, or between H. pylori CagA status and IL-1B-31 genotypes after adjustment for pork consumption and other factors. CONCLUSION: These interaction relationships among CagA, IL-1B-31 and pork consumption may have implications for development of the preventive strategies for the early detection of non-cardiac GC.