BACKGROUND: This study aimed to examine the associations of a RUNX3 T/A polymorphism at exon 1 (Asn18Ile) (rs6672420) and another RUNX3 intronic T/A polymorphism (rs760805) with the risk of gastric cancer together with the risk of H. pylori seropositivity and gastric atrophy in Japanese people. METHODS: Study subjects were 583 histologically diagnosed gastric cancer patients and age- and sex-frequency-matched 1,742 control outpatients (among whom 1,637 subjects were eligible for the analyses), who visited Aichi Cancer Center Hospital from 2001 to 2005. Serum pepsinogens were measured to evaluate gastric atrophy. RESULTS: There was no significant association between the RUNX3 polymorphisms and the seropositivity. Among H. pylori seropositive subjects, we found a significant association between RUNX3 rs760805 polymorphism and the risk of gastric atrophy with the age- and sex-adjusted OR of 1.51 (95% CI 1.11-2.05, P = 0.008) in T/A, 1.59 (95% CI 1.08-2.33, P = 0.019) in A/A, and 1.53 (95% CI 1.14-2.05, P = 0.004) in T/A + A/A, compared with T/T genotype. We found no statistically significant associations between RUNX3 rs6672420 polymorphism and risk of gastric atrophy, nor between these two RUNX3 polymorphisms and the risk of gastric cancer relative to the subjects with gastric atrophy. CONCLUSIONS: Our study results revealed that the RUNX3 intronic T/A polymorphism (rs760805) might modulate the risk of gastric atrophy among H. pylori seropositive subjects, and the RUNX3 T/A polymorphism at exon 1 (rs6672420) had little influence on the risks of H. pylori infection, gastric atrophy or gastric cancer in Japanese people. Further investigation is required to verify our findings.
BACKGROUND: This study aimed to examine the associations of a RUNX3 T/A polymorphism at exon 1 (Asn18Ile) (rs6672420) and another RUNX3 intronic T/A polymorphism (rs760805) with the risk of gastric cancer together with the risk of H. pylori seropositivity and gastric atrophy in Japanese people. METHODS: Study subjects were 583 histologically diagnosed gastric cancerpatients and age- and sex-frequency-matched 1,742 control outpatients (among whom 1,637 subjects were eligible for the analyses), who visited Aichi Cancer Center Hospital from 2001 to 2005. Serum pepsinogens were measured to evaluate gastric atrophy. RESULTS: There was no significant association between the RUNX3 polymorphisms and the seropositivity. Among H. pylori seropositive subjects, we found a significant association between RUNX3 rs760805 polymorphism and the risk of gastric atrophy with the age- and sex-adjusted OR of 1.51 (95% CI 1.11-2.05, P = 0.008) in T/A, 1.59 (95% CI 1.08-2.33, P = 0.019) in A/A, and 1.53 (95% CI 1.14-2.05, P = 0.004) in T/A + A/A, compared with T/T genotype. We found no statistically significant associations between RUNX3 rs6672420 polymorphism and risk of gastric atrophy, nor between these two RUNX3 polymorphisms and the risk of gastric cancer relative to the subjects with gastric atrophy. CONCLUSIONS: Our study results revealed that the RUNX3 intronic T/A polymorphism (rs760805) might modulate the risk of gastric atrophy among H. pylori seropositive subjects, and the RUNX3 T/A polymorphism at exon 1 (rs6672420) had little influence on the risks of H. pyloriinfection, gastric atrophy or gastric cancer in Japanese people. Further investigation is required to verify our findings.
Authors: S Fukushige; K Matsubara; M Yoshida; M Sasaki; T Suzuki; K Semba; K Toyoshima; T Yamamoto Journal: Mol Cell Biol Date: 1986-03 Impact factor: 4.272
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