Zhonghua yi xue za zhi · 2006
[Correlation between an insertion-deletion polymorphism in the pepsinogen C gene and gastric cancer as well as its precursors].
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Sun Li-ping, Guo Xiao-lin, Zhang Ye, Chen Wei, Bai Xue-lei, Liu Jin, Yuan Yuan
Аннотация
OBJECTIVE: To assess the relationship between the insert-deletion polymorphism in the Human pepsinogen (PGC) gene and susceptibility to gastric cancer, together with its precursors, and to investigate the interaction between PGC polymorphism and H. pylori infection in the development of gastric cancer.
METHODS: PGC gene polymorphism in 141 patients with gastric cancer and 564 matched non-cancer controls were detected by polymerase chain reaction (PCR), and the relation between the PGC polymorphism and gastric cancer was examined. Serum H. pylori-IgG was determined with ELISA method. The odds ratios and 95% confidence intervals (95% CI) were calculated using unconditional logistic regression model. The effect-modified model was used to evaluate the PGC-H. pylori interaction.
RESULTS: No significant association between the frequency of homogenous allele 1 of PGC gene and the sex and age of the subjects was observed. The subjects with the homogenous allele 1 had an increased risk of developing atrophic gastritis (OR: 3.103, 95% CI: 1.440-6.686), and gastric cancer (OR: 2.962, 95% CI: 1.370-6.404), and Intestinal metaplasia (OR: 1.659, 95% CI: 0.998-2.757) comparing with those with the non-homogenous allele 1. For subjects carrying both homogenous allele 1 and H. pylori-IgG positive, there was an significant increased risk of developing atrophic gastritis and gastric cancer (likelihood test ratio test: P = 0.023, P = 0.005).
CONCLUSION: PGC gene polymorphism may be associated with susceptibility to gastric cancer and atrophic gastritis. The PGC gene polymorphism and H. pylori infection seem to display an interaction in the development of gastric cancer.
METHODS: PGC gene polymorphism in 141 patients with gastric cancer and 564 matched non-cancer controls were detected by polymerase chain reaction (PCR), and the relation between the PGC polymorphism and gastric cancer was examined. Serum H. pylori-IgG was determined with ELISA method. The odds ratios and 95% confidence intervals (95% CI) were calculated using unconditional logistic regression model. The effect-modified model was used to evaluate the PGC-H. pylori interaction.
RESULTS: No significant association between the frequency of homogenous allele 1 of PGC gene and the sex and age of the subjects was observed. The subjects with the homogenous allele 1 had an increased risk of developing atrophic gastritis (OR: 3.103, 95% CI: 1.440-6.686), and gastric cancer (OR: 2.962, 95% CI: 1.370-6.404), and Intestinal metaplasia (OR: 1.659, 95% CI: 0.998-2.757) comparing with those with the non-homogenous allele 1. For subjects carrying both homogenous allele 1 and H. pylori-IgG positive, there was an significant increased risk of developing atrophic gastritis and gastric cancer (likelihood test ratio test: P = 0.023, P = 0.005).
CONCLUSION: PGC gene polymorphism may be associated with susceptibility to gastric cancer and atrophic gastritis. The PGC gene polymorphism and H. pylori infection seem to display an interaction in the development of gastric cancer.