BACKGROUND/AIMS: infection induces aberrant DNA methylation in gastric mucosa. We evaluated the long-term effect of eradication on promotor CpG island hypermethylation in gastric carcinogenesis.

METHODS

-positive patients with gastric adenoma or early gastric cancer who underwent endoscopic resection were enrolled. According to eradication after endoscopic resection, the participants were randomly assigned to eradication or non-eradication group. -negative gastric mucosa from normal participants provided the normal control. CpG island hypermethylation of tumor-related genes (p16, CDH1, and RUNX-3) was evaluated by quantitative MethyLight assay in non-tumorous gastric mucosa. The gene methylation rate and median values of hypermethylation were compared after one year by status.

RESULTS

In -positive patients, hypermethylation of p16 was found in 80.6%, of CDH1 in 80.6%, and of RUNX-3 in 48.4%. This is significantly higher than normal control (p16, 10%; CDH1, 44%; RUNX-3, 16%) (p<0.05). In the eradication group, methylation rates of p16 and CDH1 decreased in 58.1% and 61.3% of the patients, and the median values of hypermethylation were significantly lower at one year compared with the non-eradication group. However, RUNX-3 hypermethylation did not differ significantly at one year after eradication. The non-eradication group hypermethylation did not change after one year.

CONCLUSIONS

infection was associated with promotor hypermethylation of genes in gastric carcinogenesis, and eradication might reverse p16 and CDH1 hypermethylation.