Abstract
Background and aims: Aberrant DNA methylation observed in the atrophic gastritis with the past infection of Helicobacter pylori (H. pylori) is associated with the risk of gastric cancer, mainly intestinal-type. In contrast, DNA methylation in gastric mucosae at risk of diffusetype gastric cancer is not fully known. We have found that the subjects with severe gastric mucosal inflammation identified by serum markers have higher risk of the development of diffuse-type gastric cancer. Thosewho showedH. pylori antibody titer >500U/mL, pepsinogen (PG) II >30 ng/mL, or PG I >70 ng/mL and PG I/II ratio 500 U/mL) and high levels of PG II (>30 ng/mL). The methylation levels were also severely altered in the subjects with serum PG I >70 ng/mL and PG I/II ratio <3.0. Conclusions: DNA methylation in gastric mucosae was closely associated with the severity of inflammation identified by serum H. pylori antibody or PGs. These results suggest that DNAmethylation works to some extent in the occurrence of diffusetype gastric cancer resulting from severe active inflammation induced by H. pylori infection.
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