| Theme |
Risk Factors and Prevention of Gastric Cancer |
| Title |
Salt and H. pylori-associated Gastric Cancer |
| Author |
Shinji Takasu |
Division of Oncological Pathology, Aichi Cancer Center Research Institute |
| Author |
Tetsuya Tsukamoto |
Division of Oncological Pathology, Aichi Cancer Center Research Institute |
| Author |
Takeshi Toyoda |
Division of Oncological Pathology, Aichi Cancer Center Research Institute |
| Author |
Masae Tatematsu |
Division of Oncological Pathology, Aichi Cancer Center Research Institute |
| [ Summary ] |
Salt promoted gastric carcinogenesis in Mongolian gerbils with Helicobacter pylori (H. pylori) infection and N-methyl-N-nitrosourea (MNU) treatment in a dose dependent manner. Salt was a weak factor for gastric carcinogenesis compared to H. pylori infection and behaved as a co-promoter of gastric cancers, especially in combination with H. pylori. Salt induced the increase of surface mucous cell type mucins (SMCM), suitable for H. pylori colonization, and a decrease in gland mucous cell type mucins (GMCM), which have effects on inhibiting H. pylori infection. H. pylori infection induced an increase in MUC6 mRNA expression, while salt had no influence on MUC5AC and MUC6 mRNA expression. Thus, salt altered the mucousal microenvironment by increasing SMCM to help H. pylori colonize and exacerbate inflammation and increased subsequent stomach carcinogenesis by inhibiting GMCM defense mechanisms. Therefore, restriction of salt is important for the prevention of stomach cancers in patients with H. pylori infection. |