Recently, interest has focused on the association between the gut microbiota and human malignancies. Gastric cancer is one of the most common malignancies in the world. However, despite Helicobacter pylori being a well-known carcinogen for gastric cancer, studies of the association between the gut microbiota and gastric cancer are relatively few. The intestinal microbial diversity of H. pylori-infected subjects is significantly higher than that of non-infected subjects, and the abundance of the genus Streptococcus is significantly higher than that in H. pylori-infected subjects without atrophic gastritis. The gastric microbiota of patients with gastric cancer is characterized by the increase of oral bacteria, such as Streptococcus and Prevotella. An increase in oral bacteria is also a well-known characteristic of the intestinal flora of patients with colonic cancer. These findings might suggest that the progress of gastric glandular atrophy is associated with the development of colonic cancer as well as intestinal-type gastric cancer.

The liver is connected directly to the intestinal tract by the portal vein. In recent years, it has been clarified that intestinal factors play a very important role in the onset and progression of liver diseases through enterohepatic circulation. In increased intestinal permeability caused by various stresses, gut-derived LPS or LTA induce inflammatory signals via liver TLRs and promote liver fibrosis, cirrhosis and liver cancer. Moreover, although bile acids regulate metabolism-related gene expression through FXR or TGR5 signals and maintain liver homeostasis, excessive accumulation of secondary bile acids such as DCA and LCA induce liver damage and promote liver cancer. Elucidating the pathogenesis of liver disease through the gut-liver axis might lead to the development of a method for preventing liver disease through control of gut microbiota.