Helicobacter pylori (H. pylori) is a group 1 gastric carcinogen that plays a significant role in extra-gastric digestive system cancers. H. pylori disrupts host cell homeostasis through expression of virulence factors leading to immune evasion as well as persistent gastric mucosal colonization. H. pylori infection has been shown to play a role in extra-gastric cancers such as, hepatocellular cancer, cholangiocarcinoma, colorectal, pancreatic, and esophageal cancers. H. pylori are highly heterogeneous bacterium, and different strains may carry different virulence factors, which varies across geographic regions. Intercellular communication via exosomes derived from H. pylori-infected cells, and the H. pylori-related gut microbiota dysbiosis leads to extra-gastric cancer development through the "microbiota-epigenetic-cancer regulatory axis" in epigenomic reprogrammed host. Because of the regional and social variabilities, studies have conflicting results concerning the effect of the mutual interactions between the virulence factors of H. pylori, host, and host's microbiota on the development of extra-gastric cancer. Consistently, a significant increase in kynurenine production from tryptophan via indoleamine-2,3-dioxygenase activity of gut microbiome suppresses host's immune response by activating the aryl hydrocarbon receptor in H. pylori seropositive patients. Immune suppression in extra-gastric digestive system cancer development preserves the tumor cells from immune attack and promotes tumor growth.
Engin et al. (2026) studied this question.