Increased cancer risk for the disrupted co-evolution of Helicobacter pylori with hosts

Helicobacter pylori colonize the human stomach and increase the risk for gastric cancer. It is intriguing, however, that the incidence of gastric cancer is low in some geographical regions or ethnic groups with a high prevalence of H. pylori. During past hundreds of years, waves of human migration have resulted in mingled populations of multiple ethnicities in many geographical regions. The incidence of gastric cancer may vary among different ethnic groups in these regions. Studies have found newly acquired H. pylori infection or infection with strains replaced from other populations. For ethnic groups with a new acquisition of the bacterium, risk for gastric cancer is usually low owing to the low prevalence of H. pylori. In contrast, the risk is increased when an infection with strains from another population occurs. Currently, it appears that the differences in bacterial genomic contents are not responsible for the varied incidence of gastric cancer. Rather, the disruption of the original co-evolution of the bacterium and hosts could contribute to the gastric carcinogenesis. Further understanding the interaction between the bacterium and hosts would benefit for elucidating the carcinogenic mechanisms of H. pylori.