Several factors affect the likelihood that an infection with H. pylori will cause cancer. Some of these factors are features of the bacterium itself. For example, some strains of H. pylori make a toxin called CagA that gets injected into the junctions where cells of the stomach lining meet. Once inside cells, CagA can cause them to become cancerous by removing controls on cell growth and enhancing cell motility (43). Long-term exposure of cells to the toxin causes chronic inflammation. Epidemiology studies suggest that CagA-positive strains have a stronger association with non-cardia gastric cancer than CagA-negative strains (44).
Some evidence also suggests that certain lifestyle exposures may modify H. pylori–induced stomach cancer risk. For example, H. pylori–infected individuals who smoke have a higher risk of stomach cancer than H. pylori–infected individuals who do not smoke (45). Also, a high intake of salt and processed meat is associated with an increased risk of stomach cancer (29), possibly by increasing the risk that H. pylori will colonize the stomach or that CagA will enter gastric cells (46, 47).