Gastric cancer and Helicobacter pylori: the bug, the host or the environment?

Worldwide, gastric cancer is still a leading cause of cancer deaths. The association of Helicobacter pylori and gastric cancer is well established, and the bacterium was declared a class one carcinogen by the International Agency for Research on Cancer and the World Health Organisation in 1994. H pylori infection is responsible for 5.5% of all global cancers, 75% of non-cardia gastric cancer and lymphoma, and 65% of gastric cancers worldwide.1 In 2005, Marshall and Warren were awarded the Nobel Prize for Medicine for their pioneering work on H pylori (in 1984) showing the association between this bacterium and gastritis and that antibiotics could cure peptic ulcers.2 Parsonnet et al3 formally demonstrated the link to gastric cancer in 1991. However, although more than 50% of people worldwide are infected with H pylori, only a small percentage of those infected will have clinical complications, which include gastric and duodenal ulcers, precancerous lesions, atrophy and intestinal metaplasia, and progression to cancer or lymphoma. However, all those infected will have some degree of histological gastritis, likely to be present long term. It is the distribution and extent of gastritis that to some extent determines outcome: 10–15% of subjects will have antral-predominant gastritis, which is the duodenal ulcer phenotype, and 1% will have a body (corpus)-predominant phenotype, with the risk of gastric cancer.4 It has been estimated that 60–80% of gastric cancers would be preventable if H pylori was eradicated.1