Helicobacter pylori: the link with gastric cancer

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Abstract
Gastric cancer is the world's overall second most common cancer, and carries a bad prognosis. In the Correa model of gastric carcinogenesis, environmental factors (salt, nitrate, a lack of vitamin C and beta-carotene, bile reflux, bacterial overgrowth in atrophic gastritis with nitrosamine formation) are related to the evolution from normal gastric tissue through superficial gastritis, multifocal atrophic gastritis, intestinal metaplasia and dysplasia to carcinoma. The incidence ofH. pyloridecreases with progressing preneoplastic lesions. In several studies, the prevalence ofH. pyloriwas elevated in patients with gastric cancer, with a trend for a higher prevalence in intestinal type gastric cancervsdiffuse type. Family members of patients with gastric adenocarcinoma have a higherH. pyloriprevalence than controls; patients infected withH. pylorihave more family members with gastric cancer. Several epidemiological studies showed a higherH. pyloriprevalence in regions or populations with high gastric cancer riskvslow-risk populations. Large-scale studies in China and Europe showed a correlation betweenH. pyloriseroprevalence and gastric cancer incidence and mortality. Three prospective nested case-control studies showed that infection withH. pyloriincreased the risk of further development of gastric adenocarcinoma, showing thatH. pyloriinfection precedes the development of gastric cancer. Several pathways can be identified explaining the association betweenH. pyloriand gastric adenocarcinoma. We showed that gastric cell proliferation is increased in parallel with inflammation. The ascorbic acid concentrating mechanism is abolished in gastritis. Ammonia, generated byH. pylori'surease, gives rise to gastric mucosal atrophy. We showed that salt increases the gastric cell proliferation only inH. pylori-infected individuals. The organism's toxin may play a role in gastric cancer. BesidesH. pylori, other environmental factors are important in determining the gastric cancer risk. For instance, we showed that in Belgium, Maghreb immigrants have a high prevalence ofH. pyloriinfection but a low prevalence of intestinal metaplasia and gastric cancer. Gastric lymphoma is rare (about 5% of all gastric tumours), but its incidence is steadily increasing. It was shown thatH. pylorialso increases the risk for low-grade as well as high-grade gastric lymphoma. Eradication ofH. pylorihas been shown to cure several cases of unequivocally proven gastric low-grade lymphoma. WhetherH. pylorieradication and/or long-term antioxidant intervention is able to decrease the incidence of gastric preneoplastic and malignant lesions should be settled during the next years by several large-scale studies, including an European Cancer Prevention intervention study.

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