Gastric cancer

Infection with Helicobacter pylori (Hp), which affects more than half of the world population, is an established risk factor for gastric cancer, yet only 10-15% of infected individuals are estimated to experience clinically adverse sequelae, including peptic ulcers, gastric adenocarcinoma and gastric mucosa-associated lymphoid tissue lymphoma (MALT). What determines these variable clinical outcomes has not been fully elucidated, but believed to be combinations of environmental, host genetics and HP virulence factors. Work by us and others support that bacterial factors are likely to play the most decisive role. In particular, presence in the bacterial genome of a cytotoxin-associated gene pathogenicity island (cagPAI) is associated with increased risk of progression from preneoplastic lesions to cancer. We have sequenced the whole Hp genome, including the cagPAI, of Hp samples isolated from gastric biopsies of subjects with preneoplastic gastric lesions (chronic gastritis, metaplasia, dysplasia, for a total of over 2000 samples available) and with stomach cancer (about 200 samples available), in order to identify specific variants in this regions of the bacterial genome that are associated with risk of neoplastic progression.