[Helicobacter pylori and gastric carcinogenesis]

Gastric carcinogenesis is a multistep and multifactorial process beginning with chronic gastritis Helicobacter pylori (Hp) induced in most cases. There are some obstacles to an exclusive acceptance of the idea that the relation of Hp with the preneoplastic/neoplastic changes solely develops by means of the chronic gastritis with its atrophic evolution and achlorydria. Hp may be considered a trigger by means of alteration of cellular synetics without any direct influence on genetic alterations. Under the push of an intense proliferation, the expression of typical antigens of the organ is progressively lost, with acquisition of antigens from other organs. Cellular dedifferentiation displayed, with the progressive increase of immature elements that progress to the more or less total disappearance of differentiated gastric cells or differentiating ones, with the formation of metaplastic/dysplastic clones or even neoplastic ones. The bacteria, together with other environmental factors and individual genetic susceptibility, determine the final risk for the development of gastric cancer. Considering that 1-2% of the Hp positive subjects are estimated to develop gastric cancer and that Hp is considered the cause of 75% of gastric cancer, the eradication of the infection, not only in the initial phases but even in those with preneoplastic changes, involves an advantage for the prevention of gastric cancer. For the prevention among the general population testing Hp-positive subjects for serum antibodies against CagA protein might represent an effective way of identifying patients in whom Hp eradication is advisable also in term of gastric cancer prevention.