Helicobacter pylori, a Gram negative bacteria, is capable of modifying cell turnover in the interior of gastric glands, by influencing cell proliferation and apoptosis ratio. Gastric carcinogenesis is a complex, multifactorial process in which Helicobacter pylori persistence plays an important role. Initially Helicobacter pylori determines a superficial gastritis which can lead to glandular loss and multifocal atrophic gastritis; this is followed by intestinal metaplasia which can develop later in some patients in gastric displasia and cancer. This carcinogenic model is currently accepted for distal gastric cancer; cardial cancer is correlated with Helicobacter pylori infection. Usually intestinal pathologic type is associated with gastric atrophy and diffuse type is associated with non-atrophic chronic gastritis. Helicobacter pylori seems to be involved in both pathological forms of gastric cancer; epidemiological studies couldn't find significant differences between those types regarding infection prevalence. Regarding the high prevalence of Helicobacter pylori infection in general population must be explained firstly why just some individuals develop gastric cancer and secondly why others develop peptic ulcer.
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Preda, A., Burada, F., Soare, C., Birca, A., Moraru, E., & Cruce, M. (2009). Helicobacter pylori infection and the development of gastric cancer. Annals of the Romanian Society for Cell Biology, 14(2), 212–214. https://doi.org/10.1097/00042737-200111000-00023