Gastric carcinogenesis, which may well extend over decades, is characterized by a slow stepwise evolution
from superficial gastritis to glandular atrophy, intestinal metaplasia, dysplasia, and finally, adenocarcinoma. This sequence
provides an excellent opportunity for the prevention or early detection of the events preceding development of the
neoplasm. In 1994, the International Agency for Research on Cancer defined Helicobacter pylori (H. pylori) as a group
I carcinogen for gastric cancer (GC). Evidence supporting a causal association has been demonstrated by epidemiological
data as well as by experimental animal models. A meta-analysis has shown an higher risk (odds ratio: 1.92) of progression
to GC in infected compare to uninfected subjects, that increased to a value >8 considering the surveys having a follow-up
of more than 8 years. A crucial question remains whether and when precancerous lesions can reverse after H. pylori
eradication. While several prospective studies have cast doubts about this reversibility others obtained opposing results.
Currently, H. pylori is recognized as a necessary but insufficient cause of GC. The most accepted model of gastric carcinogenesis
provides, like for other cancers, a multifactorial pathogenesis, linked with a number of initiators and other
continuator agents. This review presents a multidisciplinary point of view to approaching the relationship between H. pylori
infection and GC, focusing on the potential benefits of bacterial eradication in slowing down or in inducing regression
of precancerous lesions.
Keywords: Helicobacter pylori, gastric cancer, intestinal metaplasia, Gastric carcinogenesis, glandular atrophy, dysplasia, adenocarcinoma, precancerous lesions, multifactorial pathogenesis, bacterial eradication, neoplasms, biotechnologies, gastroduodenal diseases, gastric MALT lymphoma
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