Abstract
Helicobacter pylori infection is the main risk factor for gastric cancer, which develops in a multistep process that includes chronic atrophic gastritis, intestinal metaplasia, and dysplasia.1 This process develops over decades. Progression to gastric cancer can still be observed after bacterial eradication suggesting that once a “point of no return” is reached, mechanisms triggered by the infection perpetuate and drive carcinogenesis. Atrophic gastritis is a complex lesion occurring at early stages of the carcinogenesis cascade.
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