Abstract
Helicobacter pylori infection is the most important cause of human gastric cancer worldwide. Gastric cancer develops over a long time after H. pylori infection via stepwise accumulation of genetic alterations and positive selection of cells with growth advantages. H. pylori itself and the resultant chronic inflammation lead to the emergence of genetic alterations in gastric epithelial cells via increased susceptibility of these cells to DNA damage. Reactive oxygen species (ROS) and reactive nitrogen species (RNS) in inflammatory and gastric epithelial cells, as well as the expression of cytidine deaminase in gastric epithelial cells, may link H. pylori-related inflammation and DNA damage. Recent comprehensive analyses of gastric cancer genomes provide clues for the possible molecular mechanisms of gastric carcinogenesis. In this chapter, we describe how genetic alterations emerge during gastric carcinogenesis related to H. pylori infection.
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