Helicobacter pylori infection and gastric cancer

Twenty-three years have passed since the first isolation and cultivation of H. pylori. However, such spiral microorganisms had already been discovered in the 1890s. In Japan, 85 years ago, Rokuzo Kobayashi et al. discovered that a spirochete-like organism (Helicobacter felis) colonized the stomachs of dogs and cats. It was not until 70 years later that scientists again began attempting to treat Helicobacter spp.-associated gastroduodenal diseases. H. pylori is now believed to be one of the major pathogenetic factors in the development of gastroduodenal diseases. The inflammation associated with H. pylori damages the epithelial cells, which probably links this infection to preneoplastic lesions such as gastric atrophy or intestinal metaplasia. Recently, a large-scale randomized controlled study revealed the potent link between H. pylori infection and gastric cancer development. However, the molecular pathogenesis of H. pylori-associated carcinogenesis has been unknown. According to a recent investigation, sonic hedgehog (Shh), morphogen, is also expressed in normal adult gastric fundic mucosa, and this expression disappears in the fundic glandular cells of the H. pylori-colonized stomach, demonstrating for the first time that H. pylori infection leads to deregulation of the expression of a morphogen and that its infection could be linked to the misregulation of the gastric regenerative pathway. Research to seek the relation between H. pylori and gastric cancer development is consistent with the recent trend in molecular regenerative medicine.