Helicobacter pylori infection and molecular changes in gastric carcinogenesis.
In recent years there has been much progress in understanding the pathogenesis of gastric cancer. The role of individual factors in gastric carcinogenesis continues to be debated and is also subject to further analysis. In addition to the activation of oncogenes and the inactivation of tumor suppressor genes, alteration of adhesion molecules seems to be critical for the development of gastric cancer. Helicobacter pylori has been linked to an increased risk of developing gastric cancer, and the molecular changes induced by H. pylori are currently being investigated. Recent studies indicate that H. pylori induces cell proliferation and apoptosis during the early phase of chronic inflammation of the gastric mucosa, whereas in the malignant transformation of the gastric mucosa apoptosis is inhibited and adhesion of gastric epithelial cells is impaired. This review focuses on the role of H. pylori in the development of molecular changes in gastric cancer and its preneoplastic lesions.
Ebert
Matthias P A
MP
Department of Gastroenterology, Hepatology and Infectious Diseases, Otto-von-Guericke University, Magdeburg, Germany.
Schandl
Laszlo
L
Malfertheiner
Peter
P
D016481:Helicobacter Infections / Q000150:complications* / Q000235:genetics* / Q000503:physiopathology; D016480:Helicobacter pylori / Q000235:genetics* / Q000472:pathogenicity; D006801:Humans; D025202:Molecular Diagnostic Techniques; D013274:Stomach Neoplasms / Q000209:etiology* / Q000235:genetics* / Q000503:physiopathology