Journal of Gastroenterology

, Volume 37, Supplement 13, pp 45–49

Helicobacter pylori infection and molecular changes in gastric carcinogenesis

Authors

  • Matthias P. A. Ebert
    • Department of Gastroenterology, Hepatology and Infectious DiseasesOtto-von-Guericke University
  • Laszlo Schandl
    • Department of Gastroenterology, Hepatology and Infectious DiseasesOtto-von-Guericke University
  • Peter Malfertheiner
    • Department of Gastroenterology, Hepatology and Infectious DiseasesOtto-von-Guericke University
Article

DOI: 10.1007/BF02990099

Cite this article as:
Ebert, M.P.A., Schandl, L. & Malfertheiner, P. J Gastroenterol (2002) 37: 45. doi:10.1007/BF02990099

Abstract

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 byH. pylori are currently being investigated. Recent studies indicate thatH. 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 ofH. pylori in the development of molecular changes in gastric cancer and its preneoplastic lesions.

Key words

gastric cancergenestomachpathogenesis

Copyright information

© Springer-Verlag 2002