Helicobacter pylori infection and the pathogenesis of gastric cancer

a paradigm for host-bacterial interactions

D. McNamara, E. El-Omar

Research output: Contribution to journalArticle

68 Citations (Scopus)

Abstract

Helicobacter pylori infection is the most important acquired risk factor for gastric cancer. The infection initiates a chronic inflammatory process that eventually alters the physiology of the gastric environment and leads to achlorohydria. Gastric atrophy may be part of this process but cancer can arise without this precursor. The net effect of decades of inflammation is the establishment of a milieu awash with proinflammatory cytokines and characterized by the activation of signalling pathways that cross-talk between inflammation and carcinogenesis. Many of the factors involved in chronic inflammation play a dual role in the process-promoting neoplastic progression but also facilitating cancer prevention. H. pylori bacterial virulence factors as well as host genetic factors play a major role in orchestrating the increased risk of cancer. The study of such host-bacterial interaction is key to uncovering the molecular and cellular pathways involved and will ultimately lead to developing preventive and therapeutic strategies against this global killer. (c) 2008 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.

Original languageEnglish
Pages (from-to)504-509
Number of pages6
JournalDigestive and Liver Disease
Volume40
Issue number7
Early online date16 May 2008
DOIs
Publication statusPublished - Jul 2008

Keywords

  • interleukin-1 gene polymorphisms
  • necrosis-factor-alpha
  • NF-Kappa-B
  • increased risk
  • atrophic gastritis
  • epithelial-cells
  • CAGA protein
  • promoter polymorphism
  • tyrosine phosphatase
  • Chinese population

Cite this

Helicobacter pylori infection and the pathogenesis of gastric cancer : a paradigm for host-bacterial interactions. / McNamara, D.; El-Omar, E.

In: Digestive and Liver Disease, Vol. 40, No. 7, 07.2008, p. 504-509.

Research output: Contribution to journalArticle

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