How does H. pylori infection cause gastric cancer?

Keio J Med. 2002 Dec;51 Suppl 2:53-6. doi: 10.2302/kjm.51.supplement2_53.

Abstract

H. pylori is now recognised to be an important co-factor in the aetiology of non-cardia gastric cancer of both the diffuse and intestinal histological type. The latter type develops via a complex multistage and multifactorial process. The fist stage involves progression from superficial gastritis to atrophic pangastritis with intestinal metaplasia and associated hypochlorhydria. This gastric phenotype may then progress to dysplasia and cancer. Many co-factors are involved in this progression including the strain of H. pylori, host genetic factors, such as interleukin-1 polymorphisms and gender, plus environmental factors such as smoking and diet. Intestinal colonisation with helminthic infection may retard the progression by altering the immune and inflammatory response to H. pylori and colonisation of the achlorhydric stomach with nitrosating bacteria may promote progression to cancer. H. pylori appears to be an obligatory co-factor in the aetiology of most gastric cancers. Consequently, prevention of the infection or its eradication in early life should reduce the incidence of this common and usually fatal tumour.

Publication types

  • Review

MeSH terms

  • Genotype
  • Helicobacter pylori / pathogenicity*
  • Humans
  • Interleukin-1 / genetics
  • Models, Biological
  • Phenotype
  • Polymorphism, Genetic
  • Stomach Neoplasms / etiology*
  • Stomach Neoplasms / microbiology*

Substances

  • Interleukin-1