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Helicobacter pylori infection and gastrin and cyclooxygenase expression in gastric and colorectal malignancies.

Abstract
Helicobacter pylori, infecting more than 50% of the world population, results in gastritis, usually located in the antral portion of the stomach, accompanied by hypergastrinemia, the key factor in gastric and colorectal carcinogenesis. Excessive mucosal cell proliferation for many years may eventually result in gastric atrophy, cell mutation and transformation of gastric mucosal cells into gastrin-producing cells, which also express gastrin receptors serving to stimulate cell proliferation and tumor growth. These processes may be completed by the expression of cyclooxygenase-2 (COX-2) as an inflammation enzyme to release excessive amounts of PGE(2), leading to further proliferation, reduction in apoptosis, angiogenesis and tumor growth. H. pylori eradication results in complete regression of MALT lymphoma and subsequent normalisation of excessive gastrin release and COX-2 expression. Reduction of gastrin by active immunisation (gastrimmune), blocking of gastrin receptors with specific blockers and suppression of COX-2 might be helpful in inhibiting tumor growth and invasion.
AuthorsS J Konturek, P C Konturek, A Hartwich, E G Hahn
JournalRegulatory peptides (Regul Pept) Vol. 93 Issue 1-3 Pg. 13-9 (Sep 25 2000) ISSN: 0167-0115 [Print] Netherlands
PMID11033048 (Publication Type: Journal Article, Review)
Chemical References
  • Gastrins
  • Isoenzymes
  • Membrane Proteins
  • Cyclooxygenase 2
  • PTGS2 protein, human
  • Prostaglandin-Endoperoxide Synthases
Topics
  • Animals
  • Colorectal Neoplasms (microbiology)
  • Cyclooxygenase 2
  • Gastrins (biosynthesis)
  • Helicobacter Infections (metabolism)
  • Helicobacter pylori (metabolism, physiology)
  • Humans
  • Isoenzymes (biosynthesis)
  • Lymphoma, B-Cell, Marginal Zone (microbiology)
  • Membrane Proteins
  • Mice
  • Prostaglandin-Endoperoxide Synthases (biosynthesis)
  • Stomach Neoplasms (microbiology)

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