1.Gastrointestinal Research Group, Division of Applied Medicine, School of Medicine, Dentistry, Aberdeen University, Aberdeen AB25 2ZD, Scotland, UK
The gastric mucosa is normally devoid of lymphoid tissue. H. pylori is implicated as an etiological agent in over 92% of cases of gastric MALT lymphoma. Chronic H. pylori infection results in a lymphoid follicular gastritis and so to the acquisition of gastric MALT. MALT lymphomagenesis is thought to be dependent on clonal expansion driven by H. pylori antigenic stimulation. The mechanisms involved in the transformation of low-grade gastric MALT lymphoma to high grade DLBCL are not well understood.Individual differences in the inflammatory response to H. pylori infection, as determined by host genetic polymorphisms, may predispose to the development of a gastric cancer phenotype. Pro-inflammatory polymorphisms have been described in the interleukin-1 gene cluster, and tumour necrosis factor-alpha, interleukin-10, interleukin-8, and interferon-gamma genes. Having an increasing number of such pro-inflammatory genetic polymorphisms confers an increased gastric cancer risk for an H. pylori-infected individual.
Paul Lochhead ; Emad El-Omar
Gastric Tumors: an overview
Atlas Genet Cytogenet Oncol Haematol. 2008-11-01
Online version: http://atlasgeneticsoncology.org/solid-tumor/5410/gastrictumoverviewid5410