Helicobacter pylori infection and expression of the angiogenic factor platelet-derived endothelial cell growth factor by pre-neoplastic gastric mucosal lesions and gastric carcinoma

Dig Liver Dis. 2002 Sep;34(9):621-5. doi: 10.1016/s1590-8658(02)80203-1.

Abstract

Background: Expression of the angiogenic factor platelet-derived endothelial cell growth factor is induced in some gastric carcinomas. Whether angiogenesis is induced early in the development of gastric pre-neoplastic lesions and whether Helicobacter pylori infection affects platelet-derived endothelial cell growth factor expression is not known.

Aim: To assess whether chronic gastritis, intestinal metaplasia, gastric dysplasia and gastric carcinomas express platelet-derived endothelial cell growth factor and whether Helicobacter pylori infection might affect the expression of platelet-derived endothelial cell growth factor in these lesions.

Patients and methods: Patients with gastric carcinomas, atrophic gastritis with associated intestinal metaplasia, dysplasia and controls without infection or carcinoma were studied.

Results: Platelet-derived endothelial cell growth factor was detected by immunohistochemistry in 9 out 19 gastric carcinomas (45%). Only focal immunostaining was detected in intestinal metaplasia adjacent to dysplasia and in dysplastic cells. Of the tumours, 90% contained platelet-derived endothelial cell growth factor-positive interstitial cells. A significant correlation was found between active Helicobacter pylori infection and a larger number of platelet-derived endothelial cell growth factor-positive interstitial cells in areas of intestinal metaplasia (p<0.05).

Conclusion: Helicobacter pylori infection does not influence the expression of platelet-derived endothelial cell growth factor, once gastric cancer has developed. However, Helicobacter pylori infection may increase the extension of expression of platelet-derived endothelial cell growth factor by infiltrating interstitial cells in premalignant lesions, such as intestinal metaplasia, which may help create a favourable environment for tumour development. This may possibly be due to non-specific increase in recruitment of inflammatory cells caused by Helicobacter pylori infection. Further studies, with a larger number of samples, are now needed in order to confirm this finding.

MeSH terms

  • Adenocarcinoma / metabolism
  • Adenocarcinoma / microbiology*
  • Adenocarcinoma / pathology
  • Cell Transformation, Neoplastic / pathology
  • Gastric Mucosa / pathology
  • Gastritis, Atrophic / metabolism
  • Gastritis, Atrophic / microbiology*
  • Gastritis, Atrophic / pathology
  • Helicobacter Infections / pathology*
  • Helicobacter pylori* / isolation & purification
  • Helicobacter pylori* / ultrastructure
  • Humans
  • Immunohistochemistry
  • Metaplasia / pathology
  • Stomach / blood supply
  • Stomach Neoplasms / metabolism
  • Stomach Neoplasms / microbiology*
  • Stomach Neoplasms / pathology
  • Thymidine Phosphorylase / metabolism*

Substances

  • Thymidine Phosphorylase