title: Helicobacter pylori infection and expression of the angiogenic factor platelet-derived endothelial cell growth factor by pre-neoplastic gastric mucosal lesions and gastric carcinoma.
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.
  
  
  OBJECTIVE
  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.
  
  
  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).
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Internal Medicine, Catholic University of Rome, Italy.
authors.forename: F
authors.initials: F
authors.lastname: Franceschi
authors.forename: R M
authors.initials: RM
authors.lastname: Genta
authors.forename: A
authors.initials: A
authors.lastname: Gasbarrini
authors.forename: N
authors.initials: N
authors.lastname: Gentiloni Silveri
authors.forename: G
authors.initials: G
authors.lastname: Gasbarrini
authors.forename: A R
authors.initials: AR
authors.lastname: Sepulveda
mesh_terms: D000230:Adenocarcinoma / Q000378:metabolism / Q000382:microbiology* / Q000473:pathology; D002471:Cell Transformation, Neoplastic / Q000473:pathology; D005753:Gastric Mucosa / Q000473:pathology; D005757:Gastritis, Atrophic / Q000378:metabolism / Q000382:microbiology* / Q000473:pathology; D016481:Helicobacter Infections / Q000473:pathology*; D016480:Helicobacter pylori / Q000302:isolation & purification / Q000648:ultrastructure; D006801:Humans; D007150:Immunohistochemistry; D008679:Metaplasia / Q000473:pathology; D013270:Stomach / Q000098:blood supply; D013274:Stomach Neoplasms / Q000378:metabolism / Q000382:microbiology* / Q000473:pathology; D013939:Thymidine Phosphorylase / Q000378:metabolism*
chemical_list: D013939:Thymidine Phosphorylase