title: Helicobacter pylori infection influences tumor growth of human gastric carcinomas.
abstract: BACKGROUND
  Helicobacter pylori infection is considered a risk factor for gastric carcinoma. However, the effect of eradication therapy in gastric carcinoma patients is not well known. The aim of this study was to investigate the relationship between H. pylori infection and tumor growth of gastric carcinoma.
  
  
  METHODS
  Fifty-one patients with gastric carcinoma participated in the study. Thirty-three were H. pylori-positive, 6 were H. pylori-negative, and 12 were diagnosed with gastric carcinoma after eradication of H. pylori. To investigate tumor growth of gastric carcinoma, cell proliferation and angiogenesis of the tumors were evaluated by immunohistochemical techniques using Ki-67 and CD34.
  
  
  RESULTS
  The Ki-67 labeling index was 47.9 +/- 2.6 (mean +/- s) in the H. pylori-positive group, 38.1 +/- 3.6 in the H. pylori-eradicated group, and 22.2 +/- 5.5 in the H. pylori-negative group. It was significantly lower in the H. pylori-eradicated and H. pylori-negative groups than in the H. pylori-positive one, and a significant difference was also found between the H. pylori-positive and H. pylori-eradicated groups. The microvessel counts were 62.5 +/- 3.0, 50.2 +/- 4.0, and 66.0 +/- 9.8 in the positive, eradicated, and negative groups, respectively. A significant difference was found between the H. pylori-positive and H. pylori-eradicated groups.
  
  
  CONCLUSIONS
  Our results suggest that H. pylori infection is associated with cell proliferation, and its eradication may influence tumor vascularity of gastric carcinoma. Therefore, H. pylori eradication therapy may contribute to the suppression of tumor growth.
authors.affiliation: Dept. of Medicine and Molecular Science, Graduate School of Biomedical Sciences, Hiroshima University, Hiroshima, Japan. asasaki@hiroshima-u.ac.jp
authors.forename: A
authors.initials: A
authors.lastname: Sasaki
authors.forename: Y
authors.initials: Y
authors.lastname: Kitadai
authors.forename: M
authors.initials: M
authors.lastname: Ito
authors.forename: M
authors.initials: M
authors.lastname: Sumii
authors.forename: S
authors.initials: S
authors.lastname: Tanaka
authors.forename: M
authors.initials: M
authors.lastname: Yoshihara
authors.forename: K
authors.initials: K
authors.lastname: Haruma
authors.forename: K
authors.initials: K
authors.lastname: Chayama
mesh_terms: D000368:Aged; D018952:Antigens, CD34 / Q000032:analysis; D002277:Carcinoma / Q000098:blood supply / Q000737:chemistry / Q000382:microbiology* / Q000473:pathology; D002455:Cell Division; D005260:Female; D016481:Helicobacter Infections / Q000188:drug therapy / Q000503:physiopathology*; D016480:Helicobacter pylori; D006801:Humans; D007150:Immunohistochemistry; D019394:Ki-67 Antigen / Q000032:analysis; D008297:Male; D008875:Middle Aged; D009389:Neovascularization, Pathologic; D013274:Stomach Neoplasms / Q000098:blood supply / Q000737:chemistry / Q000382:microbiology* / Q000473:pathology
chemical_list: D018952:Antigens, CD34; D019394:Ki-67 Antigen