title: Multiple gene status in Helicobacter pylori strains and risk of gastric cancer development.
abstract: OBJECTIVE
  The identification of the vacA intermediate region has provided new insights into the role of vacA heterogeneity in relation to gastro-duodenal pathogenesis. The aim of this study was to assess vacA polymorphism in Iranian Helicobacter pylori strains and its association with cagA as a major virulence determinant, gastric histopathology and disease.
  
  
  METHODS
  vacA polymorphism and serum antibody responses were studied in 207 H. pylori-infected (139 NUD, 34 PUD, and 34 GC) patients and correlated with gastric histopathology.
  
  
  RESULTS
  Multivariate logistic regression analysis found intermediate region typing superior to signal or mid region typing for screening high risk patients. vacA i1 allele was identified as an independent predictor of dysplasia (OR = 9.044; 95% CI: 1.11-73.33). Possession of s1/i1/cagA(+) strains was also identified as a predictor of intestinal metaplasia (OR = 3; 95% CI: 1.13-7.95), dysplasia (OR = 9.9; 95% CI: 1.23-80.86) and risk of GC (OR = 6.9; 95% CI: 2.5-18.66) as well as induction of anti-VacA sero-positivity (OR = 5.04; 95% CI: 1.8-13.6). Anti-VacA serology correctly detected 83.8% of s1/i1/cagA(+) strains carried by high-risk patients.
  
  
  CONCLUSIONS
  The current study emphasizes the implication of vacA polymorphic structure, especially the s1/i1/cagA(+) genotype, in increasing the risk of GC by revealing their association with gastric pre-neoplastic changes and their reflection in VacA sero-positivity which encourages the application of noninvasive procedures in population screening.
authors.affiliation: Helicobacter pylori Research Group, Biotechnology Research Center, Pasteur Institute of Iran, Tehran, Iran.
authors.forename: Masoumeh
authors.initials: M
authors.lastname: Douraghi
authors.forename: Yeganeh
authors.initials: Y
authors.lastname: Talebkhan
authors.forename: Hojjat
authors.initials: H
authors.lastname: Zeraati
authors.forename: Fatemeh
authors.initials: F
authors.lastname: Ebrahimzadeh
authors.forename: Azin
authors.initials: A
authors.lastname: Nahvijoo
authors.forename: Arman
authors.initials: A
authors.lastname: Morakabati
authors.forename: Masoud
authors.initials: M
authors.lastname: Ghafarpour
authors.forename: Maryam
authors.initials: M
authors.lastname: Esmaili
authors.forename: Maryam
authors.initials: M
authors.lastname: Bababeik
authors.forename: Akbar
authors.initials: A
authors.lastname: Oghalaie
authors.forename: Nasser
authors.initials: N
authors.lastname: Rakhshani
authors.forename: Mahmoud Eshagh
authors.initials: ME
authors.lastname: Hosseini
authors.forename: Mohammad Ali
authors.initials: MA
authors.lastname: Mohagheghi
authors.forename: Marjan
authors.initials: M
authors.lastname: Mohammadi
mesh_terms: D000230:Adenocarcinoma / Q000276:immunology / Q000382:microbiology* / Q000473:pathology; D000328:Adult; D000907:Antibodies, Bacterial / Q000097:blood; D001426:Bacterial Proteins / Q000235:genetics* / Q000276:immunology; D004415:Dyspepsia / Q000276:immunology / Q000382:microbiology; D005260:Female; D005787:Gene Frequency; D005838:Genotype; D016481:Helicobacter Infections / Q000150:complications* / Q000382:microbiology; D016480:Helicobacter pylori / Q000235:genetics* / Q000276:immunology / Q000378:metabolism; D006801:Humans; D008297:Male; D010437:Peptic Ulcer / Q000276:immunology / Q000382:microbiology; D011110:Polymorphism, Genetic; D012307:Risk Factors; D013274:Stomach Neoplasms / Q000276:immunology / Q000382:microbiology* / Q000473:pathology
chemical_list: D000907:Antibodies, Bacterial; D001426:Bacterial Proteins; C074689:VacA protein, Helicobacter pylori