title: Helicobacter pylori genotyping in gastric adenocarcinoma and MALT lymphoma by multiplex PCR analyses of paraffin wax embedded tissues.
abstract: BACKGROUND
  Gastric infection with Helicobacter pylori is the major cause of chronic active gastritis and is associated with the pathogenesis of peptic ulcer and gastric carcinoma. Gastric mucosal damage involves both host and H pylori dependent factors, such as the presence of the cag pathogenicity island and allelic variations of the vacA and iceA genes.
  
  
  OBJECTIVE
  To evaluate the association of these virulence factors with the development of gastric malignancies, a retrospective study was performed on archived tissue routinely obtained for diagnostic histopathology.
  
  
  METHODS
  DNA was extracted from formalin fixed, paraffin wax embedded gastric tissue sections of 93 patients with chronic active gastritis (n = 39), adenocarcinoma (n = 28), or mucosa associated lymphoid tissue (MALT) lymphoma (n = 24). The extracted DNA was used to perform a polymerase chain reaction based, simultaneous analysis of the following: (1) cagA status, (2) allelic variation of the iceA genes (iceA1, iceA2), allelic variation of the signal peptide (s1a, s1b, s2) and the midregion (m1, m1a, m2) of the vacA gene.
  
  
  RESULTS
  The iceA1 gene showed a 3.6 fold and the vacA s1a variant a 4.2 fold higher prevalence in gastric adenocarcinoma than in gastritis. The combined presence of both the vacA s1a and iceA1 genes had a 5.6 fold higher frequency in adenocarcinoma. The vacA m2 allele was the predominant subtype in MALT lymphoma and the combination of the vacA m2 subtypes with the vacA s1 and the iceA1 variants occurred in MALT lymphoma nearly five times more often than in chronic active gastritis.
  
  
  CONCLUSIONS
  Certain H pylori subtype combinations possess a differentiating and predictive value for the development of gastric adenocarcinoma and MALT lymphoma.
authors.affiliation: Institute for Pathology, University of Cologne, 50924 Cologne, Germany Institute for Pathology, University of Mainz, 55131 Mainz, Germany.
authors.forename: C I
authors.initials: CI
authors.lastname: Koehler
authors.forename: M B
authors.initials: MB
authors.lastname: Mues
authors.forename: H P
authors.initials: HP
authors.lastname: Dienes
authors.forename: J
authors.initials: J
authors.lastname: Kriegsmann
authors.forename: P
authors.initials: P
authors.lastname: Schirmacher
authors.forename: M
authors.initials: M
authors.lastname: Odenthal
mesh_terms: D000230:Adenocarcinoma / Q000382:microbiology*; D000368:Aged; D000483:Alleles; D002908:Chronic Disease; D004269:DNA, Bacterial / Q000032:analysis; D005753:Gastric Mucosa / Q000382:microbiology; D005756:Gastritis / Q000382:microbiology*; D005798:Genes, Bacterial / Q000235:genetics; D016481:Helicobacter Infections / Q000382:microbiology; D016480:Helicobacter pylori / Q000235:genetics* / Q000472:pathogenicity; D006801:Humans; D018442:Lymphoma, B-Cell, Marginal Zone / Q000382:microbiology*; D008875:Middle Aged; D016133:Polymerase Chain Reaction / Q000379:methods; D012189:Retrospective Studies; D013274:Stomach Neoplasms / Q000382:microbiology*; D037521:Virulence Factors / Q000235:genetics
chemical_list: D004269:DNA, Bacterial; D037521:Virulence Factors