title: Is the association between Helicobacter pylori and gastric cancer confined to CagA-positive strains?
abstract: BACKGROUND
  Infection with Helicobacter pylori is associated with an increased risk of gastric cancer. Several studies have indicated that the association differs with strain type. We aimed to find out if infection with strains lacking the virulence factor CagA is linked to gastric cancer risk.
  
  
  METHODS
  In a hospital-based case-control study, we collected sera from 100 case patients with a newly diagnosed gastric adenocarcinoma and 96 control patients with diseases unrelated to H. pylori status. Antibodies to H. pylori were analyzed by enzyme-linked immunosorbent assay (ELISA), and antibodies to CagA were detected by immunoblot. Logistic regression was used to obtain odds ratios (ORs) as estimates of relative risk, adjusted for potential confounding.
  
  
  RESULTS
  Among the case patients, 81% were ELISA positive and 86% had antibodies to CagA. The corresponding numbers among the controls were 58% and 55%, respectively. ELISA positivity was associated with an increased risk of gastric adenocarcinoma compared to ELISA negativity (OR for gastric cancer regardless of site 3.9, 95% CI 1.9-8.2). The OR was 7.4 (95% CI 3.3-16.6) for CagA-positive relative to CagA-negative subjects. Among ELISA-positive subjects the presence of CagA antibodies increased the risk 3.6 times (95% CI 1.2-11.1). ELISA-positive CagA-negative infections were associated with a fourfold increased risk (OR = 4.2, 95% CI 1.0-17.0) compared to no infection (ELISA-negative and CagA-negative).
  
  
  CONCLUSIONS
  Although patients with antibodies to CagA have the greatest risk of developing gastric cancer, those with CagA-negative infections run a significantly greater risk than uninfected persons.
authors.affiliation: Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
authors.forename: Maria
authors.initials: M
authors.lastname: Held
authors.forename: Lars
authors.initials: L
authors.lastname: Engstrand
authors.forename: Lars-Erik
authors.initials: LE
authors.lastname: Hansson
authors.forename: Reinhold
authors.initials: R
authors.lastname: Bergström
authors.forename: Torkel
authors.initials: T
authors.lastname: Wadström
authors.forename: Olof
authors.initials: O
authors.lastname: Nyrén
mesh_terms: D000230:Adenocarcinoma / Q000453:epidemiology* / Q000382:microbiology; D000368:Aged; D000907:Antibodies, Bacterial / Q000097:blood; D000942:Antigens, Bacterial / Q000276:immunology / Q000378:metabolism*; D001426:Bacterial Proteins / Q000276:immunology / Q000378:metabolism*; D016022:Case-Control Studies; D005260:Female; D016481:Helicobacter Infections / Q000150:complications* / Q000453:epidemiology / Q000382:microbiology; D016480:Helicobacter pylori / Q000302:isolation & purification*; D006761:Hospitals; D006801:Humans; D008297:Male; D012307:Risk Factors; D013274:Stomach Neoplasms / Q000453:epidemiology* / Q000382:microbiology
chemical_list: D000907:Antibodies, Bacterial; D000942:Antigens, Bacterial; D001426:Bacterial Proteins; C080866:cagA protein, Helicobacter pylori