title: An inverse relation between cagA+ strains of Helicobacter pylori infection and risk of esophageal and gastric cardia adenocarcinoma.
abstract: Gastric colonization with Helicobacter pylori, especially cagA+ strains, is a risk factor for noncardia gastric adenocarcinoma, but its relationship with gastric cardia adenocarcinoma is unclear. Although incidence rates for noncardia gastric adenocarcinoma have declined steadily, paralleling a decline in H. pylori prevalence, rates for adenocarcinomas of esophagus and gastric cardia have sharply increased in industrialized countries in recent decades. To clarify the role of H. pylori infection in these tumors with divergent incidence trends, we analyzed serum IgG antibodies to H. pylori and to a recombinant fragment of CagA by antigen-specific ELISA among 129 patients newly diagnosed with esophageal/gastric cardia adenocarcinoma, 67 patients with noncardia gastric adenocarcinoma, and 224 population controls. Cancer risks were estimated by odds ratios (OR) and 95% confidence intervals (CI) using logistic regression models. Infection with cagA+ strains was not significantly related to risk for noncardia gastric cancers (OR, 1.4; CI, 0.7-2.8) but was significantly associated with a reduced risk for esophageal/cardia cancers (OR, 0.4; CI, 0.2-0.8). However, there was little association with cagA- strains of H. pylori for either cancer site (OR, 1.0 and 1.1, respectively). These findings suggest that the effects of H. pylori strains on tumor development vary by anatomical site. Further studies are needed to confirm these results and to assess whether the decreasing prevalence of H. pylori, especially cagA+ strains, may be associated with the rising incidence of esophageal/gastric cardia adenocarcinomas in industrialized countries.
authors.affiliation: National Cancer Institute, Division of Cancer Epidemiology and Genetics, Bethesda, Maryland 20852, USA.
authors.forename: W H
authors.initials: WH
authors.lastname: Chow
authors.forename: M J
authors.initials: MJ
authors.lastname: Blaser
authors.forename: W J
authors.initials: WJ
authors.lastname: Blot
authors.forename: M D
authors.initials: MD
authors.lastname: Gammon
authors.forename: T L
authors.initials: TL
authors.lastname: Vaughan
authors.forename: H A
authors.initials: HA
authors.lastname: Risch
authors.forename: G I
authors.initials: GI
authors.lastname: Perez-Perez
authors.forename: J B
authors.initials: JB
authors.lastname: Schoenberg
authors.forename: J L
authors.initials: JL
authors.lastname: Stanford
authors.forename: H
authors.initials: H
authors.lastname: Rotterdam
authors.forename: A B
authors.initials: AB
authors.lastname: West
authors.forename: J F
authors.initials: JF
authors.lastname: Fraumeni
mesh_terms: D000230:Adenocarcinoma / Q000209:etiology*; D000328:Adult; D000368:Aged; D000942:Antigens, Bacterial; D001426:Bacterial Proteins / Q000235:genetics; D002299:Cardia; D016022:Case-Control Studies; D004938:Esophageal Neoplasms / Q000209:etiology*; D005260:Female; D005838:Genotype; D016481:Helicobacter Infections / Q000150:complications*; D016480:Helicobacter pylori / Q000235:genetics*; D006801:Humans; D008297:Male; D008875:Middle Aged; D012306:Risk; D013274:Stomach Neoplasms / Q000209:etiology*
chemical_list: D000942:Antigens, Bacterial; D001426:Bacterial Proteins; C080866:cagA protein, Helicobacter pylori