title: Association of Helicobacter pylori infection with reduced risk for esophageal cancer is independent of environmental and genetic modifiers.
abstract: OBJECTIVE
  Infection with Helicobacter pylori is associated with reduced risk of esophageal adenocarcinoma (EAC), but it is not clear whether this reduction is modified by genotype, other host characteristics, or environmental factors. Furthermore, little is known about the association between H pylori and adenocarcinomas of the esophagogastric junction (EGJAC) or squamous cell carcinomas (ESCC). We sought to measure the association between H pylori infection and esophageal cancer and identify potential modifiers.
  
  
  METHODS
  In an Australian, population-based, case-control study, we compared the prevalence of H pylori seropositivity and single nucleotide polymorphisms in interleukin (IL)-1B (-31, -511) and tumor necrosis factor (TNF)-alpha (-308, -238) among 260 EAC, 298 EGJAC, and 208 ESCC patients and 1346 controls. To estimate relative risks, we calculated odds ratios (OR) and 95% confidence intervals (CI) using multivariable logistic regression in the entire sample and within strata of phenotypic and genotypic risk factors.
  
  
  RESULTS
  H pylori infection was associated with significantly reduced risks of EAC (OR, 0.45; 95% CI: 0.30-0.67) and EGJAC (OR, 0.41; 95% CI: 0.27-0.60) but not ESCC (OR, 1.04; 95% CI: 0.71-1.50). For each cancer subtype, risks were of similar magnitude across strata of reflux frequency and smoking status. We found no evidence that polymorphisms in IL-1B or TNF-alpha modified the association between H pylori and EAC or EGJAC.
  
  
  CONCLUSIONS
  H pylori infection is inversely associated with risks of EAC and EGJAC (but not ESCC); the reduction in risk is similar across subgroups of potential modifiers.
authors.affiliation: Queensland Institute of Medical Research, Brisbane, Australia.
authors.forename: David C
authors.initials: DC
authors.lastname: Whiteman
authors.forename: Priya
authors.initials: P
authors.lastname: Parmar
authors.forename: Paul
authors.initials: P
authors.lastname: Fahey
authors.forename: Suzanne P
authors.initials: SP
authors.lastname: Moore
authors.forename: Mitchell
authors.initials: M
authors.lastname: Stark
authors.forename: Zhen Zhen
authors.initials: ZZ
authors.lastname: Zhao
authors.forename: Grant W
authors.initials: GW
authors.lastname: Montgomery
authors.forename: Adèle C
authors.initials: AC
authors.lastname: Green
authors.forename: Nicholas K
authors.initials: NK
authors.lastname: Hayward
authors.forename: Penelope M
authors.initials: PM
authors.lastname: Webb
mesh_terms: D000230:Adenocarcinoma / Q000517:prevention & control*; D000293:Adolescent; D000328:Adult; D000368:Aged; D000907:Antibodies, Bacterial / Q000097:blood; D001284:Atrophy; D016022:Case-Control Studies; D016207:Cytokines / Q000235:genetics; D004938:Esophageal Neoplasms / Q000517:prevention & control*; D004943:Esophagogastric Junction / Q000473:pathology; D005260:Female; D005753:Gastric Mucosa / Q000473:pathology; D005764:Gastroesophageal Reflux / Q000517:prevention & control; D005838:Genotype; D016481:Helicobacter Infections / Q000276:immunology*; D016480:Helicobacter pylori; D006801:Humans; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D020641:Polymorphism, Single Nucleotide
chemical_list: D000907:Antibodies, Bacterial; D016207:Cytokines