title: Helicobacter pylori protein-specific antibodies and risk of colorectal cancer.
abstract: BACKGROUND
  There is biologic plausibility as to why infection with Helicobacter pylori, the leading cause of gastric cancer, may also increase the risk of colorectal cancer, but the epidemiologic findings have been inconsistent. We assessed the association of H. pylori protein-specific infection and colorectal cancer risk in the prospective cohort, the Southern Community Cohort Study.
  
  
  METHODS
  Multiplex serology was used to measure antibodies to 15 H. pylori proteins in prediagnostic blood among 188 incident colorectal cancer cases and 370 controls matched by age, race, sex, and blood collection timing. Conditional logistic regression was used to calculate ORs and 95% confidence intervals (CI).
  
  
  RESULTS
  Overall H. pylori prevalence was not associated with colorectal cancer risk (OR, 1.03; 95% CI, 0.59-1.77). However, seropositivity to any of five specific H. pylori proteins (VacA, HP231, HP305, NapA, and HcpC) was associated with a significant 60% to 80% increase in odds of risk. These associations became even stronger when limited to colon cancer risk, particularly for the known H. pylori toxin VacA (OR, 2.24; 95% CI, 1.22-4.11), including a significant, positive dose-response association by VacA antibody levels in quartiles (P < 0.05). Associations with VacA seropositivity were especially strong for early-onset and late-stage cancers.
  
  
  CONCLUSIONS
  The findings raise the hypothesis that individuals with high levels of antibodies to specific H. pylori proteins may be at higher risk of colon cancer.
  
  
  CONCLUSIONS
  Further investigation of the H. pylori-colorectal cancer association is warranted to determine the possibility of protein-specific antibody levels as a risk biomarker.
authors.affiliation: Authors' Affiliations: Division of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center and Vanderbilt-Ingram Cancer Center, and Division of Gastroenterology, Departments of Medicine and Cancer Biology, Vanderbilt University School of Medicine, Nashville, Tennessee; International Epidemiology Institute, Rockville, Maryland; and Division of Genome Modifications and Carcinogenesis, Infection and Cancer Program, German Cancer Research Center (DFKZ), Heidelberg, Germany.
authors.forename: Meira
authors.initials: M
authors.lastname: Epplein
authors.forename: Michael
authors.initials: M
authors.lastname: Pawlita
authors.forename: Angelika
authors.initials: A
authors.lastname: Michel
authors.forename: Richard M
authors.initials: RM
authors.lastname: Peek
authors.forename: Qiuyin
authors.initials: Q
authors.lastname: Cai
authors.forename: William J
authors.initials: WJ
authors.lastname: Blot
mesh_terms: D000328:Adult; D000368:Aged; D000907:Antibodies, Bacterial / Q000097:blood* / Q000276:immunology; D015331:Cohort Studies; D015179:Colorectal Neoplasms / Q000097:blood / Q000276:immunology / Q000821:virology*; D005260:Female; D016481:Helicobacter Infections / Q000097:blood* / Q000276:immunology / Q000382:microbiology; D016480:Helicobacter pylori / Q000276:immunology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D012307:Risk Factors
chemical_list: D000907:Antibodies, Bacterial
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