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[Cancer Research 58, 588-590, February 15, 1998]
© 1998 American Association for Cancer Research
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An Inverse Relation between cagA+ Strains of Helicobacter pylori Infection and Risk of Esophageal and Gastric Cardia Adenocarcinoma1

Wong-Ho Chow2, Martin J. Blaser, William J. Blot, Marilie D. Gammon, Thomas L. Vaughan, Harvey A. Risch, Guillermo I. Perez-Perez, Janet B. Schoenberg, Janet L. Stanford, Heidi Rotterdam, A. Brian West3 and Joseph F. Fraumeni,, Jr.

National Cancer Institute, Division of Cancer Epidemiology and Genetics, Bethesda, Maryland 20852 [W-H. C., J. F. F.]; Vanderbilt University School of Medicine, Division of Infectious Diseases, Nashville, Tennessee [M. J. B., G. I. P-P.]; Medical Service, Department of Veterans Affairs Medical Center, Nashville, Tennessee [M. J. B.]; International Epidemiology Institute, Rockville, Maryland [W. J. B.]; Columbia University School of Public Health, Division of Epidemiology, New York, New York [M. D. G.]; Fred Hutchinson Cancer Research Center, Program in Epidemiology, and University of Washington, School of Public Health, Department of Epidemiology, Seattle, Washington [T. L. V., J. L. S.]; Yale University School of Medicine, Departments of Epidemiology and Public Health [H. A. R.] and Pathology [A. B. W.], New Haven, Connecticut; New Jersey Department of Health and Senior Services, Applied Cancer Epidemiology Program, Trenton, New Jersey [J. B. S.]; and College of Physicians and Surgeons of Columbia University, Department of Pathology, New York, New York [H. R.]

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.

1 Supported in part by NIH Grants U01-CA57983, U01-CA57949, 5U01-CA57923, and R01-DK58834 and National Cancer Institute Contracts N02-CP-40501 and N01-CN-05230.

2 To whom requests for reprints should be addressed, at National Cancer Institute, 6130 Executive Boulevard, EPN 418, Rockville, MD 20852.

3 Present address: University of Texas, Department of Pathology, Galveston, TX.

Received 11/11/97. Accepted 1/ 6/98.




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