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1 Division of Gastroenterology, Hepatology and Nutrition, Vanderbilt University Medical Center, Nashville, Tennessee; 2 Tumor Immunology Laboratory, Stanley S. Scott Cancer Center and 3 School of Public Health, Louisiana State University Health Sciences Center, New Orleans, Louisiana; and 4 Division of Gastroenterology, University of Alberta, Edmonton, Alberta, Canada
Requests for reprints: M. Constanza Camargo, Division of Gastroenterology, Hepatology, and Nutrition, Vanderbilt University Medical Center, 2215 Garland Avenue, 1005 MRB IV, Nashville, TN 37232-0252. Phone: 615-3433951; Fax: 615-3436229. E-mail: maria.c.camargo{at}vanderbilt.edu
Background: Polymorphisms of interleukin-1B (IL1B) and its receptor antagonist (IL1RN) genes have been inconsistently associated with gastric cancer risk. We examined these associations by performing meta-analyses.
Materials and Methods: Twenty-five studies testing the association between IL1B and/or IL1RN gene polymorphisms and gastric cancer were examined: 14 studies of IL1B-511, 14 studies of IL1B-31, 8 studies of IL1B+3954, and 23 studies of IL1RN. Overall and ethnicity-specific summary odds ratios and corresponding 95% confidence intervals for gastric cancer associated with these polymorphisms were estimated using fixed- and random-effects models. Heterogeneity and publication bias were evaluated.
Results: IL1B-511T and IL1RN*2 were associated with gastric cancer risk in Caucasians, but not in Asians. For IL1B-511T, the association in Caucasians was stronger when intestinal-subtype and noncardia gastric cancer cases were examined. A nonsignificant trend was observed between IL1B-31C and gastric cancer in Caucasians. No significant association of IL1B+3954T and gastric cancer risk was detected. Studies with better methodologic characteristics reported stronger effects. There was no evidence of publication bias.
Conclusion: IL1B-511T is associated with gastric cancer susceptibility in Caucasians. The meta-analyses suggest that the conflicting results among studies may be explained by variation in allele frequencies among the ethnic groups and variation in tumor types, as well as by the methodologic quality of the studies. (Cancer Epidemiol Biomarkers Prev 2006;15(9):1674–87)
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