title: Interleukin-1B polymorphisms and gastric cancer risk--a meta-analysis.
abstract: Some studies have reported that proinflammatory polymorphisms in interleukin-1B (IL-1B) and IL-1 receptor antagonist (IL-1RN) genes are associated with increased gastric cancer risk. However, other studies have shown null or inverse associations. This meta-analysis reviews and summarizes published evidence for these associations. Searching the PubMed Database yielded 35 studies that reported on the association between IL-1B -511 C>T, IL-1B -31 T>C, or IL-1RN variable number tandem repeat polymorphisms and gastric cancer risk. Q-statistics and I(2) statistics were calculated to examine heterogeneity. Summary odds ratios (OR) and 95% confidence intervals (95% CI) were calculated in the random-effects model using the DerSimonian-Laird method. For all gastric cancers, the overall ORs (95% CIs) for IL-1B -511 CT versus CC and TT versus CC genotypes were 1.07 (0.91-1.25) and 1.16 (0.95-1.42), respectively. ORs (95% CIs) for the association between IL-1B -31 CT versus TT and CC versus TT genotypes were 0.99 (0.83-1.19) and 0.98 (0.78-1.21), respectively. For the associations between IL-1RN and gastric cancer, ORs (95% CIs) for *2/L versus LL and *2/*2 versus L/L were 1.15 (0.96-1.38) and 1.23 (0.79-1.92). For each of the examined associations, there was significant heterogeneity among studies; P(heterogeneity) < or = 0.001 and I(2) ranged from 0.54 to 0.71. Noncardia cancers showed stronger associations with IL-1B -511 CT or TT and IL1-RN *2/*2 genotypes, but limiting the analysis to intestinal-type cancers, studies conducted in Western countries, or studies in which polymorphisms were in Hardy-Weinberg equilibrium, made no material difference in the results. The overall associations between IL-1B or IL-1RN proinflammatory polymorphisms and gastric cancer were null but several studies showed an association. The sources of this variation are unclear.
authors.affiliation: Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, 6120 Executive Boulevard, Room 3034, Bethesda, MD 20892-7232, USA. kamangaf@mail.nih.gov
authors.forename: Farin
authors.initials: F
authors.lastname: Kamangar
authors.forename: Cindy
authors.initials: C
authors.lastname: Cheng
authors.forename: Christian C
authors.initials: CC
authors.lastname: Abnet
authors.forename: Charles S
authors.initials: CS
authors.lastname: Rabkin
mesh_terms: D000569:Americas / Q000453:epidemiology; D001208:Asia / Q000453:epidemiology; D016022:Case-Control Studies; D005060:Europe / Q000453:epidemiology; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D053590:Interleukin 1 Receptor Antagonist Protein / Q000235:genetics; D053583:Interleukin-1beta / Q000235:genetics*; D016017:Odds Ratio; D011110:Polymorphism, Genetic; D012307:Risk Factors; D012680:Sensitivity and Specificity; D013274:Stomach Neoplasms / Q000453:epidemiology* / Q000235:genetics*
chemical_list: C507763:IL1RN protein, human; D053590:Interleukin 1 Receptor Antagonist Protein; D053583:Interleukin-1beta