Polymorphisms of the IL-1B and IL-1RN genes (which encode interleukin [IL]-1beta and IL-1 receptor antagonist, respectively) have been associated with hypochlorhydria and gastric cancer.
Previously we have shown that the known proinflammatory genotypes, IL-1B -31C/+ and IL-1RN *2/*2, were not associated with increased risks for gastric cancer/duodenal ulcer in the Korean population.
Our study investigates the role of the IL-1B-31, IL-1RN and TNF-A-308 gene polymorphisms as risk factors for the development of GC in a Mexican population.
IL-1B and IL-1RN polymorphisms were investigated in 138 H. pylori-negative Italian patients with sporadic gastric cancer and 100 H. pylori-negative controls.
Although no correlation was found in the analysis of the IL-1B and IL-1RN polymorphisms, IL-8 -251 A/A genotype held a higher risk of atrophic gastritis [odds ratio (OR), 2.35; 95% confidence interval (CI), 1.12-4.94] and gastric cancer (OR, 2.22; 95% CI, 1.08-4.56) compared with the T/T genotype.
We aimed to test for associations between polymorphisms in IL1B (-31 and +3954), IL10-592 and IL1RN variable number of tandem repeats (VNTR) and risk of gastric cancer in a Mexican population.
There was an association between the presence of IL-1RN*2 allele and gastric cancer [odds ratio (OR) = 2.2, 95% confidence interval (CI) = 1.0-3.3, P = 0.04).
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).
A comprehensive analysis of 207 SNP of 11 cytokine genes revealed that variations in IL-4 and IL-1RN genes are negatively associated with the risk of developing gastric cancer following H. pylori infection.
Three hundred and ninety-nine patients with gastroduodenal diseases (129 chronic gastritis, 127 duodenal ulcer and 143 non-cardiac gastric cancer) and 264 healthy controls were genotyped for IL-1B-511 and IL-1RN gene polymorphisms by the PCR-RFLP method.
Atrophic body gastritis patients harbouring the wild type of IL-1B-511/IL-1RN polymorphisms were not different from those harbouring the proinflammatory pattern as far as regards gender, age, gastric cancer family history and metaplastic atrophy.
The age-sex-adjusted odds ratios (OR) for the IL-1B-511 T genotype relative to the C/C genotype (OR = 0.82, 95% confidence interval [CI] 0.41-1.65), IL-1RN*2 genotype relative to the L/L genotype (OR = 0.85, 95% CI 0.41-1.78), and IL-2-330 T genotype relative to the G/G genotype (OR = 1.94, 95% CI 0.76-4.96) were not increased in GC.
Multivariate regression analysis showed that cagE, babA2, and IL-1RN-1/2 genotypes were independent predictors of GC, but when patients with benign disorders were grouped together (NUD + DU) and compared with patients with GC, regression analysis disclosed that babA2 (P = 0.000) and IL-1B-31 gene polymorphisms (CC or CT) (P = 0.01) were the only independent markers of GC.
IL1RN 2R/2R genotype [odds ratio (OR) 2.43; 95% confidence interval (CI) 1.19-4.96] and allele IL1RN Ex5-35C were associated with an increased risk of Hp(+) non-cardia GC.