Background. Helicobacter pylori infection is associated not only with gastr
oduodenal ulcers but with the development of gastric cancer. Interleukin-1
beta (IL-1 beta) is a potent inhibitor of gastric secretion. The -31 C-to-T
base transition in the intron of this gene has been reported to be involve
d in carcinogenic changes within the stomach, especially in H. pylori-infec
ted individuals. Methods. In this study, the -511 T-to-C polymorphism in th
e IL-1 gene was investigated in 669 patients with gastric diseases. Results
. The allelic frequencies of the C allele, which indicates low acid secreti
on and is a component of a supposedly high-risk genotype for gastric cancer
, were 0.48 in H. pylori-negative noncancer controls, 0.52 in H. pylori-pos
itive noncancer controls, 0.57 in subjects with chronic active gastritis (C
AG) with H. pylori, 0.58 in subjects with intestinal metaplasia (IM) or CAG
without H. pylori, and 0.52 in gastric cancer patients. Significant differ
ences among the groups were observed between the IM or CAG without H. pylor
i group and the gastric cancer group and between the IM or CAG without H. p
ylori group and the H. pylori-negative noncancer control group (P < 0.05).
Conclusions. The IL-1 beta -511 genetic polymorphism was not associated wit
h gastric cancer in a multistep carcinogenesis model. However, in view of t
he results for the IM or CAG without H. pylori group, the presence of the C
allele may also indicate a risk of mucosal atrophy of the stomach in the J
apanese population.