Published online Jul 7, 2014. doi: 10.3748/wjg.v20.i25.8151
Revised: February 9, 2014
Accepted: April 2, 2014
Published online: July 7, 2014
Processing time: 190 Days and 0 Hours
AIM: To explore potential interactions among Helicobacter pylori (H. pylori), CagA status, interleukin (IL)-1B-31 genotypes, and non-cardiac gastric cancer (GC) risk.
METHODS: A case-control study of non-cardia GC was performed at 3 hospitals located in Xi’an, China, between September 2008 and July 2010. We included 171 patients with histologically diagnosed primary non-cardia GC and 367 population based controls (matched by sex, age and city of residence). A standardized questionnaire was used to obtain information regarding potential risk factors, including pork consumption. H. pylori CagA status was assessed by enzyme-linked immunosorbent assay, and IL-1B-31 genotypes were determined by polymerase chain reaction-restriction fragment length polymorphism. Multivariate unconditional logistic regression was used to explore potential interactions among the factors.
RESULTS: The CagA appeared to confer an increased risk of GC (OR = 1.81, 95%CI: 1.25-2.61). The main associations with IL-1B-31C allele here were 0.98 (95%CI: 0.59-1.63) for CC vs TT and 0.99 (95%CI: 0.64-1.51) for C Carriers vs TT. However, no associations were observed for CagA or IL-1B-31 genotype status among subjects who reported low pork consumption (P for interaction = 0.11). In contrast, high pork consumption and IL-1B-31C genotypes appeared to synergistically increase GC risk (P for interaction = 0.048) after adjusting for confounding factors, particularly among subjects with CagA (OR = 3.07, 95%CI: 1.17-10.79). We did not observe effect modification of pork consumption by H. pylori CagA status, or between H. pylori CagA status and IL-1B-31 genotypes after adjustment for pork consumption and other factors.
CONCLUSION: These interaction relationships among CagA, IL-1B-31 and pork consumption may have implications for development of the preventive strategies for the early detection of non-cardiac GC.
Core tip: It is widely known that infectious, dietary, and genetic factors are implicated in gastric carcinogenesis, which is a long, complicated, and multi-stage process. The Helicobacter pylori (H. pylori) virulence factor CagA has been shown to be polymorphic and to contribute to disease pathogenesis in an allele-dependent manner. The interleukin (IL)-1 gene plays an important role in determining the long-term outcome of H. pylori infection. Dietary factors such as pork consumption may contribute to the malignancy process in synergy with these genetic factors and infectious agents. Our study further explores potential interactions among dietary (pork intake), infectious (H. pylori CagA positive) and genetic factors (IL-1B-31 genotypes) on gastric cancer risk.