## Abstract Infection with the gastric bacterium __Helicobacter pylori__ (in particular infection with CagAβpositive strains) and smoking have been identified as risk factors for the development of gastric cancer. Both risk factors are typically acquired early in life and prevail over decades if no
Interaction of Cyclooxygenase-2 promoter polymorphisms with Helicobacter pylori infection and risk of gastric cancer
β Scribed by Xuemei Zhang; Rong Zhong; Zhi Zhang; Juxiang Yuan; Li Liu; Yan Wang; Susan Kadlubar; Fumin Feng; Xiaoping Miao
- Publisher
- John Wiley and Sons
- Year
- 2011
- Tongue
- English
- Weight
- 97 KB
- Volume
- 50
- Category
- Article
- ISSN
- 0899-1987
- DOI
- 10.1002/mc.20784
No coin nor oath required. For personal study only.
β¦ Synopsis
Overexpression of cyclooxygenase (COX)-2 has been implicated in the development of cancer. This study aimed to evaluate the relationship between genetic variants in COX-2 promoter interacting with Helicobacter pylori and the susceptibility to gastric cancer (GC). Three COX-2 polymorphisms -1290A>G (rs689465), -1195G>A (rs689466), and -765G>C (rs20417) were genotyped in 323 GC patients and 944 controls. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated by logistic regression model. In GC patients, the ORs were 2.33 (95% CI = 1.50-3.63) and 2.70 (95% CI = 1.68-4.33) for -1195AA and -765CG genotype carriers, respectively. Haplotype analysis showed all -1195A allele-containing haplotypes, except G(-1290)-A(-1195)-G(-765), were associated with increased risk for GC, compared with the A(-1290)-G(-1195)-G(-765) haplotype. Moreover, significant multiplicative and additive interactions were observed between H. pylori infection and all these three polymorphisms, and H. pylori-infected subjects carrying the variant allele of -1290A>G, -1195G>A, or -765G>C had increased risk of GC compared with non-H. pylori-infected subjects with wild-type allele (OR = 4.10, 95% CI = 1.90-8.83; OR = 3.46, 95% CI = 1.31-9.11; and OR = 3.32, 95% = 1.27-8.73, respectively). Our results suggested that the COX-2 promoter polymorphisms were associated with increased risk of GC, especially interacting with H. pylori infection.
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