Genetic variations of TLR5 gene interacted with Helicobacter pylori infection among carcinogenesis of gastric cancer
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Tianwen Xu1, Deqiang Fu1, Yi Ren2, Yijun Dai1, Jianguang Lin1, Liming Tang3, Jian Ji4
1Department of Oncology, The Second Affiliated Hospital of Fujian Medical University, China
2Department of Thyroid and Breast, Huai'an First People's Hospital, Nanjing Medical University, China
3No. 2 People’s Hospital of Henan Province, China
4Department of Thoracic Surgery, Huai’an First People’s Hospital, Nanjing Medical University, China
Jian Ji, email: firstname.lastname@example.org
Keywords: gastric cancer, variation, genetic, TLR5, helicobacter pylori
Received: December 14, 2016 Accepted: January 11, 2017 Published: March 09, 2017
Gastric cancer (GC) ranks the second prevalent cancer type and the second cancer-related death in China. However, the precise mechanisms of GC development remain poorly understood. Chronic infection with Helicobacter pylori is the strongest identified risk factor for GC. Toll-like receptor (TLR) genes, which play critical roles in Helicobacter pylori induced chronic inflammation, may also be implicated in GC susceptibility. TLR5 signaling deficiency could deregulate a cascade of inflammatory events. In current study, we systematically evaluated genetic variations of TLR5, and their interaction with Helicobacter pylori infection among carcinogenesis of gastric cancer, using a large case-controls study among Chinese population. Minor alleles of three SNPS, including rs5744174 (P = 0.001), rs1640827 (P = 0.005), and rs17163737 (P = 0.004), were significantly associated with increased GC risk (OR ranged from 1.20–1.24). Significant interactions with Helicobacter pylori infection were also identified for rs1640827 (P for interaction = 0.009) and rs17163737 (P for interaction = 0.006). These findings suggest that genetic variants in TLR5 may modify the role of Helicobacter pylori infection in the process of causing GC.
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