Combined effect between WT1 methylation and Helicobacter pylori infection, smoking, and alcohol consumption on the risk of gastric cancer. Issue 5 (30th July 2019)

• Record Type: Journal Article
• Authors: Zhou, Haibo; Sun, Hongru; Liu, Xinyan; Chen, Jie; Zhang, Lei; Lin, Shangqun; Han, Xu; Nie, Chuang; Liu, Yupeng; Tian, Wenjing; Zhao, Yashuang
• Is Part Of: Helicobacter. Volume 24:Issue 5(2019)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2019-07-30
• Subjects: DNA methylation -- gastric cancer -- Helicobacter pylori -- methylation‐sensitive high‐resolution melting -- WT1; Helicobacter -- Periodicals; Helicobacter infections -- Periodicals; Stomach -- Diseases -- Periodicals; 616.3301405
• DOI: 10.1111/hel.12650
• Languages: English
• ISSNs: 1083-4389

Abstract

Abstract: Background: Peripheral blood leukocyte DNA methylation status has been proposed to be a surrogate marker for evaluating susceptibility to gastric cancer (GC). Helicobacter pylori ( H pylori ) infection, smoking, and alcohol consumption are known to induce gene methylation. A case‐control study was performed to investigate the interactions between the methylation of two candidate genes and H pylori infection, smoking, and alcohol consumption in the risk of GC. Methods: A total of 400 GC cases and 402 controls were included in this study. The methylation status of WT1 and IGF2 was semiquantitatively determined by using methylation‐sensitive high‐resolution melting assays. H pylori IgG antibodies were detected by ELISA method. Results: Based on the area under the curve (AUC), 0% methylated DNA and 0.5% methylated DNA were used as the cutoff values for WT1 and IGF2, respectively. WT1 methylation was significantly associated with increased GC risk (OR = 1.65, 95% CI = 1.09‐2.51, P = .019), especially in males (OR = 1.80, 95% CI: 1.10‐2.95, P = .019) and older individuals (≥60 years) (OR = 2.03, 95% CI: 1.15‐3.57, P = .014). A significant combination was observed between WT1 methylation and H pylori infection, alcohol consumption, and smoking for the risk of GC (ORc = 2.28, 95% CI = 1.47‐3.55, P = .003, ORc = 2.19, 95% CI = 1.37‐3.51, P = .001, ORc = 2.21, 95% CI = 1.39‐3.51, P = .001, respectively). However, no association between IGF2 methylation and the risk of GC was found in this study. Conclusions: WT1 methylation may serve as a new potential biomarker for GC susceptibility and can combine with H pylori infection, smoking, and alcohol consumption to influence GC risk.