Changes of DNA methylation in gastric mucosae after eradication of Helicobacter pylori have not been clarified yet. From this background, we investigated time course of DNA methylation following H. pylori eradication in 221 successfully H. pylori eradicated subjects with endoscopic follow-up at least for 6 months, including 114 controls, 53 subjects with gastric dysplasia and 54 patients with early gastric cancer. All dysplasia and gastric cancer patients underwent endoscopic resection at the time of enrollment. The methylation levels in LOX, APC and MOS genes from noncancerous gastric mucosae using quantitative methylation-specific PCR, as well as the histologic findings of gastric mucosae, were compared before and after eradication. Average follow-up duration was 26.0 months (range: 6 to 76 months). H. pylori eradication decreased methylation levels in LOX (p-value for slope < 0.001) but not in APC. In MOS, decrease of its methylation level following H. pylori eradication was significant among controls without intestinal metaplasia (IM) (p-value for slope < 0.05); however, it was not observed among patients with IM or those with dysplasia or gastric cancer. After H. pylori eradication, methylation level in MOS persistently increased in patients with dysplasia or gastric cancer (p < 0.01). In conclusion, H. pylori eradication decreases aberrant DNA methylation with gene-specific manner. Methylation level in MOS is associated with IM and may be used as a surrogate marker for gastric cancer risk, regardless of H. pylori eradication history. What's new? While eradication of Helicobacter pylori, a known risk factor for gastric cancer, can prevent disease progression in animal models, its eradication in gastric cancer patients has yielded inconsistent results, possibly owing to the persistence of aberrant changes in DNA methylation. In this study, methylation of the gene MOS was correlated with severity of intestinal metaplasia, a risk factor for progression to gastric cancer. MOS methylation level was persistently higher in subjects with intestinal metaplasia, dysplasia, or gastric cancer, even after H. pylori eradication. The findings strongly support the epigenetic field defect hypothesis for gastric cancer. © 2013 UICC.
CITATION STYLE
Shin, C. M., Kim, N., Lee, H. S., Park, J. H., Ahn, S., Kang, G. H., … Jung, H. C. (2013). Changes in aberrant DNA methylation after Helicobacter pylori eradication: A long-term follow-up study. International Journal of Cancer, 133(9), 2034–2042. https://doi.org/10.1002/ijc.28219
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