H. pylori eradication long-term effects on epigenetic alterations related to gastric carcinogenesis

It has been postulated that Helicobacter pylori (H. pylori) infection causes chronic gastritis, comprised of atrophic gastritis, typically with intestinal metaplasia (IM), dysplasia, and gastric cancer (GC). The stepwise nature of this infection that typically continues over decades has been outlined as a sequence of histological atomy events that confers an increased risk of malignant transformation, as represented in Correa’s hypothesis. In Japan, therefore, national insurance has covered eradication medical care in patients with endoscopically diagnosed chronic gastritis caused by H. pylori infection since 2013 to stop the event of GC. Similarly, the International Agency for analysis on Cancer working group Report in 2014 suggested that each one country explore the chance of introducing population-based H. pylori screening and treatment programs as a method for GHz prevention.

In this study, the long effects of H. pylori eradication on genetic and epigenetic molecular alterations as well as dysregulation of miRNAs and monoclonal antibody (mAb) Das-1, that is strongly related to GC22,25,33,34, were investigated in atrophic mucosa (non-IM) and IM (pre-cancerous conditions) in patients with and while not early rate (primary endpoints). The molecular markers connected to carcinogenesis risk in such patients (secondary endpoints) were additionally determined.



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