Changing the natural history of metachronous gastric cancer after H. pylori eradication

Metachronous gastric cancer occurs frequently following endoscopic removal of an early gastric cancer. H. pylori eradication significantly reduces that risk. While, the pathogenesis of this phenomenon remains unclear, it is clear that the natural history of metachronous gastric cancer is altered following H. pylori eradication. Genetic instability of host cells induced by inflammation, H. pylori, host or environmental factors can result in the production of malignant cells. H. pylori eradication reduces and alters the inflammation, and can reverse epigenetic damage and abnormal expression of miRNA's. Fundamentally, H. pylori eradication stops the progression and may reverse some of the damage to the mucosa resulting in improved acid secretion and improving the gastric microbiome. Because the risk of developing metachronous cancer varies among patients, prospective research is needed to identify reliable biomarkers to predict development of metachronous cancer as well as to define surveillance methods, intervals, and duration. Some candidate examples of prognostic or predictive biomarkers for the prediction of subsequent risk include the presence or absence, titers, and changes in anti-H. pylori IgG and or anti-CagA antibodies, serum pepsinogens, gastrin, and miRNAs.