H. pylori infection is firmly established as a risk factor for the development of gastric adenocarcinoma, but relatively little is known about how its colonization of the stomach contributes to epithelial dysfunction, particularly at the stem cell level. My current research project uses stem cell organogenesis to examine H. pylori infection in the human stomach and determine whether infection upregulates epithelial ST6Gal-I expression, a glycosyltransferase that is overexpressed in multiple mucosal cancers including ovarian, pancreatic and colonic. Recently, we have shown that ST6Gal-I is dysregulated in gastric adenocarcinoma (Alexander et al JBC 2020), but the mechanism is still undefined. Considering the prevalence of epigenetic modifications in gastric cancer and that H. pylori is the primary risk factor for gastric adenocarcinoma, we hypothesize that H. pylori colonization of the gastric stem cell niche initiates epigenetic modifications. Epigenetic modifications are heritable, making the study of these modifications especially relevant to disease pathogenesis. Interestingly, epigenetic modifications may be reversed, therefore identifying and targeting epigenetic alterations in the genome is a promising new treatment option in progressive diseases, particularly tumorigenesis and cancer.