Positions

Overview

  • immunobiology of microbiota-epithelial interactions and the epigenetics of mucosal cancers
  • Selected Publications

    Academic Article

    Year Title Altmetric
    2022 Tu1167: DIVERGENT GENE SIGNATURES IN BARRETT'S ESOPHAGUS EPITHELIAL STEM CELLS DURING DYSPLASIAGastroenterology.  162:s-333. 2022
    2022 Sialyltransferase ST6GAL-1 mediates resistance to chemoradiation in rectal cancerJournal of Biological Chemistry.  298. 2022
    2021 CD4+ T cell activation and concomitant mTOR metabolic inhibition can ablate microbiota-specific memory cells and prevent colitisScience Immunology.  5. 2021
    2021 Human Microbiota Flagellins Drive Adaptive Immune Responses in Crohn's DiseaseGastroenterology.  161:522-535.e6. 2021
    2021 Fr159 EXPRESSION OF GLYCOSYLTRANSFERASE ST6GAL-I AND TUMORIGENIC GENES IN BARRETT'S ESOPHAGUS STEM CELLS DURING DYSPLASIAGastroenterology.  160:s-241. 2021
    2020 Modulation of glycosyltransferase ST6Gal-I in gastric cancer-derived organoids disrupts homeostatic epithelial cell turnoverJournal of Biological Chemistry.  295:14153-14163. 2020
    2020 Sa1210 ST6GAL-I IS UPREGULATED IN BARRETT'S ESOPHAGUS STEM CELLS AND DYSPLASIAGastroenterology.  158:s-313. 2020
    2019 283 – The Role of St6Gal-I, a Glycosyltransferase Strongly Associated with Mucosal Carcinogenesis, in Barrett's Esophagus and Esophageal AdenocarcinomaGastroenterology.  156:s-57. 2019
    2018 Sa1102 - Barrett's Epithelium Displays Increased Expression of St6Gal-I, a Glycosyltransferase Strongly Associated with Mucosal CarcinogenesisGastroenterology.  154:s-241. 2018
    2017 CBirTox is a selective antigen-specific agonist of the Treg-IgA-microbiota homeostatic pathwayPLoS One.  12. 2017
    2017 Moms, babies, and bugs in immune developmentF1000Research.  6. 2017
    2015 Host-microbiota interactions in the intestine 2015
    2014 Microbiota activation and regulation of innate and adaptive immunityImmunological Reviews.  260:206-220. 2014
    2012 Regulation of Toll-like receptor 5 gene expression and function on mucosal dendritic cellsPLoS One.  7. 2012

    Research Overview

  • 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.
  • Education And Training

  • Doctor of Philosophy in Immunology, University of Alabama at Birmingham 2015
  • Bachelor of Science or Mathematics in Chemistry, Birmingham-Southern College 2008
  • Full Name

  • Katie Alexander