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Supplementary Table S4 from Single-cell RNA sequencing unifies developmental programs of Esophageal and Gastric Intestinal Metaplasia.

dataset

posted on 2024-09-16, 09:30 authored by Karol Nowicki-Osuch, Lizhe Zhuang, Tik Shing Cheung, Emily L. Black, Neus Masque-Soler, Ginny Devonshire, Aisling M. Redmond, Adam Freeman, Massimilliano di Pietro, Nastazja Pilonis, Wladyslaw Januszewicz, Maria O'Donovan, Simon Tavare, Jacqueline D. Shields, Rebecca C. Fitzgerald

This table contains results of pairwise differential expression analysis between E-GM and gastric tissues and Atrophic gastritis and gastric tissue.

History

ARTICLE ABSTRACT

Intestinal metaplasia in the esophagus (Barrett’s Esophagus BE-IM) and stomach (GIM) are considered precursors for esophageal and gastric adenocarcinoma, respectively. We hypothesize that BE-IM and GIM follow parallel developmental trajectories in response to differing inflammatory insults. Here, we construct a single-cell RNA-seq atlas, supported by protein expression studies, of the entire gastrointestinal tract spanning physiologically normal and pathological states including gastric metaplasia in the esophagus (E-GM), BE-IM, atrophic gastritis, and GIM. We demonstrate that BE-IM and GIM share molecular features, and individual cells simultaneously possess transcriptional properties of gastric and intestinal epithelia, suggesting phenotypic mosaicism. Transcriptionally E-GM resembles atrophic gastritis; genetically, it is clonal and has a lower mutational burden than BE-IM. Finally, we show that GIM and BE-IM acquire a pro-tumorigenic, activated fibroblast microenvironment. These findings suggest that BE-IM and GIM can be considered molecularly similar entities in adjacent organs, opening the path for shared detection and treatment strategies.