食管（Barrett食管BE-IM）和胃（GIM）中的肠上皮化生被认为是食管和胃腺癌的前体，我们假设BE-IM和GIM在对不同炎症侵害的反应中呈平行的发育轨迹。 在此，我们构建了一个单细胞RNA-seq图谱，支持蛋白质表达研究，涵盖整个肠胃道，包括生理正常和病理状态，包括食管中的胃化生（E-GM），BE-IM、萎缩性胃炎和GIM。 我们证明了BE-IM和GIM具有共同的分子特征，个体细胞同时具有胃和肠上皮细胞的转录特性，暗示表型马赛克。 从转录角度上看，E-GM类似于萎缩性胃炎。从基因上看，它是克隆的，突变负担低于BE-IM。 最后，我们展示了GIM和BE-IM获得一种促癌的、激活的成纤维细胞微环境。 这些发现表明，BE-IM和GIM可以被认为是毗邻器官中相似的分子实体，为分享的检测和治疗策略打开了道路。

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.