肠型胃癌（IGC）是高发人群中最常见的胃癌类型。IGC的早期生长阶段依次包括非萎缩性胃炎（NAG）、慢性萎缩性胃炎（CAG）和肠化生（IM）。然而，IGC在这些阶段中发展的机制尚不清楚。本研究从GEO数据库下载了与IGC相关的单细胞RNA-seq数据，并使用R软件注释了肿瘤微环境（TME）中的免疫细胞。利用R软件探索了不同疾病阶段中免疫细胞比例的变化和细胞间相互作用的改变，重点关注浆细胞。此外，使用TCGA数据库中的IGC样本进行了免疫细胞浸润分析，并构建了Cox比例风险回归模型来识别可能的预后基因。结果表明，在癌前病变中，免疫细胞之间的相互作用主要由趋化因子主导，以刺激免疫细胞的浸润和激活。在肿瘤中，上调分子的细胞间移动和信号放大与肿瘤坏死因子家族和免疫抑制有关，以逃避免疫监视并促进肿瘤生长。关于预后分析，发现IGLC3、IGLV1-44、IGKV1-16、IGHV3-21、IGLV1-51和IGLV3-19是IGC的新生物标志物。我们对IGC单细胞图谱和大规模转录组数据进行的分析有助于理解IGC发展过程中分子水平上的TME异质性，并为阐明IGC机制和发现精准治疗新靶点提供了见解。版权所有 © 2023. Elsevier B.V. 发表。

Intestinal-type gastric cancer (IGC) is the most frequent type of gastric cancer in high-incidence populations. The early stages of IGC growth successively include nonatrophic gastritis (NAG), chronic atrophic gastritis (CAG) and intestinal metaplasia (IM). However, the mechanisms of IGC development through these stages remain unclear. For this study, single-cell RNA-seq data related to IGC were downloaded from the GEO database, and immune cells of the tumor microenvironment (TME) were annotated using R software. Changes in the proportion of immune cells and altered cell-to-cell interactions were explored at different disease stages using R software, with a focus on plasma cells. Additionally, IGC samples from the TCGA database were used for immune cell infiltration analysis, and a Cox proportional risk regression model was constructed to identify possible prognostic genes. The results indicated that for precancerous lesions, interactions between immune cells were mainly dominated by chemokines to stimulate the infiltration and activation of immune cells. In tumors, intercellular movement of upregulated molecules and amplified signals were associated with the tumor necrosis factor family and immunosuppression to escape immune surveillance and promote tumor growth. Regarding prognostic analysis, IGLC3, IGLV1-44, IGKV1-16, IGHV3-21, IGLV1-51, and IGLV3-19 were found to be novel biomarkers for IGC. Our analysis of the IGC single-cell atlas together with bulk transcriptome data contributes to understanding TME heterogeneity at the molecular level during IGC development and provides insights for elucidating the mechanism of IGC and discovering novel targets for precise therapy.Copyright © 2023. Published by Elsevier B.V.