ArticlePeerJ2026
Identification of a GPR182-postive stem cell population that drives polyp progression in familial adenomatous polyposis.
Article in PeerJ, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
9 authors.
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Abstract
Background: Familial adenomatous polyposis (FAP) is characterized by hundreds of colorectal adenomas that inevitably progress into carcinomas. This study focused on the heterogeneity during the polyposis progression to identify new targets and signatures for therapeutic development. Methods: An integrated analysis of single-cell sequencing (GSE109308) and bulk transcriptomic data (GSE79460, GSE88945, GSE94919, GSE106500, GSE109812, GSE153385, and GSE156172) of FAP patients from the Gene Expression Omnibus database was conducted. The heterogeneous features of epithelial cell clusters were described in terms of evolutionary trajectory, stemness, hypoxia, epithelial-mesenchymal transition (EMT), immune infiltration and metabolism. Three machine learning algorithms were applied to identify the key cell subset driving polyp heterogeneity, followed by functional validation with cell cycle and viability experiments. Cell-cell communication landscapes of this significant cell subset and its associations with prognosis and response to chemotherapy or immunotherapy were delineated. Results: Thirteen epithelial cell clusters were determined and further classified into four heterogeneous phenotypes. A specific cell population, G protein-coupled receptor 182 (GPR182)-positive polyp stem cells (GPR182 Conclusion: Our findings map the epithelial heterogeneity in FAP and reveal that GPR182
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