ArticlePeerJ2025
Exosome and BCR-ABL mediated molecular alterations in endothelial cells in chronic myeloid leukemia: identification of seven genes and their regulatory network.
Article in PeerJ, 2025. 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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17 authors.
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Abstract
Background: Chronic myeloid leukemia (CML) progression relies on dynamic crosstalk between leukemic cells and vascular niches. Here, we investigate how exosomes and BCR/ABL overexpression influence endothelial functions, aiming to identify key mediators of leukemia-induced microenvironmental remodeling as potential therapeutic targets. Methods: Human umbilical vein endothelial cells (HUVECs) were cultured and divided into four groups: control (Z), treated with K562-derived exosomes (Zexo), BCR-ABL-overexpressing (ZBA), and BCR-ABL-overexpressing with exosome treatment (ZBAexo). Transcriptomic profiling was performed to identify DEGs, followed by functional enrichment and protein-protein interaction network analyses. Gene Set Enrichment Analysis (GSEA) was applied to uncover associated biological pathways. Results: Seven specificized expressed genes in ZBAexo group were identified: Conclusion: This study identifies seven novel candidate biomarkers dysregulated in endothelial cells under combined BCR-ABL and exosomal stimulation, shedding light on the molecular crosstalk between leukemic cells and the vascular niche.
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