ArticleTranslational pediatrics2026
Transcriptomic remodeling of bone marrow mesenchymal stromal cells in pediatric B-cell acute lymphoblastic leukemia: a four-gene signature.
Article in Translational pediatrics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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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Who cites it
1 citing paper in PubMed.
- Chasing the FoxO in Metabolic Disorders: Novel Considerations for Oxidative Stress, Programmed Cell Death, Wnt, and the Gut Microbiome.Antioxidants (Basel, Switzerland) · 2026Review
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10 authors.
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Abstract
Background: Pediatric B-cell acute lymphoblastic leukemia (B-ALL) is molecularly heterogeneous and influenced by the bone marrow microenvironment. Mesenchymal stromal cells (MSCs) provide critical niche signals, yet their transcriptomic remodeling in B-ALL is poorly defined. This study aims to define a compact gene signature that complements blast-centric diagnostics. Methods: We analyzed GSE101425 (GPL570) MSC microarrays (rather than leukemic blasts) from pediatric B-ALL at diagnosis (day 0, n=35), remission (n=29), relapse (n=6), and healthy donors (n=16). Differential expression (day 0 Results: We identified 78 differentially expressed genes (DEGs) in B-ALL-associated MSCs. A four-gene MSC signature [Dickkopf WNT Signaling Pathway Inhibitor 1 (DKK1), Regulator of G Protein Signaling 2 (RGS2), Cellular Communication Network Factor 4/WNT1-Inducible Signaling Pathway Protein 1 (CCN4/WISP1), Lysozyme (LYZ)] distinguished active B-ALL MSCs from healthy MSCs with cross-validated AUC 0.883 (95% CI: 0.783-0.966) and separated samples into two transcriptional states with distinct pathway enrichment, including extracellular matrix and immune-related programs. Single-cell data localized RGS2 and LYZ to immune compartments, whereas DKK1 and CCN4/WISP1 were low, supporting stromal specificity. Peripheral blood RT-qPCR showed decreased RGS2 and LYZ, whereas CCN4 showed a nonsignificant upward trend (P=0.053), underscoring compartment-dependent patterns. Conclusions: These data delineate transcriptional remodeling of bone marrow MSCs in pediatric B-ALL and nominate a four-gene MSC-associated signature. By centering on stromal MSC transcriptomes rather than leukemic blasts, we target a complementary microenvironmental layer of B-ALL biology that is underrepresented in blast-centric transcriptomics. The findings are hypothesis-generating and require independent MSC cohorts and functional validation.
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