ArticleBlood2026
High-dimensional spatiotemporal single-cell atlas and 3D imaging of the bone marrow microenvironment during CML progression.
Article in Blood, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed.
- Assessment of Tfh Cells and Related Molecules in CML-CP Patients With Different Molecular Responses.International journal of laboratory hematology · 2026Article
- Human biomarker navigator.iMeta · 2026Review
- No Simple Fluke: Schistosomiasis as an Emerging Regulator of Haematopoiesis.Parasite immunology · 2026Review
- Rapid 3D Immunolabeling and Light Sheet Microscopy for Quantitative Analysis of Intact Tissues.Computational and structural biotechnology journal · 2026Article
Corrections and comments
- Commented on by
- Update of
Authors and funding
17 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
abstractThe bone marrow microenvironment (BMME) is essential for hematopoiesis and immunity, yet spatiotemporal single-cell analysis during leukemogenesis remains challenging. We characterized the BMME in femurs from wild-type and chronic myeloid leukemia (CML) mice at 7, 14, and 21 days after induction by highly multiplexed and 3-dimensional (3D) microscopy. Using a 54-marker codetection by indexing panel, we profiled 2 033 725 cells in 55 regions of interest and identified 41 cell types. During CML progression, we observed myeloid and progenitor cell expansion, increased programmed death ligand 1-positive leukemic cells, programmed death 1 (PD-1) upregulation on CD4+ and CD8+ T cells, and a profound loss of B cells, plasma cells, and bone cells. Advanced CML exhibited a striking expansion of immature, pericyte-deficient vasculature that disrupted vascular niches and impaired hematopoietic stem/progenitor cell positioning. Spatial mapping revealed leukemia-specific cellular neighborhoods enriched in PD-1+CD8+ T cells, suggesting localized immune exhaustion. Early CML showed increased contacts between plasmacytoid dendritic cells and megakaryocytes (MKs), whereas advanced CML featured heightened MK emperipolesis of nonleukemic granulocytes. MKs were morphologically irregular in CML mice and patient bone marrow biopsies. In contrast, in mice with acute myeloid leukemia, vasculature and MKs were reduced, whereas the remaining MKs retained normal morphology. Laser-capture microdissected MKs from patients with newly diagnosed CML had reduced cytoskeleton gene expression, which was reversed in advanced cases treated with tyrosine kinase inhibitors. 3D imaging revealed vascular disorganization and depleted MKs in the diaphysis, underscoring region-specific pathology. Together, this study provides a spatiotemporal single-cell atlas of the BMME during leukemic progression, showing how leukemic cells reprogram it to support their expansion and immune evasion.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.