ArticleCell stem cell2013
Myeloproliferative neoplasia remodels the endosteal bone marrow niche into a self-reinforcing leukemic niche.
Article in Cell stem cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 384 papers.
What it found
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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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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.
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Who cites it
384 citing papers in PubMed, 594 citations in OpenAlex.
- Efficacy and safety of momelotinib in Janus kinase inhibitor-experienced Asian patients with myelofibrosis and anemia.International journal of hematology · 2025Trial
- Safety and efficacy of zinpentraxin alfa as monotherapy or in combination with ruxolitinib in myelofibrosis: stage I of a phase II trial.Haematologica · 2023Trial
- Identification of CXCL12-abundant reticular cells in human adult bone marrow.British journal of haematology · 2021Trial
- Silent NK/T cell reactions to dasatinib during sustained deep molecular response before cessation are associated with longer treatment-free remission.Cancer science · 2020Trial
- Inflammatory and Immune Microenvironment in Myeloproliferative Neoplasms: Pathogenic Mechanisms and Therapeutic Opportunities.Cancers · 2026Review
- Bispecific Antibodies for Acute Myeloid Leukemia: From Bone Marrow Immune Niche to Clinical Translation.Antibodies (Basel, Switzerland) · 2026Review
- Genomic insights transform diagnosis, prognosis, and therapy in BCR::ABL1-negative myeloproliferative neoplasms.International journal of hematology · 2026Review
- Engineering bone marrow in a dish-a bloody business: preclinical opportunities, translational use cases, and a call for consensus.Journal of thrombosis and haemostasis : JTH · 2026Review
- Longitudinal localization of leukaemic stem cells between the metaphysis and central marrow governs their behaviour.Nature cell biology · 2026Article
- Roles of extracellular vesicles in the pathogenesis of chronic myeloid leukemia.Journal of physiology and biochemistry · 2026Review
- Pharmacological inhibition of sclerostin protects bone from B-cell acute lymphoblastic leukemia-mediated destruction.HemaSphere · 2026Article
- Inflammation perturbs hematopoiesis by remodeling specific compartments of the bone marrow niche.Blood · 2026Article
- Non-invasive detection of bone marrow fibrosis in myeloproliferative neoplasms using cell-free RNA.iScience · 2026Article
- Epigenetic Inhibition of HDAC7 by Daidzein isolated from Macrotyloma uniflorum: A potential therapeutic approach in leukemia in silico, in-vitro and in-vivo.Medical oncology (Northwood, London, England) · 2026Article
- Conserved stromal EMT program controls regenerative capacity of mesenchymal stromal cells across multiple tissues.Science advances · 2026Article
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- Target practice: Opportunities for therapeutic intervention in CHIP and CCUS.Blood reviews · 2025Review
- Disruption of Marrow Microenvironments in Chronic Lymphocytic Leukemia by High-Resolution Synchrotron Micro-Computed Tomography.bioRxiv : the preprint server for biology · 2025Article
- Restoring resident tissue macrophages to combat aging and cancer.Nature aging · 2025Review
324 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Multipotent stromal cells (MSCs) and their osteoblastic lineage cell (OBC) derivatives are part of the bone marrow (BM) niche and contribute to hematopoietic stem cell (HSC) maintenance. Here, we show that myeloproliferative neoplasia (MPN) progressively remodels the endosteal BM niche into a self-reinforcing leukemic niche that impairs normal hematopoiesis, favors leukemic stem cell (LSC) function, and contributes to BM fibrosis. We show that leukemic myeloid cells stimulate MSCs to overproduce functionally altered OBCs, which accumulate in the BM cavity as inflammatory myelofibrotic cells. We identify roles for thrombopoietin, CCL3, and direct cell-cell interactions in driving OBC expansion, and for changes in TGF-β, Notch, and inflammatory signaling in OBC remodeling. MPN-expanded OBCs, in turn, exhibit decreased expression of many HSC retention factors and severely compromised ability to maintain normal HSCs, but effectively support LSCs. Targeting this pathological interplay could represent a novel avenue for treatment of MPN-affected patients and prevention of myelofibrosis.
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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 Socratic graph.