ArticleNature2014
Leukaemogenesis induced by an activating β-catenin mutation in osteoblasts.
Article in Nature, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 315 papers.
What it found
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Who cites it
315 citing papers in PubMed, 513 citations in OpenAlex.
- The Role of the Bone Marrow Microenvironment in the Pathogenesis of Acute Myeloid Leukemia.Biomedicines · 2026Review
- Elevated lactate in AML bone marrow contributes to macrophage polarization via GPR81 signaling.Blood advances · 2026Article
- Intrinsic and niche-dependent metabolic regulation of haematopoietic stem cells and implications for leukaemogenesis.Nature cell biology · 2026Review
- Systematic functional dissection of germline noncoding risk variants impacting clonal hematopoiesis.bioRxiv : the preprint server for biology · 2026Article
- Regulatory role of mTORC1 signaling in osteoblasts in acute myeloid leukemia progression and steady-state hematopoiesis.iScience · 2026Article
- Review
- 3DACS biomaterials science & engineering · 2026Review
- Exploring the Bone Marrow Microenvironment as a Therapeutic Barrier and Targetable Source of Crosstalk in Acute Myeloid Leukemia.Blood and lymphatic cancer : targets and therapy · 2026Review
- Avian influenza virus H5N1 and H9N2 subtypes in different birds and humans: Findings from an extensive evaluation.Open veterinary journal · 2026Review
- An inflammatory T-cell-stromal axis contributes to hematopoietic stem/progenitor cell failure and clonal evolution in human myelodysplastic syndrome.Nature communications · 2025Article
- Chromosomal abnormalities of mesenchymal stromal cells in hematological malignancies.Oncogene · 2025Review
- Review
- Galectin-3 Release in the Bone Marrow Microenvironment Promotes Drug Resistance and Relapse in Acute Myeloid Leukemia.Life (Basel, Switzerland) · 2025Review
- A niche driven mechanism determines response and a mutation-independent therapeutic approach for myeloid malignancies.Cancer cell · 2025Article
- Bone-derived factors mediate crosstalk between skeletal and extra-skeletal organs.Bone research · 2025Review
- From Chemotherapy to Targeted Therapy: Unraveling Resistance in Acute Myeloid Leukemia Through Genetic and Non-Genetic Insights.International journal of molecular sciences · 2025Review
- Article
- Elevated Lactate in the AML Bone Marrow Microenvironment Polarizes Leukemia-Associated Macrophages via GPR81 Signaling.bioRxiv : the preprint server for biology · 2025Article
- STAT signaling in the pathogenesis and therapy of acute myeloid leukemia and myelodysplastic syndromes.Neoplasia (New York, N.Y.) · 2025Review
- Evidence of Epigenetic Oncogenesis: A Turning Point in Cancer Research.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
255 more citing papers are in PubMed but not listed here.
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Authors and funding
19 authors at 4 institutions in 2 countries.
Funding
Abstract
Cells of the osteoblast lineage affect the homing and the number of long-term repopulating haematopoietic stem cells, haematopoietic stem cell mobilization and lineage determination and B cell lymphopoiesis. Osteoblasts were recently implicated in pre-leukaemic conditions in mice. However, a single genetic change in osteoblasts that can induce leukaemogenesis has not been shown. Here we show that an activating mutation of β-catenin in mouse osteoblasts alters the differentiation potential of myeloid and lymphoid progenitors leading to development of acute myeloid leukaemia with common chromosomal aberrations and cell autonomous progression. Activated β-catenin stimulates expression of the Notch ligand jagged 1 in osteoblasts. Subsequent activation of Notch signalling in haematopoietic stem cell progenitors induces the malignant changes. Genetic or pharmacological inhibition of Notch signalling ameliorates acute myeloid leukaemia and demonstrates the pathogenic role of the Notch pathway. In 38% of patients with myelodysplastic syndromes or acute myeloid leukaemia, increased β-catenin signalling and nuclear accumulation was identified in osteoblasts and these patients showed increased Notch signalling in haematopoietic cells. These findings demonstrate that genetic alterations in osteoblasts can induce acute myeloid leukaemia, identify molecular signals leading to this transformation and suggest a potential novel pharmacotherapeutic approach to acute myeloid leukaemia.
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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 OpenQuestion graph.