ArticleNature medicine2013
Differential regulation of myeloid leukemias by the bone marrow microenvironment.
Article in Nature medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 161 papers.
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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
161 citing papers in PubMed, 257 citations in OpenAlex.
- ADORE: an open platform study of ruxolitinib in combination with other novel therapies in patients with myelofibrosis.Blood advances · 2025Trial
- Assessment of the Number and Phenotype of Macrophages in the Human BMB Samples of CML.BioMed research international · 2016Trial
- Modulation of the bone marrow microenvironment by acute B-cell lymphoblastic leukemia-derived large oncosomes.Blood advances · 2026Article
- Understanding drug resistance in chronic myeloid leukemia through the lens of leukemic stem cell states: insights from single-cell analyses.Haematologica · 2026Review
- Inhibition of Pellino-1 reverts the progression and tyrosine kinase inhibitor resistance in chronic myeloid leukemia.Cell death & disease · 2026Article
- Review
- Defining the Tumor-Bone axis: the role of extracellular vesicles in a crucial exchange route for breast cancer development and progression.Clinical & experimental metastasis · 2025Review
- Construction of a prognostic risk model for acute myeloid leukemia based on exosomal genes and analysis of immune microenvironment characteristics.Scientific reports · 2025Article
- HDAC3-YY1-RAB5A axis remodels AML-supportive niche by modulating mitochondrial homeostasis in bone marrow stromal cells.Cell death & disease · 2025Article
- Article
- Exploitation of the fibrinolytic system by B-cell acute lymphoblastic leukemia and its therapeutic targeting.Nature communications · 2024Article
- Differential inflammatory conditioning of the bone marrow by acute myeloid leukemia and its impact on progression.Blood advances · 2024Article
- Remodeling of the bone marrow microenvironment during acute myeloid leukemia progression.Annals of translational medicine · 2024Review
- Leukemic Stem Cells and Hematological Malignancies.International journal of molecular sciences · 2024Review
- Computational modeling reveals key factors driving treatment-free remission in chronic myeloid leukemia patients.NPJ systems biology and applications · 2024Article
- Review
- Identifying prognostic biomarker related to immune infiltration in acute myeloid leukemia.Clinical and experimental medicine · 2023Article
- Immune-related lncRNAs pairs prognostic score model for prediction of survival in acute myeloid leukemia patients.Clinical and experimental medicine · 2023Article
- DHODH: a promising target in the treatment of T-cell acute lymphoblastic leukemia.Blood advances · 2023Article
- FLT4 as a marker for predicting prognostic risk of refractory acute myeloid leukemia.Haematologica · 2023Article
101 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 1 country.
Funding
Abstract
Like their normal hematopoietic stem cell counterparts, leukemia stem cells (LSCs) in chronic myelogenous leukemia (CML) and acute myeloid leukemia (AML) are presumed to reside in specific niches in the bone marrow microenvironment (BMM) and may be the cause of relapse following chemotherapy. Targeting the niche is a new strategy to eliminate persistent and drug-resistant LSCs. CD44 (refs. 3,4) and interleukin-6 (ref. 5) have been implicated previously in the LSC niche. Transforming growth factor-β1 (TGF-β1) is released during bone remodeling and plays a part in maintenance of CML LSCs, but a role for TGF-β1 from the BMM has not been defined. Here, we show that alteration of the BMM by osteoblastic cell-specific activation of the parathyroid hormone (PTH) receptor attenuates BCR-ABL1 oncogene-induced CML-like myeloproliferative neoplasia (MPN) but enhances MLL-AF9 oncogene-induced AML in mouse transplantation models, possibly through opposing effects of increased TGF-β1 on the respective LSCs. PTH treatment caused a 15-fold decrease in LSCs in wild-type mice with CML-like MPN and reduced engraftment of immune-deficient mice with primary human CML cells. These results demonstrate that LSC niches in CML and AML are distinct and suggest that modulation of the BMM by PTH may be a feasible strategy to reduce LSCs, a prerequisite for the cure of CML.
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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.