ArticleEMBO reports2019
Extracellular vesicles impose quiescence on residual hematopoietic stem cells in the leukemic niche.
Article in EMBO reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 50 citations in OpenAlex.
- Extracellular vesicles from aged individuals trigger mitochondrial dysfunction in hematopoietic progenitor cells.Haematologica · 2026Article
- Extracellular vesicle cargo dynamics in the bone marrow microenvironment: from hematopoietic homeostasis to malignant transformation.Extracellular vesicle · 2026Article
- Extracellular Vesicles Define Discrete Nano-Based Niches Within the Human Haematopoietic System.Journal of extracellular vesicles · 2025Article
- Breaking the Bone Marrow Barrier: Peripheral Blood as a Gateway to Measurable Residual Disease Detection in Acute Myelogenous Leukemia.American journal of hematology · 2025Review
- Bone marrow mesenchymal stromal cells support translation in refractory acute myeloid leukemia.Cell reports · 2025Article
- Small extracellular vesicles derived from acute myeloid leukemia cells promote leukemogenesis by transferring miR-221-3p.Haematologica · 2024Article
- The role of the hematopoietic stem/progenitor cells-derived extracellular vesicles in hematopoiesis.Heliyon · 2024Article
- Inflammatory recruitment of healthy hematopoietic stem and progenitor cells in the acute myeloid leukemia niche.Leukemia · 2024Article
- Extracellular Vesicles in Breast Cancer: From Biology and Function to Clinical Diagnosis and Therapeutic Management.International journal of molecular sciences · 2023Review
- Bone marrow-derived extracellular vesicles carry the TGF-β signal transducer Smad2 to preserve hematopoietic stem cells in mice.Cell death discovery · 2023Article
- Current challenges and future directions for engineering extracellular vesicles for heart, lung, blood and sleep diseases.Journal of extracellular vesicles · 2023Review
- Targeting metabolic vulnerabilities to overcome resistance to therapy in acute myeloid leukemia.Cancer drug resistance (Alhambra, Calif.) · 2023Review
- Regulation of hematopoietic stem cells differentiation, self-renewal, and quiescence through the mTOR signaling pathway.Frontiers in cell and developmental biology · 2023Review
- Emerging roles of extracellular vesicles in normal and malignant hematopoiesis.The Journal of clinical investigation · 2022Review
- Extracellular Vesicles in Myeloid Neoplasms.International journal of molecular sciences · 2022Review
- Acute lymphoblastic leukemia-derived extracellular vesicles affect quiescence of hematopoietic stem and progenitor cells.Cell death & disease · 2022Article
- Identification of potential pathways and microRNA-mRNA networks associated with benzene metabolite hydroquinone-induced hematotoxicity in human leukemia K562 cells.BMC pharmacology & toxicology · 2022Article
- Acute Myeloid Leukemia Cells Functionally Compromise Hematopoietic Stem/Progenitor Cells Inhibiting Normal Hematopoiesis Through the Release of Extracellular Vesicles.Frontiers in oncology · 2022Article
- Article
- Extracellular vesicles: General features and usefulness in diagnosis and therapeutic management of colorectal cancer.World journal of gastrointestinal oncology · 2021Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Progressive remodeling of the bone marrow microenvironment is recognized as an integral aspect of leukemogenesis. Expanding acute myeloid leukemia (AML) clones not only alter stroma composition, but also actively constrain hematopoiesis, representing a significant source of patient morbidity and mortality. Recent studies revealed the surprising resistance of long-term hematopoietic stem cells (LT-HSC) to elimination from the leukemic niche. Here, we examine the fate and function of residual LT-HSC in the BM of murine xenografts with emphasis on the role of AML-derived extracellular vesicles (EV). AML-EV rapidly enter HSC, and their trafficking elicits protein synthesis suppression and LT-HSC quiescence. Mechanistically, AML-EV transfer a panel of miRNA, including miR-1246, that target the mTOR subunit Raptor, causing ribosomal protein S6 hypo-phosphorylation, which in turn impairs protein synthesis in LT-HSC. While HSC functionally recover from quiescence upon transplantation to an AML-naive environment, they maintain relative gains in repopulation capacity. These phenotypic changes are accompanied by DNA double-strand breaks and evidence of a sustained DNA-damage response. In sum, AML-EV contribute to niche-dependent, reversible quiescence and elicit persisting DNA damage in LT-HSC.
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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.