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Updated: Jun 12, 2026

Identifying Bone Marrow Microenvironmental Populations in Myelodysplastic Syndrome and Acute Myeloid Leukemia
Published on: November 10, 2023
Modulation of the bone marrow microenvironment by acute B-cell lymphoblastic leukemia-derived large oncosomes
Foruzandeh Samangan1, Theresa Krack2, Fatima Didar Kerman1
1Center for Thrombosis and Hemostasis, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Leukemia cells release large oncosomes (LO) that reprogram bone marrow stromal cells (MSC) to support therapy-evasive growth. Targeting these LO-mediated communication pathways may offer novel leukemia treatment strategies.
Area of Science:
- Oncology
- Cell Biology
- Hematology
Background:
- Leukemia cells exploit the bone marrow microenvironment for survival and therapy evasion.
- Extracellular vesicles (EVs), particularly large oncosomes (LO), are implicated in cancer progression.
- B-cell acute lymphoblastic leukemia (B-ALL) requires specific microenvironmental support for growth.
Purpose of the Study:
- To investigate how BCR-ABL1+ B-ALL cells use LO to influence the bone marrow microenvironment.
- To determine the mechanisms by which LO reprogram mesenchymal stromal cells (MSC).
- To explore the therapeutic potential of targeting LO-mediated communication in B-ALL.
Main Methods:
- Analysis of LO released by BCR-ABL1+ B-ALL cells.
- Transcriptome and secretome profiling of MSC co-cultured with LO.
- Assessment of MSC differentiation and metabolic reprogramming.
- Evaluation of LO-educated MSC and derived adipocytes in supporting B-ALL growth.
Main Results:
- BCR-ABL1+ B-ALL derived LO reprogram MSC to a pro-tumorigenic phenotype.
- LO alter MSC expression of insulin-like growth factor binding proteins (IGFBPs) and fibrinolytic proteins.
- MSC are metabolically reprogrammed and differentiated into adipocytes that support B-ALL growth.
- LO-educated MSC and adipocytes provide distinct support mechanisms for B-ALL cells.
Conclusions:
- Leukemia cell-derived LO are key mediators of bone marrow microenvironment reprogramming.
- Targeting LO-mediated intercellular communication presents a potential strategy for B-ALL adjuvant therapy.
- Understanding these interactions can lead to novel therapeutic approaches for overcoming chemoresistance.
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