Michael Boyiadzis1, Theresa L Whiteside2. 1. Division of Hematology-Oncology, Departments of Medicine. 2. Pathology, Immunology and Otolaryngology, University of Pittsburgh, Hillman Cancer Center, Pittsburgh, Pennsylvania, USA.
Abstract
PURPOSE OF REVIEW: Exosomes are cell-derived, biologically active membrane-bound vesicles, and are emerging as key modulators of hematopoiesis. Recent studies have provided a clearer understanding of the mechanisms whereby blast-derived exosomes act to suppress hematopoiesis in acute myeloid leukemia (AML). RECENT FINDINGS: Exosomes released from leukemia blasts have been shown to suppress hematopoietic progenitor cell (HPC) functions indirectly through stromal reprogramming of niche-retention factors and also as a consequence of AML exosome-directed microRNA delivery to HPC. Furthermore, exosomes secreted by AML blasts remodel the bone marrow niche into a leukemia growth-permissive microenvironment. SUMMARY: Exosomes suppress hematopoiesis in AML. Strategies to block the production, secretion and reprogramming that exosomes induce may be a novel therapeutic approach in AML and other leukemias.
PURPOSE OF REVIEW: Exosomes are cell-derived, biologically active membrane-bound vesicles, and are emerging as key modulators of hematopoiesis. Recent studies have provided a clearer understanding of the mechanisms whereby blast-derived exosomes act to suppress hematopoiesis in acute myeloid leukemia (AML). RECENT FINDINGS: Exosomes released from leukemia blasts have been shown to suppress hematopoietic progenitor cell (HPC) functions indirectly through stromal reprogramming of niche-retention factors and also as a consequence of AML exosome-directed microRNA delivery to HPC. Furthermore, exosomes secreted by AML blasts remodel the bone marrow niche into a leukemia growth-permissive microenvironment. SUMMARY: Exosomes suppress hematopoiesis in AML. Strategies to block the production, secretion and reprogramming that exosomes induce may be a novel therapeutic approach in AML and other leukemias.
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