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Acute myeloid leukemia (AML) is a quickly aggressive hematopoietic disorder that progress due to the accumulation and clonal expansion of immature myeloid cells. Despite the latest developments in AML treatment, repeated relapses and drug resistance remain one of the major challenges in treatment of leukemia. Currently, it is well known that the components of the tumor microenvironment such as cellular and non-cellular elements play a critical function in treatment failures of AML, also they are most common cause of complications including suppression of hematopoiesis. Exosomes are membrane-bound extracellular vesicles (EVs) that transfer signaling molecules and have attracted a large amount of attention due to their important role in inter-cellular communication in health and disease. Exosomes participate in the survival and chemoresistance of many leukemia through transferring their rich cargos of molecules including miRNAs, growth factors, and cytokines. The key producers of exosomes that mainly participate to AML pathogenesis are bone marrow mesenchymal stem cell (BMSCs) and AML cell themselves. These cells release an enormous number of exosomes that affect several target cells such as natural killer (NK) and hematopoietic stem cells to the development of leukemia proliferation and progression. In the present study, a comprehensive review of the literature has been done to briefly discuss the biology of exosomes and highlight the role of exosomes derived from AML in the progress of acute myeloid leukemia. Copyright © 2022. Published by Elsevier Masson SAS.

Citation

Ali H Amin, Liqaa Mohammed Al Sharifi, Alisher Jamoliddinovich Kakhharov, Maria Jade Catalan Opulencia, Fahad Alsaikhan, Dmitry Olegovich Bokov, Hasan Sh Majdi, Mohammed Abed Jawad, Ali Thaeer Hammid, Mohammed Nader Shalaby, Yasser Fakri Mustafa, Homayoon Siahmansouri. Role of Acute Myeloid Leukemia (AML)-Derived exosomes in tumor progression and survival. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie. 2022 Jun;150:113009

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PMID: 35486974

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