Abstract
Blood cancers are a heterogeneous group of disorders including leukemia, multiple myeloma, and lymphoma. They may derive from the clonal evolution of the hemopoietic stem cell compartment or from the transformation of progenitors with immune potential. Extracellular vesicles (EVs) are membrane-bound nanovesicles which are released by cells into body fluids with a role in intercellular communication in physiology and pathology, including cancer. EV cargos are enriched in nucleic acids, proteins, and lipids, and these molecules can be delivered to target cells to influence their biological properties and modify surrounding or distant targets. In this review, we will describe the “smart strategy” on how blood cancer-derived EVs modulate tumor cell development and maintenance. Moreover, we will also depict the function of microenvironment-derived EVs in blood cancers and discuss how the interplay between tumor and microenvironment affects blood cancer cell growth and spreading, immune response, angiogenesis, thrombogenicity, and drug resistance. The potential of EVs as non-invasive biomarkers will be also discussed. Lastly, we discuss the clinical application viewpoint of EVs in blood cancers. Overall, blood cancers apply a ‘vesicular intelligence’ strategy to spread signals over their microenvironment, promoting the development and/or maintenance of the malignant clone.
Highlights
Blood cancers are a heterogeneous group of disorders including leukemia, multiple myeloma, and lymphoma
It has been demonstrated that fibroblast growth factor 2 (FGF2)-enriched exosomes from bone marrow stromal cells are endocytosed by leukemia cells (AML) and protect leukemia cells from tyrosine kinase inhibitors (TKIs)
Since microenvironmental signals are involved in the development and progression of blood cancers, new ways to detect them through Extracellular vesicles (EVs) would be highly valuable for diagnosing and monitoring hematological malignancies
Summary
Blood cancers are a heterogeneous group of disorders including leukemia, multiple myeloma, and lymphoma They may derive from the clonal evolution of the hemopoietic stem cell compartment or from the transformation of progenitors with immune potential. Blood cancer-derived EVs deeply impact stromal cell transformation, angiogenesis, and immune suppression by carrying mRNAs, microRNA (miR), lipids, and proteins and transferring the cargo to target cells including stromal cells, endothelial cells, and immune cells These effects aim to promote malignant transformation, development, and progression [19]. We will describe the “smart strategy” on how blood cancer-derived EVs regulate tumor cell development and spreading, thrombogenicity, immune response, drug resistance, and communication within the tumor microenvironment in blood cancers. We included all English-language articles published from database inception through to November 2020
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