Blood Res 2016; 51(4): 225-232  https://doi.org/10.5045/br.2016.51.4.225
Mesenchymal stromal cells in myeloid malignancies
Thomas Schroeder, Stefanie Geyh, Ulrich Germing, Rainer Haas
Department of Hematology, Oncology and Clinical Immunology, University of Duesseldorf, Medical Faculty, Düesseldorf, Germany
Correspondence to: Thomas Schroeder, M.D., Ph.D.
Department of Hematology, Oncology and
Clinical Immunology, University of
Duesseldorf, Medical Faculty, Moorenstr.
5, 40225 Düsseldorf, Germany
E-mail:
thomas.schroeder@med.uni-duesseldorf.de 
Received: December 7, 2016; Accepted: December 13, 2016; Published online: December 31, 2016.
© The Korean Journal of Hematology. All rights reserved.

cc This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) are clonal myeloid disorders characterized by hematopoietic insufficiency. As MDS and AML are considered to originate from genetic and molecular defects of hematopoietic stem and progenitor cells (HSPC), the main focus of research in this field has focused on the characterization of these cells. Recently, the contribution of BM microenvironment to the pathogenesis of myeloid malignancies, in particular MDS and AML has gained more interest. This is based on a better understanding of its physiological role in the regulation of hematopoiesis. Additionally, it was demonstrated as a ‘proof of principle’ that genetic disruption of cells of the mesenchymal or osteoblastic lineage can induce MDS, MPS or AML in mice. In this review, we summarize the current knowledge about the contribution of the BM microenvironment, in particular mesenchymal stromal cells (MSC) to the pathogenesis of AML and MDS. Furthermore, potential models integrating the BM micro-environment into the pathophysiology of these myeloid disorders are discussed. Finally, strategies to therapeutically exploit this knowledge and to interfere with the crosstalk between clonal hematopoietic cells and altered stem cell niches are introduced.
Keywords: Myelodysplastic syndromes, Acute myeloid leukemia, Mesenchymal stromal cells, Hematopoiesis, Niche


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