Myelodysplastic syndromes comprise a heterogeneous group of clonal hematopoietic stem cell malignancies characterized by ineffective bone marrow (BM) hematopoiesis, peripheral blood cytopenias and substantial risk for progression to acute myeloid leukemia. It is generally accepted that myelodysplastic syndromes originate as a result of multistep leukemogenesis, implicating genetic, epigenetic and immune-mediated alterations of an early hematopoietic stem cell. However, alterations in the BM microenvironment in terms of abnormal hematopoietic-to-stromal cell interactions, relative deficiency of hematopoietic growth factors and aberrant release of inhibitors may also have a role in myelodysplastic syndrome (MDS) pathogenesis. The possible involvement of the BM mesenchymal stem cells (MSC) in the pathogenetic/pathophysiologic process of MDS has been recently studied but existing data on MSCs cytogenetic and functional integrity are controversial. Notably, in our study we did not find any significant quantitative or qualitative deficits in MDS-derived MSCs. As no conclusive data on the characteristics of BM MSCs have been reported so far, future studies should aim at elucidating whether BM MSCs belong primarily to the abnormal clone or whether they are indirectly damaged and whether they might be safely used for therapeutic purposes in MDS patients. This article aims to give an overview of the current state of the art on the quantitative, functional, immunoregulatory and cytogenetic properties of BM MSCs in MDS.
Keywords: Bone marrow, cytogenetic abnormalities, immunosuppression, mesenchymal stem cells (MSCs), myelodysplastic syndrome (MDS), hematopoietic stem cell, peripheral blood cytopenias, immunoregulatory, acute myeloid leukemia
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