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Mol Genet Metab. 2015 Sep-Oct;116(1-2):24-8. doi: 10.1016/j.ymgme.2015.07.004. Epub 2015 Jul 20.

Biology of the bone marrow microenvironment and myelodysplastic syndromes.

Author information

1
Department of Obstetrics & Gynecologic Oncology, Stanford University School of Medicine, Stanford, CA, USA; Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA, USA.
2
Division of Hematology/Oncology, Department of Pediatrics, Stanford University School of Medicine, Stanford, CA, USA.
3
Department of Molecular, Cell & Developmental Biology, University of California, Los Angeles, CA, USA.
4
Division of Hematology/Oncology, Department of Pediatrics, Stanford University School of Medicine, Stanford, CA, USA. Electronic address: kmsakamo@stanford.edu.

Abstract

Myelodysplastic syndromes (MDS) are characterized by cytopenias resulting from ineffective hematopoiesis with a predisposition to transform to acute myeloid leukemia (AML). Recent evidence suggests that the hematopoietic stem cell microenvironment contributes to the pathogenesis of MDS. Inflammation and hypoxia within the bone marrow are key regulators of hematopoietic stem and progenitor cells that can lead to several bone marrow failure syndromes, including MDS. In this brief review, we provide an overview of the clinical and molecular features of MDS, the bone marrow microenvironment, and specific pathways that lead to abnormal blood cell development in MDS. Characterization of key steps in the pathogenesis of MDS will lead to new approaches to treat patients with this disease.

KEYWORDS:

Bone marrow microenvironment; Hypoxia; Inflammation; Myelodysplastic syndromes; Ribosomal deficiency; Signaling pathways

PMID:
26210353
PMCID:
PMC4618471
DOI:
10.1016/j.ymgme.2015.07.004
[Indexed for MEDLINE]
Free PMC Article

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