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Concise Review: The Malignant Hematopoietic Stem Cell Niche
1Departments of Medicine and Pathology & Immunology, Washington University School of Medicine, St. Louis, Missouri, USA.
Hematopoietic stem cell (HSC) proliferation, self-renewal, and trafficking are dependent, in part, upon signals generated by stromal cells in the bone marrow. Stromal cells are organized into niches that support specific subsets of hematopoietic progenitors. There is emerging evidence that malignant hematopoietic cells may generate signals that alter the number and/or function of specific stromal cell populations in the bone marrow. At least in some cases, the resulting alterations in the bone marrow microenvironment confer a competitive advantage to the malignant HSC and progenitor cells and/or render them less sensitive to chemotherapy. Targeting these signals represents a promising therapeutic strategy for selected hematopoietic malignancies. In this review, we focus on two questions. How do alterations in bone marrow stromal cells arise in hematopoietic malignancies, and how do they contribute to disease pathogenesis? Stem Cells 2017;35:3-8.
Hematopoietic stem cell (HSC) proliferation, self-renewal, and trafficking are dependent, in part, upon signals generated by stromal cells in the bone marrow. Stromal cells are organized into niches that support specific subsets of hematopoietic progenitors. There is emerging evidence that malignant hematopoietic cells may generate signals that alter the number and/or function of specific stromal cell populations in the bone marrow. At least in some cases, the resulting alterations in the bone marrow microenvironment confer a competitive advantage to the malignant HSC and progenitor cells and/or render them less sensitive to chemotherapy. Targeting these signals represents a promising therapeutic strategy for selected hematopoietic malignancies. In this review, we focus on two questions. How do alterations in bone marrow stromal cells arise in hematopoietic malignancies, and how do they contribute to disease pathogenesis? Stem Cells 2017;35:3-8.
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