Journal
LEUKEMIA
Volume 23, Issue 12, Pages 2233-2241Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/leu.2009.175
Keywords
acute leukemia; microenvironment; angiogenesis; bone marrow; endosteal niche; endovascular niche
Categories
Funding
- National Institutes of Health [DK62987, DK55001, AA13913, DK61688, CA125550]
- Champalimaud Foundation
- Department of Medicine for the Division of Matrix Biology at Beth Israel Deaconess Medical Center
- Health Research Fund, Ministry of Health, Spain [BAE-90058]
- Health Service from Comunidad Autonoma of Murcia, Spain
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Tumor microenvironment has a major role in cancer progression and resistance to treatment. The bone marrow (BM) is a dynamic network of growth factors, cytokines and stromal cells, providing a permissive environment for leukemogenesis and progression. Both BM stroma and leukemic blasts promote angiogenesis, which is increased in acute lymphoblastic leukemia and acute myeloid leukemia. Growth factors like vascular endothelial growth factor (VEGF), basic fibroblast growth factor and angiopoietins are the main proangiogenic mediators in acute leukemia. Autocrine proleukemic loops have been described for VEGF and angiopoietin in hematopoietic cells. Interactions of stromal cells and extracellular matrix with leukemic blasts can also generate antiapoptotic signals that contribute to neoplastic progression and persistence of treatment-resistant minimal residual disease. High expression of CXC chemokine ligand 4 (CXCR4) by leukemic blasts and activation of the CXCR4-CXCL12 axis is involved in leukemia progression and disruption of normal hematopoiesis. Leukemia-associated bone microenvironment markers could be used as prognostic or predictive indicators of disease progression and/or treatment outcome. Studies related to bone microenvironment would likely provide a better understanding of the treatment resistance associated with leukemia therapy and design of new treatments. Leukemia (2009) 23, 2233-2241; doi:10.1038/leu.2009.175; published online 3 September 2009
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