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Leuk Res. 2015 Apr;39(4):486-93. doi: 10.1016/j.leukres.2015.01.013. Epub 2015 Feb 2.

Mesenchymal stromal cells from patients with acute myeloid leukemia have altered capacity to expand differentiated hematopoietic progenitors.

Author information

1
Regenerative Medicine Program, Ottawa Hospital Research Institute, Canada.
2
Regenerative Medicine Program, Ottawa Hospital Research Institute, Canada; Atomic Energy of Canada Limited, Chalk River, ON, Canada.
3
Department of Medicine, Hematology, University of Ottawa, Ottawa, ON, Canada.
4
Centre for Biologics Evaluation, Health Canada, Ottawa, Canada.
5
Regenerative Medicine Program, Ottawa Hospital Research Institute, Canada; Department of Medicine, Hematology, University of Ottawa, Ottawa, ON, Canada. Electronic address: daallan@ohri.ca.

Abstract

The bone marrow microenvironment may be permissive to the emergence and progression of acute myeloid leukemia (AML). Studying interactions between the microenvironment and leukemia cells should provide new insight for therapeutic advances. Mesenchymal stromal cells (MSCs) are central to the maintenance of the hematopoietic niche. Here we compared the functions and gene expression patterns of MSCs derived from bone marrow aspirates of healthy donors and patients with AML. MSCs expanded from AML patients had heterogeneous morphology and displayed a wide range of proliferation capacity compared to MSCs from healthy controls. The ability of AML-MSCs to support the expansion of committed hematopoietic progenitors from umbilical cord blood-derived CD34+ cells may be impaired while the expression of genes associated with maintaining hematopoietic quiescence appeared to be increased in AML-MSCs compared to healthy donors. These results highlight important potential differences in the biologic profile of MSCs from AML patients compared to healthy donors that may contribute to the emergence or progression of leukemia.

KEYWORDS:

Acute myeloid leukemia; Hematopoiesis; Marrow microenvironment; Mesenchymal stromal cells

PMID:
25703353
DOI:
10.1016/j.leukres.2015.01.013
[Indexed for MEDLINE]

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