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BCR-ABL enhances differentiation of long-term repopulating hematopoietic stem cells.

Schemionek, Mirle, Elling, Christian, Steidl, Ulrich, Bäumer, Nicole, Hamilton, Ashley, Spieker, Tilmann, Göthert, Joachim R., Stehling, Martin, Wagers, Amy, Huettner, Claudia S., Tenen, Daniel G., Tickenbrock, Lara, Berdel, Wolfgang E., Serve, Hubert, Holyoake, Tessa L., Müller-Tidow, Carsten, Koschmieder, Steffen·2010·Blood
DOI 10.1182/blood-2009-04-215376
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Abstract

In a previously developed inducible transgenic mouse model of chronic myeloid leukemia, we now demonstrate that the disease is transplantable using BCR-ABL+ Lin−Sca-1+c-kit+ (LSK) cells. Interestingly, the phenotype is more severe when unfractionated bone marrow cells are transplanted, yet neither progenitor cells (Lin−Sca-1−c-kit+), nor mature granulocytes (CD11b+Gr-1+), nor potential stem cell niche cells (CD45−Ter119−) are able to transmit the disease or alter the phenotype. The phenotype is largely independent of BCR-ABL priming before transplantation. However, prolonged BCR-ABL expression abrogates the potential of LSK cells to induce full-blown disease in secondary recipients and increases the fraction of multipotent progenitor cells at the expense of long-term hematopoietic stem cells (LT-HSCs) in the bone marrow. BCR-ABL alters the expression of genes involved in proliferation, survival, and hematopoietic development, probably contributing to the reduced LT-HSC frequency within BCR-ABL+ LSK cells. Reversion of BCR-ABL, or treatment with imatinib, eradicates mature cells, whereas leukemic stem cells persist, giving rise to relapsed chronic myeloid leukemia on reinduction of BCR-ABL, or imatinib withdrawal. Our results suggest that BCR-ABL induces differentiation of LT-HSCs and decreases their self-renewal capacity.

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Metadata

Authors
Schemionek, M., Elling, C., Steidl, U., Bäumer, N., Hamilton, A., Spieker, T., Göthert, J. R., Stehling, M., Wagers, A., Huettner, C. S., Tenen, D. G., Tickenbrock, L., Berdel, W. E., Serve, H., Holyoake, T. L., Müller-Tidow, C., & Koschmieder, S.
Affiliations
  • Department of Medicine, Hematology and Oncology, University of Münster, Münster, Germany;
  • Department of Cell Biology, Albert Einstein College of Medicine, Bronx, NY;
  • Section of Experimental Haematology, University of Glasgow, Glasgow, United Kingdom;
  • Department of Pathology, University of Münster, Münster, Germany;
  • Department of Hematology, University of Duisburg-Essen, Essen, Germany;
  • Max-Planck-Institute of Molecular Biomedicine, Münster, Germany;
  • Joslin Diabetes Center, Department of Stem Cell and Regenerative Biology, Harvard University, and Harvard Stem Cell Institute, Boston, MA;
  • Department of Molecular Oncology, Dana-Farber Cancer Institute, Boston, MA;
  • Harvard Stem Cell Institute, Harvard Medical School, Boston, MA and Cancer Science Institute, National University of Singapore, Singapore;
  • University of Applied Science, Hochschule Hamm-Lippstadt, Hamm, Germany; and
  • Department of Medicine, Hematology and Oncology, University of Frankfurt, Frankfurt, Germany
Venue
Blood
Publisher
American Society of Hematology
Published
2010-04-22
Volume
115
Issue
16
Pages
3185-3195
ISSN
  • 0006-4971
  • 1528-0020
DOI
10.1182/blood-2009-04-215376
Cited by
80
References
6
Language
en

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