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Interconversion between Tumorigenic and Differentiated States in Acute Myeloid Leukemia
MD. McKenzie, M. Ghisi, EP. Oxley, S. Ngo, L. Cimmino, C. Esnault, R. Liu, JM. Salmon, CC. Bell, N. Ahmed, M. Erlichster, MT. Witkowski, GJ. Liu, M. Chopin, A. Dakic, E. Simankowicz, G. Pomilio, T. Vu, P. Krsmanovic, S. Su, L. Tian, TM. Baldwin,...
Language English Country United States
Document type Journal Article, Research Support, Non-U.S. Gov't
Grant support
NV16-31586A
MZ0
CEP Register
Digital library NLK
Full text - Article
NLK
Cell Press Free Archives
from 2007-06-07 to 1 year ago
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from 2007 to 1 year ago
- MeSH
- Leukemia, Myeloid, Acute metabolism pathology MeSH
- Cell Differentiation physiology MeSH
- Carcinogenesis MeSH
- Cells, Cultured MeSH
- Humans MeSH
- Mice MeSH
- Neoplastic Stem Cells physiology MeSH
- Cell Plasticity MeSH
- Proto-Oncogene Proteins genetics metabolism MeSH
- Trans-Activators genetics metabolism MeSH
- Cell Transdifferentiation physiology MeSH
- Tretinoin metabolism MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
Tumors are composed of phenotypically heterogeneous cancer cells that often resemble various differentiation states of their lineage of origin. Within this hierarchy, it is thought that an immature subpopulation of tumor-propagating cancer stem cells (CSCs) differentiates into non-tumorigenic progeny, providing a rationale for therapeutic strategies that specifically eradicate CSCs or induce their differentiation. The clinical success of these approaches depends on CSC differentiation being unidirectional rather than reversible, yet this question remains unresolved even in prototypically hierarchical malignancies, such as acute myeloid leukemia (AML). Here, we show in murine and human models of AML that, upon perturbation of endogenous expression of the lineage-determining transcription factor PU.1 or withdrawal of established differentiation therapies, some mature leukemia cells can de-differentiate and reacquire clonogenic and leukemogenic properties. Our results reveal plasticity of CSC maturation in AML, highlighting the need to therapeutically eradicate cancer cells across a range of differentiation states.
Assistance Publique Hôpitaux de Paris Oncologie Moléculaire Hôpital St Louis 75010 Paris France
Australian Centre for Blood Diseases Monash University Commercial Road Melbourne VIC 3004 Australia
Baker Heart and Diabetes Institute Melbourne VIC 3004 Australia
Collège de France PSL Research University 75005 Paris France
Department of Biosystems Science and Engineering ETH Zurich Mattenstrasse 26 4058 Basel Switzerland
Department of Clinical Haematology The Alfred Hospital Melbourne VIC 3004 Australia
Department of Medical Biology University of Melbourne Parkville VIC 3010 Australia
Department of Pathology New York University School of Medicine 550 1 Avenue New York NY 10016 USA
Department of Pediatrics Harvard Medical School Boston MA USA
Division of Hematology Oncology Boston Children's Hospital Boston MA USA
INSERM U944 CNRS UMR7212 Université de Paris Institut de Recherche Saint Louis 75010 Paris France
Medical University of Vienna 1030 Vienna Austria
Peter MacCallum Cancer Centre Melbourne VIC 3000 Australia
Research Institute of Molecular Pathology Campus Vienna Biocenter 1 1030 Vienna Austria
School of Mathematics and Statistics University of Melbourne Parkville VIC 3010 Australia
Sir Peter MacCallum Department of Oncology University of Melbourne Parkville VIC 3010 Australia
References provided by Crossref.org
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