A novel tumour-suppressor function for the Notch pathway in myeloid leukaemia

Apostolos Klinakis (), Camille Lobry, Omar Abdel-Wahab, Philmo Oh, Hiroshi Haeno, Silvia Buonamici, Inge van De Walle, Severine Cathelin, Thomas Trimarchi, Elisa Araldi, Cynthia Liu, Sherif Ibrahim, Miroslav Beran, Jiri Zavadil, Argiris Efstratiadis, Tom Taghon, Franziska Michor, Ross L. Levine and Iannis Aifantis ()
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Apostolos Klinakis: Biomedical Research Foundation, Academy of Athens
Camille Lobry: New York University School of Medicine
Omar Abdel-Wahab: Human Oncology and Pathogenesis Program and Leukemia Service, Memorial Sloan-Kettering Cancer Center
Philmo Oh: New York University School of Medicine
Hiroshi Haeno: Dana-Farber Cancer Institute, Harvard School of Public Health
Silvia Buonamici: New York University School of Medicine
Inge van De Walle: Microbiology and Immunology, Ghent University Hospital, Ghent University
Severine Cathelin: New York University School of Medicine
Thomas Trimarchi: New York University School of Medicine
Elisa Araldi: New York University School of Medicine
Cynthia Liu: New York University School of Medicine
Sherif Ibrahim: New York University School of Medicine
Miroslav Beran: M.D. Anderson Cancer Center
Jiri Zavadil: NYU Cancer Institute and Center for Health Informatics and Bioinformatics, NYU Langone Medical Center
Argiris Efstratiadis: Biomedical Research Foundation, Academy of Athens
Tom Taghon: Microbiology and Immunology, Ghent University Hospital, Ghent University
Franziska Michor: Dana-Farber Cancer Institute, Harvard School of Public Health
Ross L. Levine: Human Oncology and Pathogenesis Program and Leukemia Service, Memorial Sloan-Kettering Cancer Center
Iannis Aifantis: New York University School of Medicine

Nature, 2011, vol. 473, issue 7346, 230-233

Abstract: Notch signalling and tumour suppression Activating mutations in the Notch pathway promote tumorigenesis in T-cell leukaemias. Iannis Aifantis and colleagues now find that the same pathway suppresses the development of myeloid leukaemias. Inactivating the pathway in haematopoietic stem cells leads to myeloid disease resembling chronic myelomonocytic leukaemia (CMML), and mutations in Notch pathway genes can be found in patients with CMML. The Notch pathway is shown to suppress a myeloid differentiation program. These findings demonstrate that the Notch pathway exerts both oncogenic and tumour-suppressor functions in the haematopoietic system and regulates critical cell-fate decisions.

Date: 2011
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DOI: 10.1038/nature09999

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