Journal Article

DKFZ-2017-02613

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png A Tumor Suppressor Function for Notch Signaling in Forebrain Tumor Subtypes.

Giachino, C. ; Boulay, J.-L. ; Ivanek, R. ; Alvarado, A. ; Tostado, C. ; Lugert, S. ; Tchorz, J. ; Coban, M. ; Mariani, L. ; Bettler, B. ; Lathia, J. ; Frank, S. ; Pfister, S.DKFZ* ; Kool, M.DKFZ* ; Taylor, V.

2015
Cell Press Cambridge, Mass.

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Please use a persistent id in citations: doi:10.1016/j.ccell.2015.10.008

Abstract: In the brain, Notch signaling maintains normal neural stem cells, but also brain cancer stem cells, indicating an oncogenic role. Here, we identify an unexpected tumor suppressor function for Notch in forebrain tumor subtypes. Genetic inactivation of RBP-Jκ, a key Notch mediator, or Notch1 and Notch2 receptors accelerates PDGF-driven glioma growth in mice. Conversely, genetic activation of the Notch pathway reduces glioma growth and increases survival. In humans, high Notch activity strongly correlates with distinct glioma subtypes, increased patient survival, and lower tumor grade. Additionally, simultaneous inactivation of RBP-Jκ and p53 induces primitive neuroectodermal-like tumors in mice. Hence, Notch signaling cooperates with p53 to restrict cell proliferation and tumor growth in mouse models of human brain tumors.

Keyword(s): Basic Helix-Loop-Helix Transcription Factors ; Hes5 protein, mouse ; Immunoglobulin J Recombination Signal Sequence-Binding Protein ; Notch1 protein, mouse ; Notch2 protein, mouse ; Platelet-Derived Growth Factor ; Proto-Oncogene Proteins c-sis ; Rbpj protein, mouse ; Receptor, Notch1 ; Receptor, Notch2 ; Receptors, Notch ; Recombinant Proteins ; Repressor Proteins ; Tumor Suppressor Protein p53 ; Tumor Suppressor Proteins ; platelet-derived growth factor A

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Contributing Institute(s):

1. Pädiatrische Neuroonkologie (B062)

Research Program(s):

1. 312 - Functional and structural genomics (POF3-312) (POF3-312)

Appears in the scientific report 2015

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Database coverage:
; BIOSIS Previews ; Current Contents - Clinical Medicine ; Current Contents - Life Sciences ; Ebsco Academic Search ; IF >= 20 ; JCR ; NCBI Molecular Biology Database ; SCOPUS ; Science Citation Index ; Science Citation Index Expanded ; Thomson Reuters Master Journal List ; Web of Science Core Collection

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