ADAMDEC1 and FGF2/FGFR1 signaling constitute a positive feedback loop to maintain GBM cancer stem cells

Identification of targetable mechanisms that maintain glioblastoma cancer stem cells (CSCs) remain a priority. Our study reveals a new mechanism by which a disintegrin and metalloproteinase domain-like protein decysin 1 promotes CSC maintenance through the activation of a fibroblast growth factor au...

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Published inMolecular & cellular oncology Vol. 7; no. 1; p. 1684787
Main Authors Jimenez-Pascual, Ana, Lathia, Justin D., Siebzehnrubl, Florian A.
Format Journal Article
LanguageEnglish
Published United States Taylor & Francis 02.01.2020
Taylor & Francis Group
Subjects
Author's Views
FGF2
FGFR1
glioblastoma
patient-derived xenograft
ZEB1
ZEB1
glioblastoma
patient-derived xenograft
FGF2
FGFR1
Online AccessGet full text
ISSN2372-3556
2372-3556
DOI10.1080/23723556.2019.1684787

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Abstract Identification of targetable mechanisms that maintain glioblastoma cancer stem cells (CSCs) remain a priority. Our study reveals a new mechanism by which a disintegrin and metalloproteinase domain-like protein decysin 1 promotes CSC maintenance through the activation of a fibroblast growth factor autocrine signaling loop, which can be blocked pharmacologically.
AbstractList Identification of targetable mechanisms that maintain glioblastoma cancer stem cells (CSCs) remain a priority. Our study reveals a new mechanism by which a disintegrin and metalloproteinase domain-like protein decysin 1 promotes CSC maintenance through the activation of a fibroblast growth factor autocrine signaling loop, which can be blocked pharmacologically.
Identification of targetable mechanisms that maintain glioblastoma cancer stem cells (CSCs) remain a priority. Our study reveals a new mechanism by which a disintegrin and metalloproteinase domain-like protein decysin 1 promotes CSC maintenance through the activation of a fibroblast growth factor autocrine signaling loop, which can be blocked pharmacologically.Identification of targetable mechanisms that maintain glioblastoma cancer stem cells (CSCs) remain a priority. Our study reveals a new mechanism by which a disintegrin and metalloproteinase domain-like protein decysin 1 promotes CSC maintenance through the activation of a fibroblast growth factor autocrine signaling loop, which can be blocked pharmacologically.
Author Lathia, Justin D.
Siebzehnrubl, Florian A.
Jimenez-Pascual, Ana
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SubjectTerms Author's Views
FGF2
FGFR1
glioblastoma
patient-derived xenograft
ZEB1
Title ADAMDEC1 and FGF2/FGFR1 signaling constitute a positive feedback loop to maintain GBM cancer stem cells
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