Critical multiple angiogenic factors secreted by glioblastoma stem-like cells underline the need for combinatorial anti-angiogenic therapeutic strategies |
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Authors: | Cécile Thirant Julie Gavard Marie-Pierre Junier Hervé Chneiweiss |
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Affiliation: | 1. Leukemia and Stem Cell Biology Laboratory, Department of Hematological Medicine, Rayne Institute, King's College London, London, UK;2. CNRS UMR8104, Inserm U1016, Cochin Institute, Paris Descartes University, Paris, France;3. Glial Plasticity Team, Psychiatry and Neuroscience Centre, Paris Descartes University, Paris, France;4. Glial Plasticity Team, Psychiatry and Neuroscience Centre, Paris Descartes University, Paris, France Correspondence: Dr. Hervé Chneiweiss, Equipe Plasticité Gliale, Centre de Psychiatrie et Neurosciences, 2 ter rue d'Alésia, 75014 Paris, France E-mail: herve.chneiweiss@inserm.fr Fax: +33-1-4580-7213 |
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Abstract: | Glioblastomas are the most frequent adult primary brain tumors that still remain fatal despite major clinical efforts. As in other solid tumors, populations of glioblastoma stem-like cells (GSCs) endowed with tumor initiating and therapeutic resistance properties have been identified. Glioblastomas are highly vascularized tumors resulting in a rich dialog between GSCs and endothelial cells. In one direction, endothelial cells and their secreted proteins are able to sustain GSC properties while, in turn, GSCs can promote neoangiogenesis, modulate endothelial cell functions and may even transdifferentiate into endothelial cells. Accordingly, targeting tumor vasculature seems a promising issue despite incomplete and transient results obtained from anti-vascular endothelial growth factor therapeutic trials. Recent findings of novel GSC-secreted molecules with pro-angiogenic properties (Semaphorin 3A, hepatoma-derived growth factor) open the path to the design of a concerted attack of glioblastoma vasculature that could overcome the development of resistance to single-targeted therapies while keeping away the toxicity of the treatments. |
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Keywords: | Anti-angiogenic Endothelial cell Glioblastoma stem-like cells HDGF Therapeutic resistance |
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