An animal model of MYC-driven medulloblastoma
Summary Medulloblastoma (MB) is the most common malignant brain tumor in children. Patients whose tumors exhibit overexpression or amplification of the MYC oncogene (c-MYC) usually have an extremely poor prognosis, but there are no animal models of this subtype of the disease. Here, we how that cere...
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| Main Authors: | , , , |
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| Format: | Article (Journal) |
| Language: | English |
| Published: |
February 13, 2012
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| In: |
Cancer cell
Year: 2012, Volume: 21, Issue: 2, Pages: 155-167 |
| ISSN: | 1878-3686 |
| DOI: | 10.1016/j.ccr.2011.12.021 |
| Online Access: | Verlag, Volltext: http://dx.doi.org/10.1016/j.ccr.2011.12.021 Verlag, Volltext: http://www.sciencedirect.com/science/article/pii/S1535610811004831 
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| Author Notes: | Yanxin Pei, Colin E. Moore, Jun Wang, Alok K. Tewari, Alexey Eroshkin, Yoon-Jae Cho, Hendrik Witt, Andrey Korshunov, Tracy-Ann Read, Julia L. Sun, Earlene M. Schmitt, C. Ryan Miller, Anne F. Buckley, Roger E. McLendon, Thomas F. Westbrook, Paul A. Northcott, Michael D. Taylor, Stefan M. Pfister, Phillip G. Febbo and Robert J. Wechsler-Reya |
| Summary: | Summary Medulloblastoma (MB) is the most common malignant brain tumor in children. Patients whose tumors exhibit overexpression or amplification of the MYC oncogene (c-MYC) usually have an extremely poor prognosis, but there are no animal models of this subtype of the disease. Here, we how that cerebellar stem cells expressing Myc and mutant Trp53 (p53) generate aggressive tumors following orthotopic transplantation. These tumors consist of large, pleiomorphic cells and resemble human MYC-driven MB at a molecular level. Notably, antagonists of PI3K/mTOR signaling, but not Hedgehog signaling, inhibit growth of tumor cells. These findings suggest that cerebellar stem cells can give rise to MYC-driven MB and identify a novel model that can be used to test therapies for this devastating disease. |
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| Item Description: | Published: February 13, 2012 Gesehen am 05.07.2018 |
| Physical Description: | Online Resource |
| ISSN: | 1878-3686 |
| DOI: | 10.1016/j.ccr.2011.12.021 |