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Nat Genet. 2015 Aug;47(8):878-87. doi: 10.1038/ng.3323. Epub 2015 Jun 15.

An in vivo screen identifies ependymoma oncogenes and tumor-suppressor genes.

Author information

1
Department of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA.
2
Department of Chemical Biology and Therapeutics, St. Jude Children's Research Hospital, Memphis, Tennessee, USA.
3
Hartwell Center for Biotechnology and Bioinformatics, St. Jude Children's Research Hospital, Memphis, Tennessee, USA.
4
Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA.
5
Department of Oncology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA.
6
Department of Pathology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA.
7
Department of Biostatistics, St. Jude Children's Research Hospital, Memphis, Tennessee, USA.
8
1] Department of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA. [2] Department of Oncology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA.

Abstract

Cancers are characterized by non-random chromosome copy number alterations that presumably contain oncogenes and tumor-suppressor genes (TSGs). The affected loci are often large, making it difficult to pinpoint which genes are driving the cancer. Here we report a cross-species in vivo screen of 84 candidate oncogenes and 39 candidate TSGs, located within 28 recurrent chromosomal alterations in ependymoma. Through a series of mouse models, we validate eight new ependymoma oncogenes and ten new ependymoma TSGs that converge on a small number of cell functions, including vesicle trafficking, DNA modification and cholesterol biosynthesis, identifying these as potential new therapeutic targets.

PMID:
26075792
PMCID:
PMC4520751
DOI:
10.1038/ng.3323
[Indexed for MEDLINE]
Free PMC Article
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