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Cancer Cell. 2015 May 11;27(5):712-27. doi: 10.1016/j.ccell.2015.04.005.

Cross-Species Genomics Identifies TAF12, NFYC, and RAD54L as Choroid Plexus Carcinoma Oncogenes.

Author information

1
Department of Developmental Neurobiology, St Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN 38105, USA.
2
Genetics and Genome Biology Program, The Hospital for Sick Children, Department of Medical Biophysics, University of Toronto, Toronto, ON M5G 1X8, Canada.
3
Department of Pathology, St Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN 38105, USA.
4
Department of Computational Biology, St Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN 38105, USA.
5
Genetics and Genome Biology Program, The Hospital for Sick Children, Department of Medical Biophysics, University of Toronto, Toronto, ON M5G 1X8, Canada; Division of Hematology/Oncology, The Hospital for Sick Children, Department of Medical Biophysics, University of Toronto, Toronto, ON M5G 1X8, Canada.
6
Department of Developmental Neurobiology, St Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN 38105, USA; Department of Oncology, St Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN 38105, USA. Electronic address: richard.gilbertson@stjude.org.

Abstract

Choroid plexus carcinomas (CPCs) are poorly understood and frequently lethal brain tumors with few treatment options. Using a mouse model of the disease and a large cohort of human CPCs, we performed a cross-species, genome-wide search for oncogenes within syntenic regions of chromosome gain. TAF12, NFYC, and RAD54L co-located on human chromosome 1p32-35.3 and mouse chromosome 4qD1-D3 were identified as oncogenes that are gained in tumors in both species and required for disease initiation and progression. TAF12 and NFYC are transcription factors that regulate the epigenome, whereas RAD54L plays a central role in DNA repair. Our data identify a group of concurrently gained oncogenes that cooperate in the formation of CPC and reveal potential avenues for therapy.

PMID:
25965574
PMCID:
PMC4458854
DOI:
10.1016/j.ccell.2015.04.005
[Indexed for MEDLINE]
Free PMC Article

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