| Literature DB >> 25965574 |
Yiai Tong1, Diana Merino2, Birgit Nimmervoll1, Kirti Gupta3, Yong-Dong Wang4, David Finkelstein4, James Dalton3, David W Ellison3, Xiaotu Ma4, Jinghui Zhang4, David Malkin5, Richard J Gilbertson6.
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.Entities:
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Year: 2015 PMID： 25965574 PMCID： PMC4458854 DOI： 10.1016/j.ccell.2015.04.005
Source DB: PubMed Journal: Cancer Cell ISSN： 1535-6108 Impact factor: 31.743