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

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...

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Detalles Bibliográficos
Autores principales: Mohankumar, Kumarasamypet M., Currle, David S., White, Elsie, Boulos, Nidal, Dapper, Jason, Eden, Christopher, Nimmervoll, Birgit, Thiruvenkatam, Radhika, Connelly, Michele, Kranenburg, Tanya A., Neale, Geoffrey, Olsen, Scott, Wang, Yong-Dong, Finkelstein, David, Wright, Karen, Gupta, Kirti, Ellison, David W., Thomas, Arzu Onar, Gilbertson, Richard J.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4520751/
https://www.ncbi.nlm.nih.gov/pubmed/26075792
http://dx.doi.org/10.1038/ng.3323
Descripción
Sumario: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 10 ependymoma TSGs that converge on a small number of cell functions including vesicle trafficking, DNA modification and cholesterol biosynthesis, pinpointing these as potential new therapeutic targets.