Genomic characterisation of Eμ-Myc mouse lymphomas identifies Bcor as a Myc co-operative tumour-suppressor gene
Nature Communications2017Vol. 8(1), pp. 14581–14581
Citations Over TimeTop 17% of 2017 papers
Marcus Lefebure, Richard W. Tothill, Elizabeth Kruse, Edwin D. Hawkins, Jake Shortt, Geoffrey M. Matthews, Gareth P. Gregory, Benjamin P. Martin, Madison J. Kelly, Izabela Todorovski, Maria Doyle, Richard Lupat, Jason Li, Jan Schroeder, Meaghan Wall, Stuart Craig, Gretchen Poortinga, Donald P. Cameron, Megan J. Bywater, Lev M. Kats, Micah D. Gearhart, Vivian J. Bardwell, Ross A. Dickins, Ross D. Hannan, Anthony T. Papenfuss, Ricky W. Johnstone
Abstract
The Eμ-Myc mouse is an extensively used model of MYC driven malignancy; however to date there has only been partial characterization of MYC co-operative mutations leading to spontaneous lymphomagenesis. Here we sequence spontaneously arising Eμ-Myc lymphomas to define transgene architecture, somatic mutations, and structural alterations. We identify frequent disruptive mutations in the PRC1-like component and BCL6-corepressor gene Bcor. Moreover, we find unexpected concomitant multigenic lesions involving Cdkn2a loss and other cancer genes including Nras, Kras and Bcor. These findings challenge the assumed two-hit model of Eμ-Myc lymphoma and demonstrate a functional in vivo role for Bcor in suppressing tumorigenesis.
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