TY  - JOUR
AU  - Lefebure, M
AU  - Tothill, RW
AU  - Kruse, E
AU  - Hawkins, ED
AU  - Shortt, J
AU  - Matthews, GM
AU  - Gregory, GP
AU  - Martin, BP
AU  - Kelly, MJ
AU  - Todorovski, I
AU  - Doyle, MA
AU  - Lupat, R
AU  - Li, J
AU  - Schroeder, J
AU  - Wall, M
AU  - Craig, S
AU  - Poortinga, G
AU  - Cameron, D
AU  - Bywater, M
AU  - Kats, L
AU  - Gearhart, MD
AU  - Bardwell, VJ
AU  - Dickins, RA
AU  - Hannan, RD
AU  - Papenfuss, AT
AU  - Johnstone, RW
Y2  - 2020/12/22
Y1  - 2017/03/06
SN  - 2041-1723
UR  - http://hdl.handle.net/11343/258287
AB  - 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.
LA  - English
PB  - NATURE PUBLISHING GROUP
T1  - Genomic characterisation of E mu-Myc mouse lymphomas identifies Bcor as a Myc co-operative tumour-suppressor gene
DO  - 10.1038/ncomms14581
IS  - Nature Communications
VL  - 8
IS  - 1
SP  - 1-10
L1  - /bitstream/handle/11343/258287/PMC5343491.pdf?sequence=1&isAllowed=y
ER  -