%0 Journal Article
%A Delage, Lorric
%A Lambert, Mireille
%A Bardel, Emilie
%A Kundlacz, Cindy
%A Chartoire, Dimitri
%A Conchon, Axel
%A Peugnet, Anne-Laure
%A Gorka, Lucas
%A Auberger, Patrick
%A Jacquel, Arnaud
%A Soussain, Carole
%A Destaing, Olivier
%A Delecluse, Henri-Jacques
%A Delecluse, Susanne
%A Merabet, Samir
%A Traverse-Glehen, Alexandra
%A Salles, Gilles A
%A Bachy, Emmanuel
%A Billaud, Marc
%A Ghesquieres, Herve
%A Genestier, Laurent
%A Rouault, Jean Pierre
%A Sujobert, Pierre
%T BTG1 inactivation drives lymphomagenesis and promotes lymphoma dissemination through activation of BCAR1.
%J Blood
%V 141
%N 10
%@ 0006-4971
%C Washington, DC
%I American Society of Hematology
%M DKFZ-2022-02815
%P 1209-1220
%D 2023
%Z 2023 Mar 9;141(10):1209-1220
%X Understanding the functional role of mutated genes in cancer is required to translate the findings of cancer genomics into therapeutic improvement. BTG1 is recurrently mutated in the MCD/C5 subtype of diffuse large B cell lymphoma (DLBCL), which is associated with extranodal dissemination. There, we provide evidence that Btg1 knock-out accelerates the development of a lethal lymphoproliferative disease driven by Bcl2 overexpression. We further show that the scaffolding protein BCAR1 is a BTG1 partner. Furthermore, following BTG1 deletion or expression of BTG1 mutations observed in DLBCL patients, the overactivation of the BCAR1-RAC1 pathway confers increased migration ability in vitro and in vivo. These modifications are targetable with the SRC inhibitor dasatinib, which opens novel therapeutic opportunities in BTG1 mutated DLBCL.
%F PUB:(DE-HGF)16
%9 Journal Article
%$ pmid:36375119
%R 10.1182/blood.2022016943
%U https://inrepo02.dkfz.de/record/182638