TY  - JOUR
AU  - Delage, Lorric
AU  - Lambert, Mireille
AU  - Bardel, Emilie
AU  - Kundlacz, Cindy
AU  - Chartoire, Dimitri
AU  - Conchon, Axel
AU  - Peugnet, Anne-Laure
AU  - Gorka, Lucas
AU  - Auberger, Patrick
AU  - Jacquel, Arnaud
AU  - Soussain, Carole
AU  - Destaing, Olivier
AU  - Delecluse, Henri-Jacques
AU  - Delecluse, Susanne
AU  - Merabet, Samir
AU  - Traverse-Glehen, Alexandra
AU  - Salles, Gilles A
AU  - Bachy, Emmanuel
AU  - Billaud, Marc
AU  - Ghesquieres, Herve
AU  - Genestier, Laurent
AU  - Rouault, Jean Pierre
AU  - Sujobert, Pierre
TI  - BTG1 inactivation drives lymphomagenesis and promotes lymphoma dissemination through activation of BCAR1.
JO  - Blood
VL  - 141
IS  - 10
SN  - 0006-4971
CY  - Washington, DC
PB  - American Society of Hematology
M1  - DKFZ-2022-02815
SP  - 1209-1220
PY  - 2023
N1  - 2023 Mar 9;141(10):1209-1220
AB  - 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.
LB  - PUB:(DE-HGF)16
C6  - pmid:36375119
DO  - DOI:10.1182/blood.2022016943
UR  - https://inrepo02.dkfz.de/record/182638
ER  -