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BTG1 inactivation drives lymphomagenesis and promotes lymphoma dissemination through activation of BCAR1

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Delage, Lorric | Lambert, Mireille | Bardel, Émilie | Kundlacz, Cindy | Chartoire, Dimitri | Conchon, Axel | Peugnet, Anne-Laure | Gorka, Lucas | Auberger, Patrick | Jacquel, Arnaud | Soussain, Carole | Destaing, Olivier | Delecluse, Henri-Jacques | Delecluse, Susanne | Merabet, Samir | Traverse-Glehen, Alexandra | Salles, Gilles | Bachy, Emmanuel | Billaud, Marc | Ghesquières, Hervé | Genestier, Laurent | Rouault, Jean-Pierre | Sujobert, Pierre

Edité par CCSD ; American Society of Hematology -

International audience. Abstract 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. Here, we provide evidence that Btg1 knock out accelerates the development of a lethal lymphoproliferative disease driven by Bcl2 overexpression. Furthermore, we show that the scaffolding protein BCAR1 is a BTG1 partner. Moreover, after BTG1 deletion or expression of BTG1 mutations observed in patients with DLBCL, 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.

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