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001     182638
005     20240229145726.0
024 7 _ |a 10.1182/blood.2022016943
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024 7 _ |a pmid:36375119
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024 7 _ |a 0006-4971
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024 7 _ |a 1528-0020
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037 _ _ |a DKFZ-2022-02815
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Delage, Lorric
|0 0000-0002-3838-8763
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245 _ _ |a BTG1 inactivation drives lymphomagenesis and promotes lymphoma dissemination through activation of BCAR1.
260 _ _ |a Washington, DC
|c 2023
|b American Society of Hematology
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500 _ _ |a 2023 Mar 9;141(10):1209-1220
520 _ _ |a 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.
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700 1 _ |a Lambert, Mireille
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700 1 _ |a Bardel, Emilie
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700 1 _ |a Kundlacz, Cindy
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700 1 _ |a Chartoire, Dimitri
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700 1 _ |a Conchon, Axel
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700 1 _ |a Peugnet, Anne-Laure
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700 1 _ |a Gorka, Lucas
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700 1 _ |a Auberger, Patrick
|0 0000-0002-2481-8275
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700 1 _ |a Jacquel, Arnaud
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700 1 _ |a Soussain, Carole
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700 1 _ |a Destaing, Olivier
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700 1 _ |a Delecluse, Henri-Jacques
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700 1 _ |a Delecluse, Susanne
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700 1 _ |a Merabet, Samir
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700 1 _ |a Traverse-Glehen, Alexandra
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700 1 _ |a Salles, Gilles A
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700 1 _ |a Bachy, Emmanuel
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700 1 _ |a Billaud, Marc
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700 1 _ |a Ghesquieres, Herve
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700 1 _ |a Genestier, Laurent
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700 1 _ |a Rouault, Jean Pierre
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700 1 _ |a Sujobert, Pierre
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773 _ _ |a 10.1182/blood.2022016943
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