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@ARTICLE{Delage:182638,
      author       = {L. Delage and M. Lambert and E. Bardel and C. Kundlacz and
                      D. Chartoire and A. Conchon and A.-L. Peugnet and L. Gorka
                      and P. Auberger and A. Jacquel and C. Soussain and O.
                      Destaing and H.-J. Delecluse$^*$ and S. Delecluse$^*$ and S.
                      Merabet and A. Traverse-Glehen and G. A. Salles and E. Bachy
                      and M. Billaud and H. Ghesquieres and L. Genestier and J. P.
                      Rouault and P. Sujobert},
      title        = {{BTG}1 inactivation drives lymphomagenesis and promotes
                      lymphoma dissemination through activation of {BCAR}1.},
      journal      = {Blood},
      volume       = {141},
      number       = {10},
      issn         = {0006-4971},
      address      = {Washington, DC},
      publisher    = {American Society of Hematology},
      reportid     = {DKFZ-2022-02815},
      pages        = {1209-1220},
      year         = {2023},
      note         = {2023 Mar 9;141(10):1209-1220},
      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. 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.},
      cin          = {F100},
      ddc          = {610},
      cid          = {I:(DE-He78)F100-20160331},
      pnm          = {316 - Infektionen, Entzündung und Krebs (POF4-316)},
      pid          = {G:(DE-HGF)POF4-316},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36375119},
      doi          = {10.1182/blood.2022016943},
      url          = {https://inrepo02.dkfz.de/record/182638},
}