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@ARTICLE{Peschke:277703,
      author       = {J. C. Peschke and R. Bergmann and M. Mehnert and K. E.
                      Gonzalez Soto and L. R. Loureiro and N. Mitwasi and A.
                      Kegler and H. Altmann$^*$ and M. Wobus$^*$ and D. Máthé
                      and K. Szigeti and A. Feldmann$^*$ and M. Bornhäuser and M.
                      Bachmann$^*$ and F. Fasslrinner and C. Arndt},
      title        = {{FLT}3-directed {U}ni{CAR} {T}-cell therapy of acute
                      myeloid leukaemia.},
      journal      = {British journal of haematology},
      volume       = {202},
      number       = {6},
      issn         = {0007-1048},
      address      = {Oxford [u.a.]},
      publisher    = {Wiley-Blackwell},
      reportid     = {DKFZ-2023-01420},
      pages        = {1137-1150},
      year         = {2023},
      note         = {2023 Sep;202(6):1137-1150},
      abstract     = {Adaptor chimeric antigen receptor (CAR) T-cell therapy
                      offers solutions for improved safety and antigen escape,
                      which represent main obstacles for the clinical translation
                      of CAR T-cell therapy in myeloid malignancies. The adaptor
                      CAR T-cell platform 'UniCAR' is currently under early
                      clinical investigation. Recently, the first proof of concept
                      of a well-tolerated, rapidly switchable, CD123-directed
                      UniCAR T-cell product treating patients with acute myeloid
                      leukaemia (AML) was reported. Relapsed and refractory AML is
                      prone to high plasticity under therapy pressure targeting
                      one single tumour antigen. Thus, targeting of multiple
                      tumour antigens seems to be required to achieve durable
                      anti-tumour responses, underlining the need to further
                      design alternative AML-specific target modules (TM) for the
                      UniCAR platform. We here present the preclinical development
                      of a novel FMS-like tyrosine kinase 3 (FLT3)-directed UniCAR
                      T-cell therapy, which is highly effective for in vitro
                      killing of both AML cell lines and primary AML samples.
                      Furthermore, we show in vivo functionality in a murine
                      xenograft model. PET analyses further demonstrate a short
                      serum half-life of FLT3 TMs, which will enable a rapid
                      on/off switch of UniCAR T cells. Overall, the presented
                      preclinical data encourage the further development and
                      clinical translation of FLT3-specific UniCAR T cells for the
                      therapy of AML.},
      keywords     = {CAR T cells (Other) / CD135 (Other) / FLT3 (Other) / UniCAR
                      (Other) / acute myeloid leukaemia (Other)},
      cin          = {DD01},
      ddc          = {610},
      cid          = {I:(DE-He78)DD01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37460273},
      doi          = {10.1111/bjh.18971},
      url          = {https://inrepo02.dkfz.de/record/277703},
}