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@ARTICLE{Givi:304580,
      author       = {S. Givi and B. J. Lohnes and S. Ebrahimi and S. Riedel and
                      S. Khokhali and S. A. Khan and M. Keller and C. Wölfel and
                      H. Echchannaoui$^*$ and E. Bockamp and M. C. Andre and H.
                      Abken and M. Theobald$^*$ and U. F. Hartwig$^*$},
      title        = {{CRISPR}/{C}as9 {TCR}-{E}dited {NK}p30 {CAR} {T} {C}ells
                      {E}xhibit {S}uperior {A}nti-{T}umor {I}mmunity to
                      {B}7{H}6-{E}xpressing {L}eukemia and {M}elanoma.},
      journal      = {International journal of molecular sciences},
      volume       = {26},
      number       = {17},
      issn         = {1422-0067},
      address      = {Basel},
      publisher    = {Molecular Diversity Preservation International},
      reportid     = {DKFZ-2025-01903},
      pages        = {8235},
      year         = {2025},
      abstract     = {Chimeric antigen receptor (CAR) T-cell therapy directed to
                      CD19 and B-cell maturation antigen has revolutionized
                      treatment of B-cell leukemia and lymphoma, and multiple
                      myeloma. However, identifying suitable targets for acute
                      myeloid leukemia (AML) remains challenging due to concurrent
                      expression of potential target antigens on normal
                      hematopoietic stem cells or tissues. As the stress-induced
                      B7H6 molecule is rarely found on normal tissues but
                      expressed on many cancers including AML and melanoma, the
                      NKp30-ligand B7H6 emerges as a promising target for
                      NKp30-based CAR T therapy for these tumors. In this study,
                      we report a comprehensive B7H6 expression analysis on
                      primary AML and melanoma as well as on different tumor
                      cell-lines examined by RT-qPCR and flow cytometry, and
                      efficient anti-tumor reactivity of NKp30-CAR T cells to AML
                      and melanoma. To overcome limitations of autologous CAR
                      T-cell fitness-dependent efficacy and patient-tailored
                      production, we generated CRISPR/Cas9-mediated TCR-knockout
                      (TCRKO) NKp30-CAR T cells as an off-the-shelf approach for
                      CAR T therapy. Functional studies comparing NKp30-CD28 CAR
                      or NKp30-CD137 CAR TCR+ and TCRKO T lymphocytes revealed
                      superior anti-tumoral immunity of NKp30-CD28 CAR TCRKO T
                      cells to AML and melanoma cell lines in vitro, and effective
                      control of tumor burden in an NSG melanoma-xenograft mouse
                      model. In conclusion, these findings highlight the
                      therapeutic potential of NKp30 CAR TCRKO T cells for
                      adoptive T-cell therapy to B7H6-expressing cancers,
                      including melanoma and AML.},
      keywords     = {B7H6 expressing tumors (Other) / CAR T-cell therapy (Other)
                      / NKp30-based CAR T-cell therapy (Other) / acute myeloid
                      leukemia (Other) / immunotherapy (Other) / melanoma (Other)},
      cin          = {FM01},
      ddc          = {540},
      cid          = {I:(DE-He78)FM01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40943160},
      pmc          = {pmc:PMC12428420},
      doi          = {10.3390/ijms26178235},
      url          = {https://inrepo02.dkfz.de/record/304580},
}