% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Heim:282514,
      author       = {C. Heim and L. M. Moser$^*$ and H. Kreyenberg and H. B.
                      Bonig and T. Tonn$^*$ and W. S. Wels$^*$ and E. Gradhand and
                      E. Ullrich$^*$ and M. T. Meister and M. G. Koerkamp and F.
                      C. P. Holstege and J. Drost and J.-H. Klusmann$^*$ and P.
                      Bader and M. Merker and E. Rettinger$^*$},
      title        = {{E}rb{B}2 ({HER}2)-{CAR}-{NK}-92 cells for enhanced
                      immunotherapy of metastatic fusion-driven alveolar
                      rhabdomyosarcoma.},
      journal      = {Frontiers in immunology},
      volume       = {14},
      issn         = {1664-3224},
      address      = {Lausanne},
      publisher    = {Frontiers Media},
      reportid     = {DKFZ-2023-01803},
      pages        = {1228894},
      year         = {2023},
      abstract     = {Metastatic rhabdomyosarcoma (RMS) is a challenging tumor
                      entity that evades conventional treatments and endogenous
                      antitumor immune responses, highlighting the need for novel
                      therapeutic strategies. Applying chimeric antigen receptor
                      (CAR) technology to natural killer (NK) cells may offer
                      safe, effective, and affordable therapies that enhance
                      cancer immune surveillance.Here, we assess the efficacy of
                      clinically usable CAR-engineered NK cell line NK-92/5.28.z
                      against ErbB2-positive RMS in vitro and in a metastatic
                      xenograft mouse model.Our results show that NK-92/5.28.z
                      cells effectively kill RMS cells in vitro and significantly
                      prolong survival and inhibit tumor progression in mice. The
                      persistence of NK-92/5.28.z cells at tumor sites
                      demonstrates efficient antitumor response, which could help
                      overcome current obstacles in the treatment of solid
                      tumors.These findings encourage further development of
                      NK-92/5.28.z cells as off-the-shelf immunotherapy for the
                      treatment of metastatic RMS.},
      keywords     = {Humans / Animals / Mice / Rhabdomyosarcoma, Alveolar:
                      therapy / Receptors, Chimeric Antigen: genetics /
                      Immunotherapy / Rhabdomyosarcoma: therapy / Disease Models,
                      Animal / Killer Cells, Natural / Neoplasms, Second Primary /
                      ERBB2 (HER2/neu) (Other) / cancer immunotherapy (Other) /
                      chimeric antigen receptor (Other) / rhabdomyosarcoma (Other)
                      / xenograft (Other) / Receptors, Chimeric Antigen (NLM
                      Chemicals)},
      cin          = {FM01 / DD01},
      ddc          = {610},
      cid          = {I:(DE-He78)FM01-20160331 / I:(DE-He78)DD01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37662907},
      pmc          = {pmc:PMC10471977},
      doi          = {10.3389/fimmu.2023.1228894},
      url          = {https://inrepo02.dkfz.de/record/282514},
}