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@ARTICLE{Kaidun:282728,
      author       = {P. Kaidun$^*$ and S. Holzmayer$^*$ and S. M. Greiner$^*$
                      and A. Seller$^*$ and C. M. Tegeler and I. Hagelstein$^*$
                      and J. Mauermann$^*$ and T. Engler and A. Koch and A. D.
                      Hartkopf and H. Salih$^*$ and M. Märklin$^*$},
      title        = {{T}argeting {NKG}2{DL} with {B}ispecific {NKG}2{D}-{CD}16
                      and {NKG}2{D}-{CD}3 {F}usion {P}roteins on
                      {T}riple-{N}egative {B}reast {C}ancer.},
      journal      = {International journal of molecular sciences},
      volume       = {24},
      number       = {17},
      issn         = {1422-0067},
      address      = {Basel},
      publisher    = {Molecular Diversity Preservation International},
      reportid     = {DKFZ-2023-01854},
      pages        = {13156},
      year         = {2023},
      abstract     = {Triple-negative breast cancer (TNBC) is a particularly
                      aggressive subtype of breast cancer with a poor response
                      rate to conventional systemic treatment and high relapse
                      rates. Members of the natural killer group 2D ligand
                      (NKG2DL) family are expressed on cancer cells but are
                      typically absent from healthy tissues; thus, they are
                      promising tumor antigens for novel immunotherapeutic
                      approaches. We developed bispecific fusion proteins (BFPs)
                      consisting of the NKG2D receptor domain targeting multiple
                      NKG2DLs, fused to either anti-CD3 (NKG2D-CD3) or anti-CD16
                      (NKG2D-CD16) Fab fragments. First, we characterized the
                      expression of the NKG2DLs (MICA, MICB, ULBP1-4) on TNBC cell
                      lines and observed the highest surface expression for MICA
                      and ULBP2. Targeting TNBC cells with NKG2D-CD3/CD16
                      efficiently activated both NK and T cells, leading to their
                      degranulation and cytokine release and lysis of TNBC cells.
                      Furthermore, PBMCs from TNBC patients currently undergoing
                      chemotherapy showed significantly higher NK and T cell
                      activation and tumor cell lysis when stimulated with
                      NKG2D-CD3/CD16. In conclusions, BFPs activate and direct the
                      NK and T cells of healthy and TNBC patients against TNBC
                      cells, leading to efficient eradication of tumor cells.
                      Therefore, NKG2D-based NK and T cell engagers could be a
                      valuable addition to the treatment options for TNBC
                      patients.},
      keywords     = {Humans / Triple Negative Breast Neoplasms: drug therapy /
                      Triple Negative Breast Neoplasms: genetics / NK Cell
                      Lectin-Like Receptor Subfamily K: genetics / Ligands /
                      Administration, Cutaneous / Aggression / NK cell (Other) /
                      NKG2D (Other) / T cell (Other) / TNBC (Other) / bispecific
                      (Other) / breast cancer (Other) / fusion protein (Other) /
                      immunotherapy (Other) / NK Cell Lectin-Like Receptor
                      Subfamily K (NLM Chemicals) / Ligands (NLM Chemicals)},
      cin          = {TU01},
      ddc          = {540},
      cid          = {I:(DE-He78)TU01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37685962},
      pmc          = {pmc:PMC10487695},
      doi          = {10.3390/ijms241713156},
      url          = {https://inrepo02.dkfz.de/record/282728},
}