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@ARTICLE{Fischer:304502,
      author       = {C. Fischer and S.-S. Chen and J. Nimmerfroh and A. Eugster
                      and S. Stücheli and C. Schultheiß and C. Widmer and D.
                      Heim and B. Kasenda and J. Passweg and S. Kobold$^*$ and L.
                      Egli and N. Coianiz and O. Chijioke and N. Chiorazzi and M.
                      Follo and H. Läubli and M. Peipp and M. Binder},
      title        = {{IGLV}3-21{R}110-directed bispecific antibodies activate
                      {T} cells and promote killing in a high-risk subset of
                      chronic lymphocytic leukemia.},
      journal      = {Haematologica},
      volume       = {nn},
      issn         = {0390-6078},
      address      = {Pavia},
      publisher    = {Ferrata Storti Foundation},
      reportid     = {DKFZ-2025-01891},
      pages        = {nn},
      year         = {2025},
      note         = {epub},
      abstract     = {We previously used a disease-specific B cell receptor (BCR)
                      point mutation (IGLV3-21R110) for selective targeting of a
                      high-risk subset of chronic lymphocytic leukemia (CLL) with
                      chimeric antigen receptor (CAR) T cells. Since CLL is a
                      disease of the elderly and a significant fraction of
                      patients is not able to physically tolerate CAR T cell
                      treatment, we explored bispecific antibodies as an
                      alternative for precision targeting of this tumor mutation.
                      Heterodimeric IgG1-based antibodies consisting of a fragment
                      crystallizable region (Fc) attached to both an
                      anti-IGLV3-21R110 Fab and an anti-CD3 (UCHT1) single chain
                      variable fragment (R110-bsAb) selectively killed cell lines
                      engineered to express high levels of the neoepitope as well
                      as primary CLL cells using healthy donor and CLL
                      patient-derived T cells as effectors. R110-bsAb spared
                      polyclonal human B cells (as opposed to CD19-targeting
                      Blinatumomab) as well as CD34+ human stem cells. Yet, R110-
                      bsAb induced lower T cell activation than Blinatumomab with
                      primary CLL cells likely due to lower expression of target
                      antigen. In vivo, R110-bsAb specifically killed
                      IGLV3-21R110-expressing cell lines and CLL cells while
                      sparing peripheral blood mononuclear cells. These findings
                      highlight bispecific antibodies as a potential off-the-shelf
                      immunotherapy for high-risk CLL patients, offering selective
                      targeting while preserving healthy B cells.},
      cin          = {MU01},
      ddc          = {610},
      cid          = {I:(DE-He78)MU01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40931870},
      doi          = {DOI:10.3324/haematol.2025.287697},
      url          = {https://inrepo02.dkfz.de/record/304502},
}