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@ARTICLE{Tate:272834,
      author       = {T. Tate and S. Matsumoto and K. Nemoto and M. Leisegang$^*$
                      and S. Nagayama and K. Obama and Y. Nakamura and K.
                      Kiyotani},
      title        = {{I}dentification of {T} {C}ell {R}eceptors {T}argeting a
                      {N}eoantigen {D}erived from {R}ecurrently {M}utated
                      {FGFR}3.},
      journal      = {Cancers},
      volume       = {15},
      number       = {4},
      issn         = {2072-6694},
      address      = {Basel},
      publisher    = {MDPI},
      reportid     = {DKFZ-2023-00407},
      pages        = {1031},
      year         = {2023},
      abstract     = {Immunotherapies, including immune checkpoint blockades,
                      play a critically important role in cancer treatments. For
                      immunotherapies, neoantigens, which are generated by somatic
                      mutations in cancer cells, are thought to be good targets
                      due to their tumor specificity. Because neoantigens are
                      unique in individual cancers, it is challenging to develop
                      personalized immunotherapy targeting neoantigens. In this
                      study, we screened 'shared neoantigens', which are specific
                      types of neoantigens derived from mutations observed
                      commonly in a subset of cancer patients. Using exome
                      sequencing data in the Cancer Genome Atlas (TCGA), we
                      predicted shared neoantigen peptides and performed in vitro
                      screening of shared neoantigen-reactive CD8+ T cells using
                      peripheral blood from healthy donors. We examined the
                      functional activity of neoantigen-specific T cell receptors
                      (TCRs) by generating TCR-engineered T cells. Among the
                      predicted shared neoantigens from TCGA data, we found that
                      the mutated FGFR3Y373C peptide induced antigen-specific CD8+
                      T cells from the donor with HLA-A*02:06 via an ELISPOT
                      assay. Subsequently, we obtained FGFR3Y373C-specific CD8+ T
                      cell clones and identified two different sets of TCRs
                      specifically reactive to FGFR3Y373C. We found that the
                      TCR-engineered T cells expressing FGFR3Y373C-specific TCRs
                      recognized the mutated FGFR3Y373C peptide but not the
                      corresponding wild-type peptide. These two
                      FGFR3Y373C-specific TCR-engineered T cells showed cytotoxic
                      activity against mutated FGFR3Y373C-loaded cells. These
                      results imply the possibility of strategies of
                      immunotherapies targeting shared neoantigens, including
                      cancer vaccines and TCR-engineered T cell therapies.},
      keywords     = {cancer precision medicine (Other) / cancer vaccine (Other)
                      / immunopharmacogenomics (Other) / shared neoantigens
                      (Other)},
      cin          = {BE01},
      ddc          = {610},
      cid          = {I:(DE-He78)BE01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36831375},
      pmc          = {pmc:PMC9953830},
      doi          = {10.3390/cancers15041031},
      url          = {https://inrepo02.dkfz.de/record/272834},
}