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@ARTICLE{Meng:285421,
      author       = {Z. Meng$^*$ and A. Rodriguez Ehrenfried$^*$ and C. L.
                      Tan$^*$ and L. K. Steffens$^*$ and H. Kehm$^*$ and S.
                      Zens$^*$ and C. Lauenstein$^*$ and A. Paul$^*$ and M.
                      Schwab$^*$ and J. Förster$^*$ and M. Salek$^*$ and A.
                      Riemer$^*$ and H. Wu and C. Eckert and C.-S. Leonhardt and
                      O. Strobel and M. Volkmar$^*$ and I. Poschke$^*$ and R.
                      Offringa$^*$},
      title        = {{T}ranscriptome-based identification of tumor-reactive and
                      bystander {CD}8+ {T} cell receptor clonotypes in human
                      pancreatic cancer.},
      journal      = {Science translational medicine},
      volume       = {15},
      number       = {722},
      issn         = {1946-6234},
      address      = {Washington, DC},
      publisher    = {AAAS},
      reportid     = {DKFZ-2023-02366},
      pages        = {eadh9562},
      year         = {2023},
      note         = {#EA:D200#EA:D170#LA:D200#LA:D170# / HI-TRON},
      abstract     = {Pancreatic ductal adenocarcinoma (PDAC) is generally
                      refractory to immune checkpoint blockade, although patients
                      with genetically unstable tumors can show modest therapeutic
                      benefit. We previously demonstrated the presence of
                      tumor-reactive CD8+ T cells in PDAC samples. Here, we
                      charted the tumor-infiltrating T cell repertoire in PDAC by
                      combining single-cell transcriptomics with functional
                      testing of T cell receptors (TCRs) for reactivity against
                      autologous tumor cells. On the basis of a comprehensive
                      dataset including 93 tumor-reactive and 65 bystander TCR
                      clonotypes, we delineated a gene signature that effectively
                      distinguishes between these T cell subsets in PDAC, as well
                      as in other tumor indications. This revealed a high
                      frequency of tumor-reactive TCR clonotypes in three
                      genetically unstable samples. In contrast, the T cell
                      repertoire in six genetically stable PDAC tumors was largely
                      dominated by bystander T cells. Nevertheless, multiple
                      tumor-reactive TCRs were successfully identified in each of
                      these samples, thereby providing a perspective for
                      personalized immunotherapy in this treatment-resistant
                      indication.},
      cin          = {D200 / D190 / D170 / F130},
      ddc          = {500},
      cid          = {I:(DE-He78)D200-20160331 / I:(DE-He78)D190-20160331 /
                      I:(DE-He78)D170-20160331 / I:(DE-He78)F130-20160331},
      pnm          = {314 - Immunologie und Krebs (POF4-314)},
      pid          = {G:(DE-HGF)POF4-314},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37967201},
      doi          = {10.1126/scitranslmed.adh9562},
      url          = {https://inrepo02.dkfz.de/record/285421},
}