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@ARTICLE{Vornholz:274320,
      author       = {L. Vornholz and S. E. Isay and Z. Kurgyis and D. C. Strobl
                      and P. Loll and M. H. Mosa and M. D. Luecken and M. Sterr
                      and H. Lickert and C. Winter$^*$ and F. R. Greten$^*$ and H.
                      Farin$^*$ and F. J. Theis and J. Ruland$^*$},
      title        = {{S}ynthetic enforcement of {STING} signaling in cancer
                      cells appropriates the immune microenvironment for
                      checkpoint inhibitor therapy.},
      journal      = {Science advances},
      volume       = {9},
      number       = {11},
      issn         = {2375-2548},
      address      = {Washington, DC [u.a.]},
      publisher    = {Assoc.},
      reportid     = {DKFZ-2023-00534},
      pages        = {eadd8564},
      year         = {2023},
      abstract     = {Immune checkpoint inhibitors (ICIs) enhance anticancer
                      immunity by releasing repressive signals into tumor
                      microenvironments (TMEs). To be effective, ICIs require
                      preexisting immunologically 'hot' niches for tumor antigen
                      presentation and lymphocyte recruitment. How the mutational
                      landscape of cancer cells shapes these immunological niches
                      remains poorly defined. We found in human and murine
                      colorectal cancer (CRC) models that the superior antitumor
                      immune response of mismatch repair (MMR)-deficient CRC
                      required tumor cell-intrinsic activation of cGAS-STING
                      signaling triggered by genomic instability. Subsequently, we
                      synthetically enforced STING signaling in CRC cells with
                      intact MMR signaling using constitutively active STING
                      variants. Even in MMR-proficient CRC, genetically encoded
                      gain-of-function STING was sufficient to induce cancer
                      cell-intrinsic interferon signaling, local activation of
                      antigen-presenting cells, recruitment of effector
                      lymphocytes, and sensitization of previously 'cold' TMEs to
                      ICI therapy in vivo. Thus, our results introduce a rational
                      strategy for modulating cancer cell-intrinsic programs via
                      engineered STING enforcement to sensitize resistant tumors
                      to ICI responsiveness.},
      cin          = {MU01 / FM01},
      ddc          = {500},
      cid          = {I:(DE-He78)MU01-20160331 / I:(DE-He78)FM01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36921054},
      doi          = {10.1126/sciadv.add8564},
      url          = {https://inrepo02.dkfz.de/record/274320},
}