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@ARTICLE{Kandala:285438,
      author       = {S. Kandala$^*$ and M. Ramos$^*$ and L. Voith von
                      Voithenberg$^*$ and A. Diaz-Jimenez$^*$ and S. Chocarro$^*$
                      and S. J. E. Keding$^*$ and B. Brors$^*$ and C. D.
                      Imbusch$^*$ and R. Sotillo$^*$},
      title        = {{C}hronic chromosome instability induced by {P}lk1 results
                      in immune suppression in breast cancer.},
      journal      = {Cell reports},
      volume       = {42},
      number       = {12},
      issn         = {2211-1247},
      address      = {[New York, NY]},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2023-02372},
      pages        = {113266},
      year         = {2023},
      note         = {#EA:B220#EA:B330#LA:B220#},
      abstract     = {Chromosome instability (CIN) contributes to resistance to
                      therapies and tumor evolution. Although natural killer (NK)
                      cells can eliminate cells with complex karyotypes, high-CIN
                      human tumors have an immunosuppressive phenotype. To
                      understand which CIN-associated molecular features alter
                      immune recognition during tumor evolution, we overexpress
                      Polo-like kinase 1 (Plk1) in a Her2+ breast cancer model.
                      These high-CIN tumors activate a senescence-associated
                      secretory phenotype (SASP), upregulate PD-L1 and CD206, and
                      induce non-cell-autonomous nuclear factor κB (NF-κβ)
                      signaling, facilitating immune evasion. Single-cell RNA
                      sequencing from pre-neoplastic mammary glands unveiled the
                      presence of Arg1+ macrophages, NK cells with reduced
                      effector functions, and increased resting regulatory T cell
                      infiltration. We further show that high PLK1-expressing
                      human breast tumors display gene expression patterns
                      associated with SASP, NF-κβ signaling, and immune
                      suppression. These findings underscore the need to
                      understand the immune landscape in CIN tumors to identify
                      more effective therapies, potentially combining immune
                      checkpoint or NF-κβ inhibitors with current treatments.},
      keywords     = {CP: Cancer (Other) / CP: Cell biology (Other) / Her2(+)
                      breast cancer (Other) / NF-κβ signaling (Other) /
                      chromosomal instability (Other) / immune evasion (Other) /
                      senescence-associated secretory phenotype, SASP (Other) /
                      single-cell sequencing (Other)},
      cin          = {B220 / B330},
      ddc          = {610},
      cid          = {I:(DE-He78)B220-20160331 / I:(DE-He78)B330-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37979172},
      doi          = {10.1016/j.celrep.2023.113266},
      url          = {https://inrepo02.dkfz.de/record/285438},
}