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@ARTICLE{Baumann:154701,
      author       = {D. Baumann$^*$ and T. Hägele$^*$ and J. Mochayedi$^*$ and
                      J. Drebant$^*$ and C. Vent$^*$ and S. Blobner$^*$ and J. H.
                      Noll$^*$ and I. Nickel$^*$ and C. Schumacher$^*$ and S. L.
                      Boos$^*$ and A. S. Daniel$^*$ and S. Wendler$^*$ and M.
                      Volkmar$^*$ and O. Strobel and R. Offringa$^*$},
      title        = {{P}roimmunogenic impact of {MEK} inhibition synergizes with
                      agonist anti-{CD}40 immunostimulatory antibodies in tumor
                      therapy.},
      journal      = {Nature Communications},
      volume       = {11},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DKFZ-2020-00959},
      pages        = {2176},
      year         = {2020},
      note         = {#EA:D220#LA:D200#},
      abstract     = {Cancer types with lower mutational load and a
                      non-permissive tumor microenvironment are intrinsically
                      resistant to immune checkpoint blockade. While the
                      combination of cytostatic drugs and immunostimulatory
                      antibodies constitutes an attractive concept for overcoming
                      this refractoriness, suppression of immune cell function by
                      cytostatic drugs may limit therapeutic efficacy. Here we
                      show that targeted inhibition of mitogen-activated protein
                      kinase (MAPK) kinase (MEK) does not impair dendritic
                      cell-mediated T cell priming and activation. Accordingly,
                      combining MEK inhibitors (MEKi) with agonist antibodies
                      (Abs) targeting the immunostimulatory CD40 receptor results
                      in potent synergistic antitumor efficacy. Detailed analysis
                      of the mechanism of action of MEKi shows that this drug
                      exerts multiple pro-immunogenic effects, including the
                      suppression of M2-type macrophages, myeloid derived
                      suppressor cells and T-regulatory cells. The combination of
                      MEK inhibition with agonist anti-CD40 Ab is therefore a
                      promising therapeutic concept, especially for the treatment
                      of mutant Kras-driven tumors such as pancreatic ductal
                      adenocarcinoma.},
      cin          = {D200 / D220},
      ddc          = {500},
      cid          = {I:(DE-He78)D200-20160331 / I:(DE-He78)D220-20160331},
      pnm          = {314 - Tumor immunology (POF3-314)},
      pid          = {G:(DE-HGF)POF3-314},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:32358491},
      doi          = {10.1038/s41467-020-15979-2},
      url          = {https://inrepo02.dkfz.de/record/154701},
}