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@ARTICLE{DiTacchio:148865,
      author       = {M. Di Tacchio$^*$ and J. Macas and J. Weissenberger and K.
                      Sommer and O. Bähr$^*$ and J. P. Steinbach$^*$ and C.
                      Senft$^*$ and V. Seifert$^*$ and M. Glas$^*$ and U.
                      Herrlinger and D. Krex$^*$ and M. Meinhardt and A.
                      Weyerbrock and M. Timmer and R. Goldbrunner and M. Deckert
                      and A. H. Scheel and R. Büttner and O. M. Grauer and J.
                      Schittenhelm and G. Tabatabai$^*$ and P. Harter$^*$ and S.
                      Günther and K. Devraj and K. H. Plate$^*$ and Y. Reiss$^*$},
      title        = {{T}umor {V}essel {N}ormalization, {I}mmunostimulatory
                      {R}eprogramming, and {I}mproved {S}urvival in {G}lioblastoma
                      with {C}ombined {I}nhibition of {PD}-1, {A}ngiopoietin-2,
                      and {VEGF}.},
      journal      = {Cancer immunology research},
      volume       = {7},
      number       = {12},
      issn         = {2326-6074},
      address      = {Philadelphia, Pa.},
      publisher    = {AACR},
      reportid     = {DKFZ-2020-00057},
      pages        = {1910 - 1927},
      year         = {2019},
      abstract     = {Glioblastoma (GBM) is a non-T-cell-inflamed cancer
                      characterized by an immunosuppressive microenvironment that
                      impedes dendritic cell maturation and T-cell cytotoxicity.
                      Proangiogenic cytokines such as VEGF and angiopoietin-2
                      (Ang-2) have high expression in glioblastoma in a
                      cell-specific manner and not only drive tumor angiogenesis
                      and vascular permeability but also negatively regulate
                      T-lymphocyte and innate immune cell responses. Consequently,
                      the alleviation of immunosuppression might be a prerequisite
                      for successful immune checkpoint therapy in GBM. We here
                      combined antiangiogenic and immune checkpoint therapy and
                      demonstrated improved therapeutic efficacy in syngeneic,
                      orthotopic GBM models. We observed that blockade of VEGF,
                      Ang-2, and programmed cell death protein-1 (PD-1)
                      significantly extended survival compared with vascular
                      targeting alone. In the GBM microenvironment, triple therapy
                      increased the numbers of CTLs, which inversely correlated
                      with myeloid-derived suppressor cells and regulatory T
                      cells. Transcriptome analysis of GBM microvessels indicated
                      a global vascular normalization that was highest after
                      triple therapy. Our results propose a rationale to overcome
                      tumor immunosuppression and the current limitations of VEGF
                      monotherapy by integrating the synergistic effects of
                      VEGF/Ang-2 and PD-1 blockade to reinforce antitumor immunity
                      through a normalized vasculature.},
      cin          = {L501 / L401 / L301 / L801},
      ddc          = {610},
      cid          = {I:(DE-He78)L501-20160331 / I:(DE-He78)L401-20160331 /
                      I:(DE-He78)L301-20160331 / I:(DE-He78)L801-20160331},
      pnm          = {899 - ohne Topic (POF3-899)},
      pid          = {G:(DE-HGF)POF3-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:31597643},
      doi          = {10.1158/2326-6066.CIR-18-0865},
      url          = {https://inrepo02.dkfz.de/record/148865},
}