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@ARTICLE{Goswami:148826,
      author       = {S. Goswami and T. Walle$^*$ and A. E. Cornish and S. Basu
                      and S. Anandhan and I. Fernandez and L. Vence and J. Blando
                      and H. Zhao and S. S. Yadav and M. Ott and L. Y. Kong and A.
                      B. Heimberger and J. de Groot and B. Sepesi and M. Overman
                      and S. Kopetz and J. P. Allison and D. Pe'er and P. Sharma},
      title        = {{I}mmune profiling of human tumors identifies {CD}73 as a
                      combinatorial target in glioblastoma.},
      journal      = {Nature medicine},
      volume       = {26},
      number       = {1},
      issn         = {1546-170X},
      address      = {New York, NY},
      publisher    = {Nature America Inc.},
      reportid     = {DKFZ-2020-00018},
      pages        = {39-46},
      year         = {2020},
      note         = {26 (1), 39-46Jan 2020 / #EA:E055#},
      abstract     = {Immune checkpoint therapy with anti-CTLA-4 and
                      anti-PD-1/PD-L1 has revolutionized the treatment of many
                      solid tumors. However, the clinical efficacy of immune
                      checkpoint therapy is limited to a subset of patients with
                      specific tumor types1,2. Multiple clinical trials with
                      combinatorial immune checkpoint strategies are ongoing;
                      however, the mechanistic rationale for tumor-specific
                      targeting of immune checkpoints is elusive. To garner an
                      insight into tumor-specific immunomodulatory targets, we
                      analyzed 94 patients representing five different cancer
                      types, including those that respond relatively well to
                      immune checkpoint therapy and those that do not, such as
                      glioblastoma multiforme, prostate cancer and colorectal
                      cancer. Through mass cytometry and single-cell RNA
                      sequencing, we identified a unique population of CD73hi
                      macrophages in glioblastoma multiforme that persists after
                      anti-PD-1 treatment. To test if targeting CD73 would be
                      important for a successful combination strategy in
                      glioblastoma multiforme, we performed reverse translational
                      studies using CD73-/- mice. We found that the absence of
                      CD73 improved survival in a murine model of glioblastoma
                      multiforme treated with anti-CTLA-4 and anti-PD-1. Our data
                      identified CD73 as a specific immunotherapeutic target to
                      improve antitumor immune responses to immune checkpoint
                      therapy in glioblastoma multiforme and demonstrate that
                      comprehensive human and reverse translational studies can be
                      used for rational design of combinatorial immune checkpoint
                      strategies.},
      cin          = {E055},
      ddc          = {610},
      cid          = {I:(DE-He78)E055-20160331},
      pnm          = {315 - Imaging and radiooncology (POF3-315)},
      pid          = {G:(DE-HGF)POF3-315},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:31873309},
      doi          = {10.1038/s41591-019-0694-x},
      url          = {https://inrepo02.dkfz.de/record/148826},
}