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@ARTICLE{Bunse:136849,
      author       = {L. Bunse$^*$ and S. Pusch$^*$ and T. Bunse$^*$ and F.
                      Sahm$^*$ and K. Sanghvi$^*$ and M. Friedrich$^*$ and D.
                      Alansary and J. Sonner$^*$ and E. Green$^*$ and K.
                      Deumelandt$^*$ and M. Kilian$^*$ and C. Neftel and S. Uhlig
                      and T. Kessler$^*$ and A. von Landenberg$^*$ and A. S.
                      Berghoff$^*$ and K. Marsh and M. Steadman and D. Zhu and B.
                      Nicolay and B. Wiestler and M. Breckwoldt$^*$ and R. Al-Ali
                      and S. Karcher-Bausch$^*$ and M. Bozza$^*$ and I. Oezen$^*$
                      and M. Kramer$^*$ and J. Meyer$^*$ and A. Habel$^*$ and J.
                      Eisel$^*$ and G. Poschet and M. Weller and M. Preusser and
                      M. Nadji-Ohl and N. Thon and M. C. Burger$^*$ and P.
                      Harter$^*$ and M. Ratliff$^*$ and R. Harbottle$^*$ and A.
                      Benner$^*$ and D. Schrimpf$^*$ and J. Okun and C.
                      Herold-Mende and S. Turcan and S. Kaulfuss and H.
                      Hess-Stumpp and K. Bieback and D. P. Cahill and K. H.
                      Plate$^*$ and D. Hänggi and M. Dorsch and M. L. Suvà and
                      B. A. Niemeyer and A. von Deimling$^*$ and W. Wick$^*$ and
                      M. Platten$^*$},
      title        = {{S}uppression of antitumor {T} cell immunity by the
                      oncometabolite ({R})-2-hydroxyglutarate.},
      journal      = {Nature medicine},
      volume       = {24},
      number       = {8},
      issn         = {1546-170X},
      address      = {New York, NY},
      publisher    = {Nature America Inc.},
      reportid     = {DKFZ-2018-01287},
      pages        = {1192 - 1203},
      year         = {2018},
      abstract     = {The oncometabolite (R)-2-hydroxyglutarate (R-2-HG) produced
                      by isocitrate dehydrogenase (IDH) mutations promotes
                      gliomagenesis via DNA and histone methylation. Here, we
                      identify an additional activity of R-2-HG: tumor
                      cell-derived R-2-HG is taken up by T cells where it induces
                      a perturbation of nuclear factor of activated T cells
                      transcriptional activity and polyamine biosynthesis,
                      resulting in suppression of T cell activity. IDH1-mutant
                      gliomas display reduced T cell abundance and altered calcium
                      signaling. Antitumor immunity to experimental syngeneic
                      IDH1-mutant tumors induced by IDH1-specific vaccine or
                      checkpoint inhibition is improved by inhibition of the
                      neomorphic enzymatic function of mutant IDH1. These data
                      attribute a novel, non-tumor cell-autonomous role to an
                      oncometabolite in shaping the tumor immune
                      microenvironment.},
      cin          = {G160 / L101 / G380 / F160 / L501 / C060},
      ddc          = {610},
      cid          = {I:(DE-He78)G160-20160331 / I:(DE-He78)L101-20160331 /
                      I:(DE-He78)G380-20160331 / I:(DE-He78)F160-20160331 /
                      I:(DE-He78)L501-20160331 / I:(DE-He78)C060-20160331},
      pnm          = {317 - Translational cancer research (POF3-317)},
      pid          = {G:(DE-HGF)POF3-317},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:29988124},
      doi          = {10.1038/s41591-018-0095-6},
      url          = {https://inrepo02.dkfz.de/record/136849},
}