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@ARTICLE{Friedrich:155564,
      author       = {Friedrich, Mirco and Sankowski, Roman and Bunse, Lukas and
                      Kilian, Michael and Green, Edward and Ramallo Guevara,
                      Carina and Pusch, Stefan and Poschet, Gernot and Sanghvi,
                      Khwab and Hahn, Markus and Bunse, Theresa and Münch,
                      Philipp and Gegner, Hagen M. and Sonner, Jana K. and von
                      Landenberg, Anna and Cichon, Frederik and Aslan, Katrin and
                      Trobisch, Tim and Schirmer, Lucas and Abu-Sammour, Denis and
                      Kessler, Tobias and Ratliff, Miriam and Schrimpf, Daniel and
                      Sahm, Felix and Hopf, Carsten and Heiland, Dieter H. and
                      Schnell, Oliver and Beck, Jürgen and Böttcher, Chotima and
                      Fernandez-Zapata, Camila and Priller, Josef and Heiland,
                      Sabine and Gutcher, Ilona and Quintana, Francisco J. and von
                      Deimling, Andreas and Wick, Wolfgang and Prinz, Marco and
                      Platten, Michael},
      title        = {{T}ryptophan metabolism drives dynamic immunosuppressive
                      myeloid states in {IDH}-mutant gliomas},
      journal      = {Nature cancer},
      volume       = {2},
      number       = {7},
      issn         = {2662-1347},
      address      = {London},
      publisher    = {Nature Research},
      reportid     = {DZNE-2021-00742},
      pages        = {723 - 740},
      year         = {2021},
      abstract     = {The dynamics and phenotypes of intratumoral myeloid cells
                      during tumor progression are poorly understood. Here we
                      define myeloid cellular states in gliomas by longitudinal
                      single-cell profiling and demonstrate their strict control
                      by the tumor genotype: in isocitrate dehydrogenase
                      (IDH)-mutant tumors, differentiation of infiltrating myeloid
                      cells is blocked, resulting in an immature phenotype. In
                      late-stage gliomas, monocyte-derived macrophages drive
                      tolerogenic alignment of the microenvironment, thus
                      preventing T cell response. We define the IDH-dependent
                      tumor education of infiltrating macrophages to be causally
                      related to a complex re-orchestration of tryptophan
                      metabolism, resulting in activation of the aryl hydrocarbon
                      receptor. We further show that the altered metabolism of
                      IDH-mutant gliomas maintains this axis in bystander cells
                      and that pharmacological inhibition of tryptophan metabolism
                      can reverse immunosuppression. In conclusion, we provide
                      evidence of a glioma genotype-dependent intratumoral network
                      of resident and recruited myeloid cells and identify
                      tryptophan metabolism as a target for immunotherapy of
                      IDH-mutant tumors.},
      keywords     = {Brain Neoplasms: genetics / Glioma: genetics / Humans /
                      Immunotherapy / Isocitrate Dehydrogenase: genetics /
                      Tryptophan: therapeutic use / Tumor Microenvironment:
                      genetics / Tryptophan (NLM Chemicals) / Isocitrate
                      Dehydrogenase (NLM Chemicals)},
      cin          = {Clinical Study Team Berlin 1 ; AG Priller},
      ddc          = {610},
      cid          = {I:(DE-2719)5000007},
      pnm          = {353 - Clinical and Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:35121943},
      doi          = {10.1038/s43018-021-00201-z},
      url          = {https://pub.dzne.de/record/155564},
}