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@ARTICLE{Sadik:157610,
      author       = {A. Sadik$^*$ and L. F. Somarribas Patterson$^*$ and S.
                      Öztürk$^*$ and S. R. Mohapatra$^*$ and V. Panitz$^*$ and
                      P. F. Secker$^*$ and P. Pfänder$^*$ and S. Loth and H.
                      Salem$^*$ and M. T. Prentzell$^*$ and B. Berdel$^*$ and M.
                      Iskar$^*$ and E. Faessler and F. Reuter$^*$ and I. Kirst$^*$
                      and V. Kalter$^*$ and K. I. Foerster and E. Jäger and C. R.
                      Guevara and M. Sobeh and T. Hielscher$^*$ and G. Poschet and
                      A. Reinhardt$^*$ and J. C. Hassel and M. Zapatka$^*$ and U.
                      Hahn and A. von Deimling$^*$ and C. Hopf and R. Schlichting
                      and B. I. Escher and J. Burhenne and W. E. Haefeli and N.
                      Ishaque and A. Böhme and S. Schäuble and K. Thedieck and
                      S. Trump and M. Seiffert$^*$ and C. Opitz$^*$},
      title        = {{IL}4{I}1 {I}s a {M}etabolic {I}mmune {C}heckpoint that
                      {A}ctivates the {AHR} and {P}romotes {T}umor {P}rogression.},
      journal      = {Cell},
      volume       = {182},
      number       = {5},
      issn         = {0092-8674},
      address      = {New York, NY},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2020-01707},
      pages        = {1252-1270.e34},
      year         = {2020},
      note         = {2020 Sep 3;182(5):1252-1270.e34#EA:B350#LA:B350#},
      abstract     = {Aryl hydrocarbon receptor (AHR) activation by tryptophan
                      (Trp) catabolites enhances tumor malignancy and suppresses
                      anti-tumor immunity. The context specificity of AHR target
                      genes has so far impeded systematic investigation of AHR
                      activity and its upstream enzymes across human cancers. A
                      pan-tissue AHR signature, derived by natural language
                      processing, revealed that across 32 tumor entities,
                      interleukin-4-induced-1 (IL4I1) associates more frequently
                      with AHR activity than IDO1 or TDO2, hitherto recognized as
                      the main Trp-catabolic enzymes. IL4I1 activates the AHR
                      through the generation of indole metabolites and kynurenic
                      acid. It associates with reduced survival in glioma
                      patients, promotes cancer cell motility, and suppresses
                      adaptive immunity, thereby enhancing the progression of
                      chronic lymphocytic leukemia (CLL) in mice. Immune
                      checkpoint blockade (ICB) induces IDO1 and IL4I1. As IDO1
                      inhibitors do not block IL4I1, IL4I1 may explain the failure
                      of clinical studies combining ICB with IDO1 inhibition.
                      Taken together, IL4I1 blockade opens new avenues for cancer
                      therapy.},
      cin          = {B350 / HD01 / B060 / C060 / B300},
      ddc          = {610},
      cid          = {I:(DE-He78)B350-20160331 / I:(DE-He78)HD01-20160331 /
                      I:(DE-He78)B060-20160331 / I:(DE-He78)C060-20160331 /
                      I:(DE-He78)B300-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:32818467},
      doi          = {10.1016/j.cell.2020.07.038},
      url          = {https://inrepo02.dkfz.de/record/157610},
}