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@ARTICLE{Yuan:124440,
      author       = {D. Yuan$^*$ and S. Huang$^*$ and E. Berger and L. Liu and
                      N. Gross and F. Heinzmann and M. Ringelhan and T. O.
                      Connor$^*$ and M. Stadler$^*$ and M. Meister$^*$ and J.
                      Weber and R. Öllinger and N. Simonavicius and F. Reisinger
                      and D. Hartmann and R. Meyer and M. Reich and M. Seehawer
                      and V. Leone and B. Höchst and D. Wohlleber and S. Jörs
                      and M. Prinz and D. Spalding and U. Protzer and T. Luedde
                      and L. Terracciano and M. Matter and T. Longerich and P.
                      Knolle and T. Ried and V. Keitel and F. Geisler and K. Unger
                      and E. Cinnamon and E. Pikarsky and N. Hüser and R. J.
                      Davis and D. F. Tschaharganeh$^*$ and R. Rad and A. Weber
                      and L. Zender$^*$ and D. Haller and M. Heikenwälder$^*$},
      title        = {{K}upffer {C}ell-{D}erived {T}nf {T}riggers
                      {C}holangiocellular {T}umorigenesis through {JNK} due to
                      {C}hronic {M}itochondrial {D}ysfunction and {ROS}.},
      journal      = {Cancer cell},
      volume       = {31},
      number       = {6},
      issn         = {1535-6108},
      address      = {Cambridge, Mass.},
      publisher    = {Cell Press},
      reportid     = {DKFZ-2017-01317},
      pages        = {771 - 789.e6},
      year         = {2017},
      abstract     = {Intrahepatic cholangiocarcinoma (ICC) is a highly
                      malignant, heterogeneous cancer with poor treatment options.
                      We found that mitochondrial dysfunction and oxidative stress
                      trigger a niche favoring cholangiocellular overgrowth and
                      tumorigenesis. Liver damage, reactive oxygen species (ROS)
                      and paracrine tumor necrosis factor (Tnf) from Kupffer cells
                      caused JNK-mediated cholangiocellular proliferation and
                      oncogenic transformation. Anti-oxidant treatment, Kupffer
                      cell depletion, Tnfr1 deletion, or JNK inhibition reduced
                      cholangiocellular pre-neoplastic lesions. Liver-specific
                      JNK1/2 deletion led to tumor reduction and enhanced survival
                      in Akt/Notch- or p53/Kras-induced ICC models. In human ICC,
                      high Tnf expression near ICC lesions, cholangiocellular
                      JNK-phosphorylation, and ROS accumulation in surrounding
                      hepatocytes are present. Thus, Kupffer cell-derived Tnf
                      favors cholangiocellular proliferation/differentiation and
                      carcinogenesis. Targeting the ROS/Tnf/JNK axis may provide
                      opportunities for ICC therapy.},
      cin          = {F180 / V076 / F190 / L801 / L701},
      ddc          = {610},
      cid          = {I:(DE-He78)F180-20160331 / I:(DE-He78)V076-20160331 /
                      I:(DE-He78)F190-20160331 / I:(DE-He78)L801-20160331 /
                      I:(DE-He78)L701-20160331},
      pnm          = {316 - Infections and cancer (POF3-316)},
      pid          = {G:(DE-HGF)POF3-316},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:28609656},
      doi          = {10.1016/j.ccell.2017.05.006},
      url          = {https://inrepo02.dkfz.de/record/124440},
}