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@ARTICLE{Seehawer:137637,
      author       = {M. Seehawer and F. Heinzmann and L. D'Artista and J. Harbig
                      and P.-F. Roux and L. Hoenicke and H. Dang and S. Klotz and
                      L. Robinson and G. Doré and N. Rozenblum and T.-W. Kang and
                      R. Chawla and T. Buch and M. Vucur and M. Roth and J. Zuber
                      and T. Luedde and B. Sipos and T. Longerich and M.
                      Heikenwälder$^*$ and X. W. Wang and O. Bischof and L.
                      Zender$^*$},
      title        = {{N}ecroptosis microenvironment directs lineage commitment
                      in liver cancer.},
      journal      = {Nature},
      volume       = {562},
      number       = {7725},
      issn         = {1476-4687},
      address      = {London [u.a.]},
      publisher    = {Nature Publ. Group},
      reportid     = {DKFZ-2018-01517},
      pages        = {69-75},
      year         = {2018},
      abstract     = {Primary liver cancer represents a major health problem. It
                      comprises hepatocellular carcinoma (HCC) and intrahepatic
                      cholangiocarcinoma (ICC), which differ markedly with regards
                      to their morphology, metastatic potential and responses to
                      therapy. However, the regulatory molecules and tissue
                      context that commit transformed hepatic cells towards HCC or
                      ICC are largely unknown. Here we show that the hepatic
                      microenvironment epigenetically shapes lineage commitment in
                      mosaic mouse models of liver tumorigenesis. Whereas a
                      necroptosis-associated hepatic cytokine microenvironment
                      determines ICC outgrowth from oncogenically transformed
                      hepatocytes, hepatocytes containing identical oncogenic
                      drivers give rise to HCC if they are surrounded by apoptotic
                      hepatocytes. Epigenome and transcriptome profiling of mouse
                      HCC and ICC singled out Tbx3 and Prdm5 as major
                      microenvironment-dependent and epigenetically regulated
                      lineage-commitment factors, a function that is conserved in
                      humans. Together, our results provide insight into lineage
                      commitment in liver tumorigenesis, and explain molecularly
                      why common liver-damaging risk factors can lead to either
                      HCC or ICC.},
      cin          = {F180 / V076 / L801},
      ddc          = {500},
      cid          = {I:(DE-He78)F180-20160331 / I:(DE-He78)V076-20160331 /
                      I:(DE-He78)L801-20160331},
      pnm          = {316 - Infections and cancer (POF3-316)},
      pid          = {G:(DE-HGF)POF3-316},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30209397},
      doi          = {10.1038/s41586-018-0519-y},
      url          = {https://inrepo02.dkfz.de/record/137637},
}