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@ARTICLE{Runge:128185,
      author       = {A. Runge$^*$ and J. Hu and M. Wieland$^*$ and J.-P.
                      Bergeest$^*$ and C. Mogler$^*$ and A. Neumann$^*$ and C.
                      Géraud and B. Arnold$^*$ and K. Rohr$^*$ and D.
                      Komljenovic$^*$ and P. Schirmacher$^*$ and S. Goerdt and H.
                      Augustin$^*$},
      title        = {{A}n inducible hepatocellular carcinoma model for
                      preclinical evaluation of antiangiogenic therapy in adult
                      mice.},
      journal      = {Cancer research},
      volume       = {74},
      number       = {15},
      issn         = {1538-7445},
      address      = {Philadelphia, Pa.},
      publisher    = {AACR},
      reportid     = {DKFZ-2017-04203},
      pages        = {4157 - 4169},
      year         = {2014},
      abstract     = {The limited availability of experimental tumor models that
                      faithfully mimic the progression of human tumors and their
                      response to therapy remains a major bottleneck to the
                      clinical translation and application of novel therapeutic
                      principles. To address this challenge in hepatocellular
                      carcinoma (HCC), one of the deadliest and most common
                      cancers in the world, we developed and validated an
                      inducible model of hepatocarcinogenesis in adult mice.
                      Tumorigenesis was triggered by intravenous adenoviral
                      delivery of Cre recombinase in transgenic mice expressing
                      the hepatocyte-specific albumin promoter, a loxP-flanked
                      stop cassette, and the SV40 large T-antigen (iAST). Cre
                      recombinase-mediated excision of the stop cassette led to a
                      transient viral hepatitis and resulted in multinodular
                      tumorigenesis within 5 to 8 weeks. Tumor nodules with
                      histologic characteristics of human HCC established a
                      functional vasculature by cooption, remodeling, and
                      angiogenic expansion of the preexisting sinusoidal liver
                      vasculature with increasing signs of vascular immaturity
                      during tumor progression. Treatment of mice with sorafenib
                      rapidly resulted in the induction of vascular regression,
                      inhibition of tumor growth, and enhanced overall survival.
                      Vascular regression was characterized by loss of endothelial
                      cells leaving behind avascular type IV collagen-positive
                      empty sleeves with remaining pericytes. Sorafenib treatment
                      led to transcriptional changes of Igf1, Id1, and cMet over
                      time, which may reflect the emergence of potential escape
                      mechanisms. Taken together, our results established the iAST
                      model of inducible hepatocarcinogenesis as a robust and
                      versatile preclinical model to study HCC progression and
                      validate novel therapies.},
      keywords     = {Angiogenesis Inhibitors (NLM Chemicals) / Phenylurea
                      Compounds (NLM Chemicals) / Niacinamide (NLM Chemicals) /
                      sorafenib (NLM Chemicals)},
      cin          = {A190 / D050 / B080 / E020 / L101},
      ddc          = {610},
      cid          = {I:(DE-He78)A190-20160331 / I:(DE-He78)D050-20160331 /
                      I:(DE-He78)B080-20160331 / I:(DE-He78)E020-20160331 /
                      I:(DE-He78)L101-20160331},
      pnm          = {311 - Signalling pathways, cell and tumor biology
                      (POF3-311)},
      pid          = {G:(DE-HGF)POF3-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:24906623},
      doi          = {10.1158/0008-5472.CAN-13-2311},
      url          = {https://inrepo02.dkfz.de/record/128185},
}