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@ARTICLE{Stoy:127576,
      author       = {C. Stoy$^*$ and A. Sundaram$^*$ and M. Rios Garcia$^*$ and
                      X. Wang$^*$ and O. Seibert$^*$ and A. Zota and S. Wendler
                      and D. Männle and U. Hinz and C. Sticht and M. Muciek and
                      N. Gretz and A. J. Rose and V. Greiner$^*$ and T.
                      Hofmann$^*$ and A. Bauer$^*$ and J. Hoheisel$^*$ and M.
                      Berriel Diaz and M. M. Gaida and J. Werner and T. Schafmeier
                      and O. Strobel and S. Herzig$^*$},
      title        = {{T}ranscriptional co-factor {T}ransducin beta-like ({TBL})
                      1 acts as a checkpoint in pancreatic cancer malignancy.},
      journal      = {EMBO molecular medicine},
      volume       = {7},
      number       = {8},
      issn         = {1757-4684},
      address      = {Weinheim},
      publisher    = {Wiley-VCH},
      reportid     = {DKFZ-2017-03599},
      pages        = {1048 - 1062},
      year         = {2015},
      abstract     = {Pancreatic ductal adenocarcinoma (PDAC) is the fourth
                      leading cause of cancer fatalities in Western societies,
                      characterized by high metastatic potential and resistance to
                      chemotherapy. Critical molecular mechanisms of these
                      phenotypical features still remain unknown, thus hampering
                      the development of effective prognostic and therapeutic
                      measures in PDAC. Here, we show that transcriptional
                      co-factor Transducin beta-like (TBL) 1 was over-expressed in
                      both human and murine PDAC. Inactivation of TBL1 in human
                      and mouse pancreatic cancer cells reduced cellular
                      proliferation and invasiveness, correlating with diminished
                      glucose uptake, glycolytic flux, and oncogenic PI3 kinase
                      signaling which in turn could rescue TBL1
                      deficiency-dependent phenotypes. TBL1 deficiency both
                      prevented and reversed pancreatic tumor growth, mediated
                      transcriptional PI3 kinase inhibition, and increased
                      chemosensitivity of PDAC cells in vivo. As TBL1 mRNA levels
                      were also found to correlate with PI3 kinase levels and
                      overall survival in a cohort of human PDAC patients, TBL1
                      was identified as a checkpoint in the malignant behavior of
                      pancreatic cancer and its expression may serve as a novel
                      molecular target in the treatment of human PDAC.},
      keywords     = {TBL1X protein, human (NLM Chemicals) / Tbl1x protein, mouse
                      (NLM Chemicals) / Transducin (NLM Chemicals)},
      cin          = {A210 / B070 / A170},
      ddc          = {610},
      cid          = {I:(DE-He78)A210-20160331 / I:(DE-He78)B070-20160331 /
                      I:(DE-He78)A170-20160331},
      pnm          = {311 - Signalling pathways, cell and tumor biology
                      (POF3-311)},
      pid          = {G:(DE-HGF)POF3-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:26070712},
      pmc          = {pmc:PMC4551343},
      doi          = {10.15252/emmm.201404837},
      url          = {https://inrepo02.dkfz.de/record/127576},
}