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@ARTICLE{Steinert:128376,
      author       = {G. Steinert and S. Schölch and T. Niemietz and N. Iwata
                      and S. A. García and B. Behrens and A. Voigt and M.
                      Kloor$^*$ and A. Benner$^*$ and U. Bork and N. N. Rahbari
                      and M. W. Büchler and N. H. Stoecklein and J. Weitz and M.
                      Koch},
      title        = {{I}mmune escape and survival mechanisms in circulating
                      tumor cells of colorectal cancer.},
      journal      = {Cancer research},
      volume       = {74},
      number       = {6},
      issn         = {1538-7445},
      address      = {Philadelphia, Pa.},
      publisher    = {AACR},
      reportid     = {DKFZ-2017-04393},
      pages        = {1694 - 1704},
      year         = {2014},
      abstract     = {The prognosis of colorectal cancer is closely linked to the
                      occurrence of distant metastases. Systemic dissemination is
                      most likely caused by circulating tumor cells (CTC). Despite
                      the fundamental role of CTC within the metastatic cascade,
                      technical obstacles have so far prevented detailed genomic
                      and, in particular, phenotypic analyses of CTC, which may
                      provide molecular targets to delay or prevent distant
                      metastases. We show here a detailed genomic analysis of
                      single colorectal cancer-derived CTC by array comparative
                      genomic hybridization (aCGH), mutational profiling, and
                      microsatellite instability (MSI) analysis. Furthermore, we
                      report the first gene expression analysis of manually
                      selected colorectal cancer-derived CTC by quantitative
                      real-time PCR (qRT-PCR) to investigate transcriptional
                      changes, enabling CTC to survive in circulation and form
                      distant metastases. aCGH confirmed the tumor cell identity
                      of CellSearch-isolated colorectal cancer-derived CTC.
                      Mutational and MSI analyses revealed mutational profiles of
                      CTC to be similar, but not identical to the corresponding
                      tumor tissue. Several CTC exhibited mutations in key genes
                      such as KRAS or TP53 that could not be detected in the
                      tumor. Gene expression analyses revealed both a pronounced
                      upregulation of CD47 as a potential immune-escape mechanism
                      and a significant downregulation of several other pathways,
                      suggesting a dormant state of viable CTC. Our results
                      suggest mutational heterogeneity between tumor tissue and
                      CTC that should be considered in future trials on targeted
                      therapy and monitoring of response. The finding of
                      upregulated immune-escape pathways, which may be responsible
                      for survival of CTC in circulation, could provide a
                      promising target to disrupt the metastatic cascade in
                      colorectal cancer. Cancer Res; 74(6); 1694-704. ©2014
                      AACR.},
      cin          = {G105 / C060},
      ddc          = {610},
      cid          = {I:(DE-He78)G105-20160331 / I:(DE-He78)C060-20160331},
      pnm          = {313 - Cancer risk factors and prevention (POF3-313)},
      pid          = {G:(DE-HGF)POF3-313},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:24599131},
      doi          = {10.1158/0008-5472.CAN-13-1885},
      url          = {https://inrepo02.dkfz.de/record/128376},
}