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@ARTICLE{Pajtler:120072,
      author       = {K. Pajtler$^*$ and E. Mahlow and A. Odersky and S. Lindner
                      and H. Stephan and I. Bendix and A. Eggert and A. Schramm
                      and J. Schulte$^*$},
      title        = {{N}euroblastoma in dialog with its stroma: {NTRK}1 is a
                      regulator of cellular cross-talk with {S}chwann cells.},
      journal      = {OncoTarget},
      volume       = {5},
      number       = {22},
      issn         = {1949-2553},
      address      = {[S.l.]},
      publisher    = {Impact Journals LLC},
      reportid     = {DKFZ-2017-00659},
      pages        = {11180 - 11192},
      year         = {2014},
      abstract     = {In neuroblastoma, the most common solid tumor of childhood,
                      excellent prognosis is associated with extensive Schwann
                      cell (SC) content and high-level expression of the
                      neurotrophin receptor, NTRK1/TrkA, which is known to mediate
                      neuroblastoma cell differentiation. We hypothesized that
                      both stromal composition and neuroblastic differentiation
                      are based on bidirectional neuroblastoma-SC interaction.
                      Reanalysis of microarray data from human SY5Y neuroblastoma
                      cells stably transfected with either NTRK1 or NTRK2 revealed
                      upregulation of the mRNA for the SC growth factor, NRG1, in
                      NTRK1-positive cells. Media conditioned by NTRK1-expressing
                      neuroblastoma cells induced SC proliferation and migration,
                      while antibody-based NRG1 neutralization significantly
                      decreased these effects. Vice versa, NRG1-stimulated SC
                      secreted the NTRK1-specific ligand, NGF. SC-conditioned
                      medium activated the NTRK1 receptor in a neuroblastoma cell
                      culture model conditionally expressing NTRK1 and induced
                      differentiation markers in NTRK1-expressing cells. NTRK1
                      induction in neuroblastoma xenografts mixed with primary SC
                      also significantly reduced tumor growth in vivo. We propose
                      a model for NTRK1-mediated and NRG1-dependent attraction of
                      adjacent SC, which in turn induce neuroblastic
                      differentiation by secretion of the NTRK1-specific ligand,
                      NGF. These findings have implications for understanding the
                      mature and less malignant neuroblastoma phenotype associated
                      with NTRK1 expression, and could assist the development of
                      new therapeutic strategies for neuroblastoma
                      differentiation.},
      keywords     = {Membrane Glycoproteins (NLM Chemicals) / Protein-Tyrosine
                      Kinases (NLM Chemicals) / tropomyosin-related kinase-B,
                      human (NLM Chemicals)},
      cin          = {B062 / L401},
      ddc          = {610},
      cid          = {I:(DE-He78)B062-20160331 / I:(DE-He78)L401-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:25361003},
      pmc          = {pmc:PMC4294349},
      doi          = {10.18632/oncotarget.2611},
      url          = {https://inrepo02.dkfz.de/record/120072},
}