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@ARTICLE{Venkataramani:144849,
      author       = {V. Venkataramani and D. I. Tanev$^*$ and C. Strahle and A.
                      Studier-Fischer$^*$ and L. Fankhauser$^*$ and T. Kessler$^*$
                      and C. Körber and M. Kardorff and M. Ratliff$^*$ and R.
                      Xie$^*$ and H. Horstmann and M. Messer$^*$ and S. P. Paik
                      and J. Knabbe and F. Sahm$^*$ and F. T. Kurz and A. A.
                      Acikgöz$^*$ and F. Herrmannsdörfer and A. Agarwal and D.
                      E. Bergles and A. Chalmers and H. Miletic and S. Turcan and
                      C. Mawrin and D. Hänggi and H.-K. Liu$^*$ and W. Wick$^*$
                      and F. Winkler$^*$ and T. Kuner},
      title        = {{G}lutamatergic synaptic input to glioma cells drives brain
                      tumour progression.},
      journal      = {Nature},
      volume       = {573},
      number       = {7775},
      issn         = {1476-4687},
      address      = {London [u.a.]},
      publisher    = {Nature Publ. Group52462},
      reportid     = {DKFZ-2019-02273},
      pages        = {532-538},
      year         = {2019},
      note         = {DKFZ-ZMBH Alliance},
      abstract     = {A network of communicating tumour cells that is connected
                      by tumour microtubes mediates the progression of incurable
                      gliomas. Moreover, neuronal activity can foster malignant
                      behaviour of glioma cells by non-synaptic paracrine and
                      autocrine mechanisms. Here we report a direct communication
                      channel between neurons and glioma cells in different
                      disease models and human tumours: functional bona fide
                      chemical synapses between presynaptic neurons and
                      postsynaptic glioma cells. These neurogliomal synapses show
                      a typical synaptic ultrastructure, are located on tumour
                      microtubes, and produce postsynaptic currents that are
                      mediated by glutamate receptors of the AMPA subtype.
                      Neuronal activity including epileptic conditions generates
                      synchronised calcium transients in
                      tumour-microtube-connected glioma networks.
                      Glioma-cell-specific genetic perturbation of AMPA receptors
                      reduces calcium-related invasiveness of
                      tumour-microtube-positive tumour cells and glioma growth.
                      Invasion and growth are also reduced by anaesthesia and the
                      AMPA receptor antagonist perampanel, respectively. These
                      findings reveal a biologically relevant direct synaptic
                      communication between neurons and glioma cells with
                      potential clinical implications.},
      cin          = {B320 / B300 / A240 / L101},
      ddc          = {500},
      cid          = {I:(DE-He78)B320-20160331 / I:(DE-He78)B300-20160331 /
                      I:(DE-He78)A240-20160331 / I:(DE-He78)L101-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:31534219},
      doi          = {10.1038/s41586-019-1564-x},
      url          = {https://inrepo02.dkfz.de/record/144849},
}