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TMIC-27. GLUTAMATERGIC NEURON-GLIOMA SYNAPSES DRIVE BRAIN TUMOUR PROGRESSION
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| Zeitschriftentitel: | Neuro-Oncology |
|---|---|
| Personen und Körperschaften: | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| In: | Neuro-Oncology, 21, 2019, Supplement_6, S. vi253-vi253 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Oxford University Press (OUP)
|
| Schlagwörter: |
| author_facet |
Venkataramani, Varun Tanev, Dimitar Strahle, Christopher Studier-Fischer, Alexander Fankhauser, Laura Kessler, Tobias Losada Perez, Maria Körber, Christoph Kardorff, Markus Ratliff, Miriam Xie, Ruifan Horstmann, Heinz Messer, Mirko Paik, Sang Knabbe, Johannes Sahm, Felix Kurz, Felix Acikgoez, Azer Herrrmannsdörfer, Frank Agarwal, Amit Bergles, Dwight Chalmers, Anthony Miletic, Hrvoje Turcan, Sevin Mawrin, Christian Hänggi, Daniel Liu, Hai-Kun Casas Tinto, Sergio Wick, Wolfgang Winkler, Frank Kuner, Thomas Venkataramani, Varun Tanev, Dimitar Strahle, Christopher Studier-Fischer, Alexander Fankhauser, Laura Kessler, Tobias Losada Perez, Maria Körber, Christoph Kardorff, Markus Ratliff, Miriam Xie, Ruifan Horstmann, Heinz Messer, Mirko Paik, Sang Knabbe, Johannes Sahm, Felix Kurz, Felix Acikgoez, Azer Herrrmannsdörfer, Frank Agarwal, Amit Bergles, Dwight Chalmers, Anthony Miletic, Hrvoje Turcan, Sevin Mawrin, Christian Hänggi, Daniel Liu, Hai-Kun Casas Tinto, Sergio Wick, Wolfgang Winkler, Frank Kuner, Thomas |
|---|---|
| author |
Venkataramani, Varun Tanev, Dimitar Strahle, Christopher Studier-Fischer, Alexander Fankhauser, Laura Kessler, Tobias Losada Perez, Maria Körber, Christoph Kardorff, Markus Ratliff, Miriam Xie, Ruifan Horstmann, Heinz Messer, Mirko Paik, Sang Knabbe, Johannes Sahm, Felix Kurz, Felix Acikgoez, Azer Herrrmannsdörfer, Frank Agarwal, Amit Bergles, Dwight Chalmers, Anthony Miletic, Hrvoje Turcan, Sevin Mawrin, Christian Hänggi, Daniel Liu, Hai-Kun Casas Tinto, Sergio Wick, Wolfgang Winkler, Frank Kuner, Thomas |
| spellingShingle |
Venkataramani, Varun Tanev, Dimitar Strahle, Christopher Studier-Fischer, Alexander Fankhauser, Laura Kessler, Tobias Losada Perez, Maria Körber, Christoph Kardorff, Markus Ratliff, Miriam Xie, Ruifan Horstmann, Heinz Messer, Mirko Paik, Sang Knabbe, Johannes Sahm, Felix Kurz, Felix Acikgoez, Azer Herrrmannsdörfer, Frank Agarwal, Amit Bergles, Dwight Chalmers, Anthony Miletic, Hrvoje Turcan, Sevin Mawrin, Christian Hänggi, Daniel Liu, Hai-Kun Casas Tinto, Sergio Wick, Wolfgang Winkler, Frank Kuner, Thomas Neuro-Oncology TMIC-27. GLUTAMATERGIC NEURON-GLIOMA SYNAPSES DRIVE BRAIN TUMOUR PROGRESSION Cancer Research Neurology (clinical) Oncology |
| author_sort |
venkataramani, varun |
| spelling |
Venkataramani, Varun Tanev, Dimitar Strahle, Christopher Studier-Fischer, Alexander Fankhauser, Laura Kessler, Tobias Losada Perez, Maria Körber, Christoph Kardorff, Markus Ratliff, Miriam Xie, Ruifan Horstmann, Heinz Messer, Mirko Paik, Sang Knabbe, Johannes Sahm, Felix Kurz, Felix Acikgoez, Azer Herrrmannsdörfer, Frank Agarwal, Amit Bergles, Dwight Chalmers, Anthony Miletic, Hrvoje Turcan, Sevin Mawrin, Christian Hänggi, Daniel Liu, Hai-Kun Casas Tinto, Sergio Wick, Wolfgang Winkler, Frank Kuner, Thomas 1522-8517 1523-5866 Oxford University Press (OUP) Cancer Research Neurology (clinical) Oncology http://dx.doi.org/10.1093/neuonc/noz175.1061 <jats:title>Abstract</jats:title> <jats:p>A network of communicating tumour cells established by tumour microtubes (TMs) is supposed to mediate relevant aspects of progression and resistance of incurable gliomas. Moreover, neuronal activity has been shown to foster malignant behavior of glioma cells by non-synaptic paracrine and autocrine mechanisms. Here, we report an unexpected direct communication channel between neurons and glioma cells in multiple disease models as well as in astrocytomas and glioblastomas (GBs) of adult patients: functional bona fide chemical synapses formed between presynaptic neurons and postsynaptic glioma cells. These neurogliomal synapses (NGS) show a typical synaptic ultrastructure, are located on TM networks, and produce depolarizing postsynaptic currents mediated by glutamate receptors of the AMPA subtype. AMPA-type glutamate receptors (AMPAR) are expressed by a molecularly and morphologically distinct subpopulation of network-integrated glioma cells. Increased neuronal activity under epileptic conditions ex vivo or neuronal optogenetic stimulation in vivo enhanced, while general anesthesia diminished synchronized calcium transients in TM-connected glioma networks. Accordingly, anesthesia reduced invasiveness of TM-positive tumour cells in mice. Genetic perturbation of AMPAR or chronic AMPAR inhibition by perampanel decreased glioma invasion and proliferation in mice and deletion of GluRII in Drosophila glioma increased survival. These findings reveal a hitherto unappreciated direct synaptic communication between neurons and glioma cells that appears relevant for brain tumour biology, implying new avenues for glioma treatment.</jats:p> TMIC-27. GLUTAMATERGIC NEURON-GLIOMA SYNAPSES DRIVE BRAIN TUMOUR PROGRESSION Neuro-Oncology |
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| title |
TMIC-27. GLUTAMATERGIC NEURON-GLIOMA SYNAPSES DRIVE BRAIN TUMOUR PROGRESSION |
| title_unstemmed |
TMIC-27. GLUTAMATERGIC NEURON-GLIOMA SYNAPSES DRIVE BRAIN TUMOUR PROGRESSION |
| title_full |
TMIC-27. GLUTAMATERGIC NEURON-GLIOMA SYNAPSES DRIVE BRAIN TUMOUR PROGRESSION |
| title_fullStr |
TMIC-27. GLUTAMATERGIC NEURON-GLIOMA SYNAPSES DRIVE BRAIN TUMOUR PROGRESSION |
| title_full_unstemmed |
TMIC-27. GLUTAMATERGIC NEURON-GLIOMA SYNAPSES DRIVE BRAIN TUMOUR PROGRESSION |
| title_short |
TMIC-27. GLUTAMATERGIC NEURON-GLIOMA SYNAPSES DRIVE BRAIN TUMOUR PROGRESSION |
| title_sort |
tmic-27. glutamatergic neuron-glioma synapses drive brain tumour progression |
| topic |
Cancer Research Neurology (clinical) Oncology |
| url |
http://dx.doi.org/10.1093/neuonc/noz175.1061 |
| publishDate |
2019 |
| physical |
vi253-vi253 |
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<jats:title>Abstract</jats:title>
<jats:p>A network of communicating tumour cells established by tumour microtubes (TMs) is supposed to mediate relevant aspects of progression and resistance of incurable gliomas. Moreover, neuronal activity has been shown to foster malignant behavior of glioma cells by non-synaptic paracrine and autocrine mechanisms. Here, we report an unexpected direct communication channel between neurons and glioma cells in multiple disease models as well as in astrocytomas and glioblastomas (GBs) of adult patients: functional bona fide chemical synapses formed between presynaptic neurons and postsynaptic glioma cells. These neurogliomal synapses (NGS) show a typical synaptic ultrastructure, are located on TM networks, and produce depolarizing postsynaptic currents mediated by glutamate receptors of the AMPA subtype. AMPA-type glutamate receptors (AMPAR) are expressed by a molecularly and morphologically distinct subpopulation of network-integrated glioma cells. Increased neuronal activity under epileptic conditions ex vivo or neuronal optogenetic stimulation in vivo enhanced, while general anesthesia diminished synchronized calcium transients in TM-connected glioma networks. Accordingly, anesthesia reduced invasiveness of TM-positive tumour cells in mice. Genetic perturbation of AMPAR or chronic AMPAR inhibition by perampanel decreased glioma invasion and proliferation in mice and deletion of GluRII in Drosophila glioma increased survival. These findings reveal a hitherto unappreciated direct synaptic communication between neurons and glioma cells that appears relevant for brain tumour biology, implying new avenues for glioma treatment.</jats:p> |
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| author | Venkataramani, Varun, Tanev, Dimitar, Strahle, Christopher, Studier-Fischer, Alexander, Fankhauser, Laura, Kessler, Tobias, Losada Perez, Maria, Körber, Christoph, Kardorff, Markus, Ratliff, Miriam, Xie, Ruifan, Horstmann, Heinz, Messer, Mirko, Paik, Sang, Knabbe, Johannes, Sahm, Felix, Kurz, Felix, Acikgoez, Azer, Herrrmannsdörfer, Frank, Agarwal, Amit, Bergles, Dwight, Chalmers, Anthony, Miletic, Hrvoje, Turcan, Sevin, Mawrin, Christian, Hänggi, Daniel, Liu, Hai-Kun, Casas Tinto, Sergio, Wick, Wolfgang, Winkler, Frank, Kuner, Thomas |
| author_facet | Venkataramani, Varun, Tanev, Dimitar, Strahle, Christopher, Studier-Fischer, Alexander, Fankhauser, Laura, Kessler, Tobias, Losada Perez, Maria, Körber, Christoph, Kardorff, Markus, Ratliff, Miriam, Xie, Ruifan, Horstmann, Heinz, Messer, Mirko, Paik, Sang, Knabbe, Johannes, Sahm, Felix, Kurz, Felix, Acikgoez, Azer, Herrrmannsdörfer, Frank, Agarwal, Amit, Bergles, Dwight, Chalmers, Anthony, Miletic, Hrvoje, Turcan, Sevin, Mawrin, Christian, Hänggi, Daniel, Liu, Hai-Kun, Casas Tinto, Sergio, Wick, Wolfgang, Winkler, Frank, Kuner, Thomas, Venkataramani, Varun, Tanev, Dimitar, Strahle, Christopher, Studier-Fischer, Alexander, Fankhauser, Laura, Kessler, Tobias, Losada Perez, Maria, Körber, Christoph, Kardorff, Markus, Ratliff, Miriam, Xie, Ruifan, Horstmann, Heinz, Messer, Mirko, Paik, Sang, Knabbe, Johannes, Sahm, Felix, Kurz, Felix, Acikgoez, Azer, Herrrmannsdörfer, Frank, Agarwal, Amit, Bergles, Dwight, Chalmers, Anthony, Miletic, Hrvoje, Turcan, Sevin, Mawrin, Christian, Hänggi, Daniel, Liu, Hai-Kun, Casas Tinto, Sergio, Wick, Wolfgang, Winkler, Frank, Kuner, Thomas |
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| description | <jats:title>Abstract</jats:title> <jats:p>A network of communicating tumour cells established by tumour microtubes (TMs) is supposed to mediate relevant aspects of progression and resistance of incurable gliomas. Moreover, neuronal activity has been shown to foster malignant behavior of glioma cells by non-synaptic paracrine and autocrine mechanisms. Here, we report an unexpected direct communication channel between neurons and glioma cells in multiple disease models as well as in astrocytomas and glioblastomas (GBs) of adult patients: functional bona fide chemical synapses formed between presynaptic neurons and postsynaptic glioma cells. These neurogliomal synapses (NGS) show a typical synaptic ultrastructure, are located on TM networks, and produce depolarizing postsynaptic currents mediated by glutamate receptors of the AMPA subtype. AMPA-type glutamate receptors (AMPAR) are expressed by a molecularly and morphologically distinct subpopulation of network-integrated glioma cells. Increased neuronal activity under epileptic conditions ex vivo or neuronal optogenetic stimulation in vivo enhanced, while general anesthesia diminished synchronized calcium transients in TM-connected glioma networks. Accordingly, anesthesia reduced invasiveness of TM-positive tumour cells in mice. Genetic perturbation of AMPAR or chronic AMPAR inhibition by perampanel decreased glioma invasion and proliferation in mice and deletion of GluRII in Drosophila glioma increased survival. These findings reveal a hitherto unappreciated direct synaptic communication between neurons and glioma cells that appears relevant for brain tumour biology, implying new avenues for glioma treatment.</jats:p> |
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| spelling | Venkataramani, Varun Tanev, Dimitar Strahle, Christopher Studier-Fischer, Alexander Fankhauser, Laura Kessler, Tobias Losada Perez, Maria Körber, Christoph Kardorff, Markus Ratliff, Miriam Xie, Ruifan Horstmann, Heinz Messer, Mirko Paik, Sang Knabbe, Johannes Sahm, Felix Kurz, Felix Acikgoez, Azer Herrrmannsdörfer, Frank Agarwal, Amit Bergles, Dwight Chalmers, Anthony Miletic, Hrvoje Turcan, Sevin Mawrin, Christian Hänggi, Daniel Liu, Hai-Kun Casas Tinto, Sergio Wick, Wolfgang Winkler, Frank Kuner, Thomas 1522-8517 1523-5866 Oxford University Press (OUP) Cancer Research Neurology (clinical) Oncology http://dx.doi.org/10.1093/neuonc/noz175.1061 <jats:title>Abstract</jats:title> <jats:p>A network of communicating tumour cells established by tumour microtubes (TMs) is supposed to mediate relevant aspects of progression and resistance of incurable gliomas. Moreover, neuronal activity has been shown to foster malignant behavior of glioma cells by non-synaptic paracrine and autocrine mechanisms. Here, we report an unexpected direct communication channel between neurons and glioma cells in multiple disease models as well as in astrocytomas and glioblastomas (GBs) of adult patients: functional bona fide chemical synapses formed between presynaptic neurons and postsynaptic glioma cells. These neurogliomal synapses (NGS) show a typical synaptic ultrastructure, are located on TM networks, and produce depolarizing postsynaptic currents mediated by glutamate receptors of the AMPA subtype. AMPA-type glutamate receptors (AMPAR) are expressed by a molecularly and morphologically distinct subpopulation of network-integrated glioma cells. Increased neuronal activity under epileptic conditions ex vivo or neuronal optogenetic stimulation in vivo enhanced, while general anesthesia diminished synchronized calcium transients in TM-connected glioma networks. Accordingly, anesthesia reduced invasiveness of TM-positive tumour cells in mice. Genetic perturbation of AMPAR or chronic AMPAR inhibition by perampanel decreased glioma invasion and proliferation in mice and deletion of GluRII in Drosophila glioma increased survival. These findings reveal a hitherto unappreciated direct synaptic communication between neurons and glioma cells that appears relevant for brain tumour biology, implying new avenues for glioma treatment.</jats:p> TMIC-27. GLUTAMATERGIC NEURON-GLIOMA SYNAPSES DRIVE BRAIN TUMOUR PROGRESSION Neuro-Oncology |
| spellingShingle | Venkataramani, Varun, Tanev, Dimitar, Strahle, Christopher, Studier-Fischer, Alexander, Fankhauser, Laura, Kessler, Tobias, Losada Perez, Maria, Körber, Christoph, Kardorff, Markus, Ratliff, Miriam, Xie, Ruifan, Horstmann, Heinz, Messer, Mirko, Paik, Sang, Knabbe, Johannes, Sahm, Felix, Kurz, Felix, Acikgoez, Azer, Herrrmannsdörfer, Frank, Agarwal, Amit, Bergles, Dwight, Chalmers, Anthony, Miletic, Hrvoje, Turcan, Sevin, Mawrin, Christian, Hänggi, Daniel, Liu, Hai-Kun, Casas Tinto, Sergio, Wick, Wolfgang, Winkler, Frank, Kuner, Thomas, Neuro-Oncology, TMIC-27. GLUTAMATERGIC NEURON-GLIOMA SYNAPSES DRIVE BRAIN TUMOUR PROGRESSION, Cancer Research, Neurology (clinical), Oncology |
| title | TMIC-27. GLUTAMATERGIC NEURON-GLIOMA SYNAPSES DRIVE BRAIN TUMOUR PROGRESSION |
| title_full | TMIC-27. GLUTAMATERGIC NEURON-GLIOMA SYNAPSES DRIVE BRAIN TUMOUR PROGRESSION |
| title_fullStr | TMIC-27. GLUTAMATERGIC NEURON-GLIOMA SYNAPSES DRIVE BRAIN TUMOUR PROGRESSION |
| title_full_unstemmed | TMIC-27. GLUTAMATERGIC NEURON-GLIOMA SYNAPSES DRIVE BRAIN TUMOUR PROGRESSION |
| title_short | TMIC-27. GLUTAMATERGIC NEURON-GLIOMA SYNAPSES DRIVE BRAIN TUMOUR PROGRESSION |
| title_sort | tmic-27. glutamatergic neuron-glioma synapses drive brain tumour progression |
| title_unstemmed | TMIC-27. GLUTAMATERGIC NEURON-GLIOMA SYNAPSES DRIVE BRAIN TUMOUR PROGRESSION |
| topic | Cancer Research, Neurology (clinical), Oncology |
| url | http://dx.doi.org/10.1093/neuonc/noz175.1061 |