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Start Over Author "Acker, Till" Language english Journal acta neuropathologica communications
4 results on '"Acker, Till"'

2. KLF4K409Q–mutated meningiomas show enhanced hypoxia signaling and respond to mTORC1 inhibitor treatment

Author

von Spreckelsen, Niklas, Waldt, Natalie, Poetschke, Rebecca, Kesseler, Christoph, Dohmen, Hildegard, Jiao, Hui-Ke, Nemeth, Attila, Schob, Stefan, Scherlach, Cordula, Sandalcioglu, Ibrahim Erol, Deckert, Martina, Angenstein, Frank, Krischek, Boris, Stavrinou, Pantelis, Timmer, Marco, Remke, Marc, Kirches, Elmar, Goldbrunner, Roland, Chiocca, E. Antonio, Huettelmaier, Stefan, Acker, Till, and Mawrin, Christian

Published
2020
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3. Tumors diagnosed as cerebellar glioblastoma comprise distinct molecular entities

Author

Reinhardt, Annekathrin, Stichel, Damian, Schrimpf, Daniel, Koelsche, Christian, Wefers, Annika K., Ebrahimi, Azadeh, Sievers, Philipp, Huang, Kristin, Casalini, M. Belén, Fernández-Klett, Francisco, Suwala, Abigail, Weller, Michael, Gramatzki, Dorothee, Felsberg, Joerg, Reifenberger, Guido, Becker, Albert, Hans, Volkmar H., Prinz, Marco, Staszewski, Ori, Acker, Till, Dohmen, Hildegard, Hartmann, Christian, Paulus, Werner, Heß, Katharina, Brokinkel, Benjamin, Schittenhelm, Jens, Buslei, Rolf, Deckert, Martina, Mawrin, Christian, Hewer, Ekkehard, Pohl, Ute, Jaunmuktane, Zane, Brandner, Sebastian, Unterberg, Andreas, Hänggi, Daniel, Platten, Michael, Pfister, Stefan M., Wick, Wolfgang, Herold-Mende, Christel, Korshunov, Andrey, Reuss, David E., Sahm, Felix, Jones, David T. W., Capper, David, and von Deimling, Andreas

Published
2019
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4. KLF4 K409Q –mutated meningiomas show enhanced hypoxia signaling and respond to mTORC1 inhibitor treatment

Author

von Spreckelsen, Niklas, Waldt, Natalie, Poetschke, Rebecca, Kesseler, Christoph, Dohmen, Hildegard, Jiao, Hui-Ke, Nemeth, Attila, Schob, Stefan, Scherlach, Cordula, Sandalcioglu, Ibrahim Erol, Deckert, Martina, Angenstein, Frank, Krischek, Boris, Stavrinou, Pantelis, Timmer, Marco, Remke, Marc, Kirches, Elmar, Goldbrunner, Roland, Chiocca, E. Antonio, Huettelmaier, Stefan, Acker, Till, and Mawrin, Christian

Subjects
pharmacology [Protein Kinase Inhibitors], drug effects [Gene Expression Regulation, Neoplastic], analogs & derivatives [Sirolimus], genetics [Gene Expression Regulation, Neoplastic], lcsh:RC346-429, drug effects [Kruppel-Like Transcription Factors], Mice, Meningeal Neoplasms, Edema, RNA-Seq, Hypoxia, antagonists & inhibitors [Mechanistic Target of Rapamycin Complex 1], genetics [Meningeal Neoplasms], Reverse Transcriptase Polymerase Chain Reaction, genetics [Meningioma], KLF4, genetics [Tumor Hypoxia], Up-Regulation, Gene Expression Regulation, Neoplastic, K409Q, Meningioma, Signal Transduction, Kruppel-Like Transcription Factors, pharmacology [Sirolimus], Mice, Nude, Mechanistic Target of Rapamycin Complex 1, genetics [Hypoxia], Skull Base Neoplasms, Prolyl Hydroxylases, Kruppel-Like Factor 4, metabolism [Meningeal Neoplasms], Cell Line, Tumor, genetics [Hypoxia-Inducible Factor 1, alpha Subunit], otorhinolaryngologic diseases, Animals, Humans, HIF, ddc:610, neoplasms, Protein Kinase Inhibitors, lcsh:Neurology. Diseases of the nervous system, Cell Proliferation, Sirolimus, Research, metabolism [Hypoxia-Inducible Factor 1, alpha Subunit], genetics [Kruppel-Like Transcription Factors], Hypoxia-Inducible Factor 1, alpha Subunit, metabolism [Hypoxia], nervous system diseases, metabolism [Meningioma], Mutation, Tumor Hypoxia, drug effects [Hypoxia-Inducible Factor 1, alpha Subunit], Neoplasm Transplantation
Abstract

Meningioma represents the most common primary brain tumor in adults. Recently several non-NF2 mutations in meningioma have been identified and correlated with certain pathological subtypes, locations and clinical observations. Alterations of cellular pathways due to these mutations, however, have largely remained elusive. Here we report that the Krueppel like factor 4 (KLF4)-K409Q mutation in skull base meningiomas triggers a distinct tumor phenotype. Transcriptomic analysis of 17 meningioma samples revealed that KLF4 K409Q mutated tumors harbor an upregulation of hypoxia dependent pathways. Detailed in vitro investigation further showed that the KLF4 K409Q mutation induces HIF-1α through the reduction of prolyl hydroxylase activity and causes an upregulation of downstream HIF-1α targets. Finally, we demonstrate that KLF4 K409Q mutated tumors are susceptible to mTOR inhibition by Temsirolimus. Taken together, our data link the KLF4K409Q mediated upregulation of HIF pathways to the clinical and biological characteristics of these skull base meningiomas possibly opening new therapeutic avenues for this distinct meningioma subtype.

Published
2020

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