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3. Pathologist Computer-Aided Diagnostic Scoring of Tumor Cell Fraction: A Swiss National Study

Author

Frei, Ana Leni, Oberson, Raphaël, Baumann, Elias, Perren, Aurel, Grobholz, Rainer, Lugli, Alessandro, Dawson, Heather, Abbet, Christian, Lertxundi, Ibai, Reinhard, Stefan, Mookhoek, Aart, Feichtinger, Johann, Sarro, Rossella, Gadient, Gallus, Dommann-Scherrer, Corina, Barizzi, Jessica, Berezowska, Sabina, Glatz, Katharina, Dertinger, Susanne, Banz, Yara, Schoenegg, Rene, Rubbia-Brandt, Laura, Fleischmann, Achim, Saile, Guenter, Mainil-Varlet, Pierre, Biral, Ruggero, Giudici, Luca, Soltermann, Alex, Chaubert, Audrey Baur, Stadlmann, Sylvia, Diebold, Joachim, Egervari, Kristof, Bénière, Charles, Saro, Francesca, Janowczyk, Andrew, and Zlobec, Inti

Published
2023
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5. Cytological features of ependymal and choroid plexus tumours.

Author

Egervari, Kristof and Hewer, Ekkehard

Subjects
*CHOROID plexus, *SYMPTOMS, *CYTOLOGY, *DIFFERENTIAL diagnosis, *EPENDYMOMA
Abstract

Ependymal and choroid plexus tumours arise in anatomically related regions. Their intraoperative differential diagnosis is large and depends on factors such as age, tumour site and clinical presentation. Squash cytology can provide valuable information in this context. Cytological features of conventional ependymomas, subependymomas and myxopapillary ependymomas as well as choroid plexus tumours are reviewed and illustrated. Differential diagnostic considerations integrating morphological and clinical information are discussed. [ABSTRACT FROM AUTHOR]

Published
2024
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7. Seizure outcome and use of antiepileptic drugs after epilepsy surgery according to histopathological diagnosis: a retrospective multicentre cohort study

Author

Aichholzer, Martin, Amorim, Isabel, Aparicio, Javier, Aronica, Eleonora, Arzimanoglou, Alexis, Barba, Carmen, Beck, Jürgen, Becker, Albert, Beckervordersandforth, Jan C, Bien, Christian G, Blümcke, Ingmar, Bodi, Istvan, Braun, Kees PJ, Catenoix, Helene, Chassoux, Francine, Chipaux, Mathilde, Cloppenborg, Thomas, Coras, Roland, Cross, J Helen, De Palma, Luca, De Tisi, Jane, Deleo, Francesco, Devaux, Bertrand, Di Gennaro, Giancarlo, Dorfmüller, Georg, Duncan, John S, Elger, Christian, Ernst, Katharina, Esposito, Vincenzo, Feucht, Martha, Gadze, Zeljka Petelin, Garbelli, Rita, Geleijns, Karin, Gil-Nagel, Antonio, Grote, Alexander, Grunwald, Thomas, Guerrini, Renzo, Hamer, Hajo, Honavar, Mrinalini, Jacques, Thomas S, Jakovcevic, Antonia, Jutila, Leena, Kalina, Adam, Kälviäinen, Reetta, Klein, Karl Martin, Koenig, Kristina, Krsek, Pavel, Kudernatsch, Manfred, Kudr, Martin, Lamberink, Herm J, Malmgren, Kristina, Marusic, Petr, Melikyan, Armen, Menzler, Katja, Noachtar, Soheyl, Otte, Willem M, Özkara, Çiğdem, Pieper, Tom, Pimentel, Jose, Raicevic, Savo, Rheims, Sylvain, Ribeiro, Joana, Rosenow, Felix, Rössler, Karl, Rydenhag, Bertil, Sales, Francisco, San Antonio-Arce, Victoria, Schaller, Karl Lothar, Schijns, Olaf, Scholl, Theresa, Schramm, Johannes, Schulze-Bonhage, Andreas, Sciot, Raf, Seeck, Margitta, Shishkina, Lyudmila, Sokic, Dragoslav, Specchio, Nicola, Theys, Tom, Thom, Maria, Delgado, Rafael Toledano, Toulouse, Joseph, Uzan, Mustafa, van Loon, Johannes, Van Paesschen, Wim, von Oertzen, Tim J, Jansen, Floor, Leijten, Frans, van Rijen, Peter, Spliet, Wim GM, Mühlebner, Angelika, Kasper, Burkhard S, Fauser, Susanne, Polster, Tilman, Kalbhenn, Thilo, Delev, Daniel, McEvoy, Andrew, Miserocchi, Anna, Landré, Elisabeth, Turak, Bares, Varlet, Pascale, Ferrand-Sorbets, Sarah, Fohlen, Martine, Bulteau, Christine, Edelvik, Anna, Shah, Mukesch J, Scheiwe, Christian, Delicado, Eva Gutierrez, Tisdall, Martin, Eltze, Christin, Akkol, Serdar, Deniz, Kaancan, Oz, Buge, Holthausen, Hans, Hartlieb, Till, Staudt, Martin, Casciato, Sara, Quarato, Pier P, Giangaspero, Felice, Streichenberger, Nathalie, Guenot, Marc, Isnard, Jean, Valentijn, Antonio, Chang, Amanda, Mullatti, Nandini, Zamecnik, Josef, Zarubova, Jana, Tomasek, Martin, Immonen, Arto, Saarela, Anni, Rauramaa, Tuomas, Lobrinus, Johannes A, Egervari, Kristof, Momjian, Shahan, Harti, Elisabeth, Lohr, Hannah, Kroell, Judith, Vermeulen, Lynn, Cleeren, Evy, Vlasov, Pavel, Kozlova, Antonia, Vorobyev, Alexey, Goeppel, Gudrun, Samueli, Sharon, Czech, Thomas, Hainfellner, Johannes, Puttinger, Gertraud, Schwarz, Gabriele, Stefanits, Harald, Weis, Serge, Spreafico, Roberto, Villani, Flavio, Rossini, Laura, Hermsen, Anke, Knake, Susanne, Nimsky, Christopher, Carl, Barbara, Belohlavkova, Anezka, Benova, Barbora, Bisschop, Jeroen, Colon, Albert, van Kranen-Mastenbroek, Vivianne, Rouhl, Rob PW, Hoogland, Govert, Rumiá, Jordi, Ramírez-Camacho, Alia, Candela-Cantó, Santiago, Ostrowsky-Coste, Karine, Panagiotakaki, Eleni, Montavont, Alexandra, Kosal, Pascale Keo, Gokce-Samar, Zeynep, Milleret, Clara, Buccoliero, Anna M, Giordano, Flavio, Sulentic, Vlatko, Mrak, Goran, Desnica, Andrej, CarfíPavia, Giusy, De Benedictis, Alessandro, Marras, Carlo E, Bascarevic, Vladimir, Vojvodic, Nikola, Ristic, Aleksandar, Rebelo, Olinda, Aledo-Serrano, Angel, Garcia-Morales, Irene, Anciones, Carla, and Braun, Kees P J

Published
2020
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10. Methylation-Based Characterization of a New IDH2 Mutation in Sinonasal Undifferentiated Carcinoma.

Author

Burgermeister, Simon, Stoykova, Simona, Krebs, Fanny S., Zoete, Vincent, Mbefo, Martial, Egervari, Kristof, Reinhard, Antoine, Bisig, Bettina, and Hewer, Ekkehard

Subjects
CARCINOMA, PARANASAL sinuses, ACUTE myeloid leukemia, ISOCITRATE dehydrogenase, GENETIC mutation
Abstract

Mutations affecting codon 172 of the isocitrate dehydrogenase 2 (IDH2) gene define a subgroup of sinonasal undifferentiated carcinomas (SNUCs) with a relatively favorable prognosis and a globally hypermethylated phenotype. They are also recurrent (along with IDH1 mutations) in gliomas, acute myeloid leukemia, and intrahepatic cholangiocarcinoma. Commonly reported mutations, all associated with aberrant IDH2 enzymatic activity, include R172K, R172S, R172T, R172G, and R172M. We present a case of SNUC with a never-before-described IDH2 mutation, R172A. Our report compares the methylation pattern of our sample to other cases from the Gene Expression Omnibus database. Hierarchical clustering suggests a strong association between our sample and other IDH-mutant SNUCs and a clear distinction between sinonasal normal tissues and tumors. Principal component analysis (PCA), using 100 principal components explaining 94.5% of the variance, showed the position of our sample to be within 1.02 standard deviation of the other IDH-mutant SNUCs. A molecular modeling analysis of the IDH2 R172A versus other R172 variants provides a structural explanation to how they affect the protein active site. Our findings thus suggest that the R172A mutation in IDH2 confers a gain of function similar to other R172 mutations in IDH2, resulting in a similar hypermethylated profile. [ABSTRACT FROM AUTHOR]

Published
2024
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11. MicroRNA-92a–CPEB3 axis protects neurons against inflammatory neurodegeneration

Author

Winkler, Iris, primary, Engler, Jan Broder, additional, Vieira, Vanessa, additional, Bauer, Simone, additional, Liu, Yi-Hsiang, additional, Di Liberto, Giovanni, additional, Grochowska, Katarzyna M., additional, Wagner, Ingrid, additional, Bier, Jasmina, additional, Bal, Lukas C., additional, Rothammer, Nicola, additional, Meurs, Nina, additional, Egervari, Kristof, additional, Schattling, Benjamin, additional, Salinas, Gabriela, additional, Kreutz, Michael R., additional, Huang, Yi-Shuian, additional, Pless, Ole, additional, Merkler, Doron, additional, and Friese, Manuel A., additional

Published
2023
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12. Developmental and oncogenic programs in H3K27M gliomas dissected by single-cell RNA-seq

Author

Filbin, Mariella G., Tirosh, Itay, Hovestadt, Volker, Shaw, McKenzie L., Escalante, Leah E., Mathewson, Nathan D., Neftel, Cyril, Frank, Nelli, Pelton, Kristine, Hebert, Christine M., Haberler, Christine, Yizhak, Keren, Gojo, Johannes, Egervari, Kristof, Mount, Christopher, van Galen, Peter, Bonal, Dennis M., Nguyen, Quang-De, Beck, Alexander, Sinai, Claire, Czech, Thomas, Dorfer, Christian, Goumnerova, Liliana, Lavarino, Cinzia, Carcaboso, Angel M., Mora, Jaume, Mylvaganam, Ravindra, Luo, Christina C., Peyr, Andreas, Popović, Mara, Azizi, Amedeo, Batchelor, Tracy. T., Frosch, Matthew P., Martinez-Lage, Maria, Kieran, Mark W., Bandopadhayay, Pratiti, Beroukhim, Rameen, Fritsch, Gerhard, Getz, Gad, Rozenblatt-Rosen, Orit, Wucherpfennig, Kai W., Louis, David N., Monje, Michelle, Slavc, Irene, Ligon, Keith L., Golub, Todd R., Regev, Aviv, Bernstein, Bradley E., and Suvà, Mario L.

Published
2018

13. Neurons under T Cell Attack Coordinate Phagocyte-Mediated Synaptic Stripping

Author

Di Liberto, Giovanni, Pantelyushin, Stanislav, Kreutzfeldt, Mario, Page, Nicolas, Musardo, Stefano, Coras, Roland, Steinbach, Karin, Vincenti, Ilena, Klimek, Bogna, Lingner, Thomas, Salinas, Gabriela, Lin-Marq, Nathalie, Staszewski, Ori, Costa Jordão, Marta Joana, Wagner, Ingrid, Egervari, Kristof, Mack, Matthias, Bellone, Camilla, Blümcke, Ingmar, Prinz, Marco, Pinschewer, Daniel D., and Merkler, Doron

Published
2018
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15. ChatGPT in glioma adjuvant therapy decision making: ready to assume the role of a doctor in the tumour board?

Author

Haemmerli, Julien, primary, Sveikata, Lukas, additional, Nouri, Aria, additional, May, Adrien, additional, Egervari, Kristof, additional, Freyschlag, Christian, additional, Lobrinus, Johannes A, additional, Migliorini, Denis, additional, Momjian, Shahan, additional, Sanda, Nicolae, additional, Schaller, Karl, additional, Tran, Sebastien, additional, Yeung, Jacky, additional, and Bijlenga, Philippe, additional

Published
2023
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16. Pituitary macroadenoma apoplexy following treatment with pembrolizumab

Author

Lopes, Stephanie Andrade, primary, Sciotto-Canel, Lucie, additional, Momjian, Shahan, additional, Aissa, Assma Ben, additional, Brocco, Elise, additional, Becquart, Ondine, additional, Egervari, Kristof, additional, Merkler, Doron, additional, Jornayvaz, Francois, additional, Leboulleux, Sophie, additional, and Mavromati, Maria, additional

Published
2023
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20. G9a dictates neuronal vulnerability to inflammatory stress via transcriptional control of ferroptosis

Author

Rothammer, Nicola, primary, Woo, Marcel S., additional, Bauer, Simone, additional, Binkle-Ladisch, Lars, additional, Di Liberto, Giovanni, additional, Egervari, Kristof, additional, Wagner, Ingrid, additional, Haferkamp, Undine, additional, Pless, Ole, additional, Merkler, Doron, additional, Engler, Jan Broder, additional, and Friese, Manuel A., additional

Published
2022
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22. Tissue-resident memory CD8+T cells cooperate with CD4+T cells to drive compartmentalized immunopathology in the CNS

Author

Vincenti, Ilena, primary, Page, Nicolas, additional, Steinbach, Karin, additional, Yermanos, Alexander, additional, Lemeille, Sylvain, additional, Nunez, Nicolas, additional, Kreutzfeldt, Mario, additional, Klimek, Bogna, additional, Di Liberto, Giovanni, additional, Egervari, Kristof, additional, Piccinno, Margot, additional, Shammas, Ghazal, additional, Mariotte, Alexandre, additional, Fonta, Nicolas, additional, Liaudet, Nicolas, additional, Shlesinger, Danielle, additional, Liuzzi, Anna Rita, additional, Wagner, Ingrid, additional, Saadi, Cynthia, additional, Stadelmann, Christine, additional, Reddy, Sai, additional, Becher, Burkhard, additional, and Merkler, Doron, additional

Published
2022
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23. G9a dictates neuronal vulnerability to inflammatory stress via transcriptional control of ferroptosis

Author

Rothammer, Nicola, Woo, Marcel S., Bauer, Simone, Binkle-Ladisch, Lars, Di Liberto, Giovanni, Egervari, Kristof, Wagner, Ingrid, Haferkamp, Undine, Pless, Ole, Merkler, Doron, Engler, Jan Broder, Friese, Manuel A., and Publica

Subjects
Inflammation, Neurons, Mice, Multidisciplinary, Encephalomyelitis, Autoimmune, Experimental, Multiple Sclerosis, Gene Expression Regulation, Animals, Ferroptosis, Humans, Histone-Lysine N-Methyltransferase
Abstract

Neuroinflammation leads to neuronal stress responses that contribute to neuronal dysfunction and loss. However, treatments that stabilize neurons and prevent their destruction are still lacking. Here, we identify the histone methyltransferase G9a as a druggable epigenetic regulator of neuronal vulnerability to inflammation. In murine experimental autoimmune encephalomyelitis (EAE) and human multiple sclerosis (MS), we found that the G9a-catalyzed repressive epigenetic mark H3K9me2 was robustly induced by neuroinflammation. G9a activity repressed anti-ferroptotic genes, diminished intracellular glutathione levels, and triggered the iron-dependent programmed cell death pathway ferroptosis. Conversely, pharmacological treatment of EAE mice with a G9a inhibitor restored anti-ferroptotic gene expression, reduced inflammation-induced neuronal loss, and improved clinical outcome. Similarly, neuronal anti-ferroptotic gene expression was reduced in MS brain tissue and was boosted by G9a inhibition in human neuronal cultures. This study identifies G9a as a critical transcriptional enhancer of neuronal ferroptosis and potential therapeutic target to counteract inflammation-induced neurodegeneration.

Published
2022

29. Neurodegenerative phagocytes mediate synaptic stripping in Neuro-HIV.

Author

Liberto, Giovanni Di, Egervari, Kristof, Kreutzfeldt, Mario, Schürch, Christian M, Hewer, Ekkehard, Wagner, Ingrid, Pasquier, Renaud Du, Merkler, Doron, Di Liberto, Giovanni, and Du Pasquier, Renaud

Abstract

Glial cell activation is a hallmark of several neurodegenerative and neuroinflammatory diseases. During HIV infection, neuroinflammation is associated with cognitive impairment, even during sustained long-term suppressive antiretroviral therapy. However, the cellular subsets contributing to neuronal damage in the CNS during HIV infection remain unclear. Using post-mortem brain samples from eight HIV patients and eight non-neurological disease controls, we identify a subset of CNS phagocytes highly enriched in LGALS3, CTSB, GPNMB and HLA-DR, a signature identified in the context of ageing and neurodegeneration. In HIV patients, the presence of this phagocyte phenotype was associated with synaptic stripping, suggesting an involvement in the pathogenesis of HIV-associated neurocognitive disorder. Taken together, our findings elucidate some of the molecular signatures adopted by CNS phagocytes in HIV-positive patients and contribute to the understanding of how HIV might pave the way to other forms of cognitive decline in ageing HIV patient populations. [ABSTRACT FROM AUTHOR]

Published
2022
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31. Neuronal metabotropic glutamate receptor 8 protects against neurodegeneration in CNS inflammation

Author

Woo, Marcel S., primary, Ufer, Friederike, additional, Rothammer, Nicola, additional, Di Liberto, Giovanni, additional, Binkle, Lars, additional, Haferkamp, Undine, additional, Sonner, Jana K., additional, Engler, Jan Broder, additional, Hornig, Sönke, additional, Bauer, Simone, additional, Wagner, Ingrid, additional, Egervari, Kristof, additional, Raber, Jacob, additional, Duvoisin, Robert M., additional, Pless, Ole, additional, Merkler, Doron, additional, and Friese, Manuel A., additional

Published
2021
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32. A tumor like no other

Author

Corniola, Marco V., primary, Egervari, Kristof, additional, Vargas, Maria I., additional, and Meling, Torstein R., additional

Published
2021
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33. Neuropathology associated with SARS-CoV-2 infection

Author

Egervari, Kristof, primary, Thomas, Christian, additional, Lobrinus, Johannes A, additional, Kuhlmann, Tanja, additional, Brück, Wolfgang, additional, Love, Seth, additional, Crary, John F, additional, Stadelmann, Christine, additional, Paulus, Werner, additional, and Merkler, Doron, additional

Published
2021
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34. Tissue-resident memory CD8+ T cells cooperate with CD4+ T cells to drive compartmentalized immunopathology in the CNS.

Author

Vincenti, Ilena, Page, Nicolas, Steinbach, Karin, Yermanos, Alexander, Lemeille, Sylvain, Nunez, Nicolas, Kreutzfeldt, Mario, Klimek, Bogna, Di Liberto, Giovanni, Egervari, Kristof, Piccinno, Margot, Shammas, Ghazal, Mariotte, Alexandre, Fonta, Nicolas, Liaudet, Nicolas, Shlesinger, Danielle, Liuzzi, Anna Rita, Wagner, Ingrid, Saadi, Cynthia, and Stadelmann, Christine

Subjects
T cells, IMMUNOLOGIC memory, IMMUNOPATHOLOGY, LYMPHOCYTIC choriomeningitis virus, CENTRAL nervous system diseases, AUTOIMMUNE diseases, CENTRAL nervous system physiology
Abstract

In chronic inflammatory diseases of the central nervous system (CNS), immune cells persisting behind the blood-brain barrier are supposed to promulgate local tissue destruction. The drivers of such compartmentalized inflammation remain unclear, but tissue-resident memory T cells (TRM) represent a potentially important cellular player in this process. Here, we investigated whether resting CD8+ TRM persisting after cleared infection with attenuated lymphocytic choriomeningitis virus (LCMV) can initiate immune responses directed against cognate self-antigen in the CNS. We demonstrated that time-delayed conditional expression of the LCMV glycoprotein as neo-self-antigen by glia cells reactivated CD8+ TRM. Subsequently, CD8+ TRM expanded and initiated CNS inflammation and immunopathology in an organ-autonomous manner independently of circulating CD8+ T cells. However, in the absence of CD4+ T cells, TCF-1+ CD8+ TRM failed to expand and differentiate into terminal effectors. Similarly, in human demyelinating CNS autoimmune lesions, we found CD8+ T cells expressing TCF-1 that predominantly exhibited a TRM-like phenotype. Together, our study provides evidence for CD8+ TRM-driven CNS immunopathology and sheds light on why inflammatory processes may evade current immunomodulatory treatments in chronic autoimmune CNS conditions. A local contribution to CNS autoimmunity: Aberrantly activated tissue-resident memory T cells (TRM) have been shown to contribute to inflammatory conditions. Their role in the CNS remains unclear. Now, in two complementary studies, Vincenti et al. and Frieser et al. investigated the role of TRM in the CNS. Vincenti and colleagues reported that after viral brain infection, TRM triggered CNS inflammation, promoting autoimmune reactions in mice. Cells with TRM-like phenotype were also identified in brain tissue from patients with CNS autoimmune diseases. Frieser et al. used rodent models of CNS autoimmunity to show that pathogenic CD8+ T cells infiltrating the CNS adopted a TRM phenotype that contributes to the disease. The results suggest that targeting TRM can be effective in treating CNS autoimmune diseases. [ABSTRACT FROM AUTHOR]

Published
2022
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36. Seizure outcome and use of antiepileptic drugs after epilepsy surgery according to histopathological diagnosis: a retrospective multicentre cohort study

Author

Lamberink, Herm J, primary, Otte, Willem M, additional, Blümcke, Ingmar, additional, Braun, Kees P J, additional, Aichholzer, Martin, additional, Amorim, Isabel, additional, Aparicio, Javier, additional, Aronica, Eleonora, additional, Arzimanoglou, Alexis, additional, Barba, Carmen, additional, Beck, Jürgen, additional, Becker, Albert, additional, Beckervordersandforth, Jan C, additional, Bien, Christian G, additional, Bodi, Istvan, additional, Braun, Kees PJ, additional, Catenoix, Helene, additional, Chassoux, Francine, additional, Chipaux, Mathilde, additional, Cloppenborg, Thomas, additional, Coras, Roland, additional, Cross, J Helen, additional, De Palma, Luca, additional, De Tisi, Jane, additional, Deleo, Francesco, additional, Devaux, Bertrand, additional, Di Gennaro, Giancarlo, additional, Dorfmüller, Georg, additional, Duncan, John S, additional, Elger, Christian, additional, Ernst, Katharina, additional, Esposito, Vincenzo, additional, Feucht, Martha, additional, Gadze, Zeljka Petelin, additional, Garbelli, Rita, additional, Geleijns, Karin, additional, Gil-Nagel, Antonio, additional, Grote, Alexander, additional, Grunwald, Thomas, additional, Guerrini, Renzo, additional, Hamer, Hajo, additional, Honavar, Mrinalini, additional, Jacques, Thomas S, additional, Jakovcevic, Antonia, additional, Jutila, Leena, additional, Kalina, Adam, additional, Kälviäinen, Reetta, additional, Klein, Karl Martin, additional, Koenig, Kristina, additional, Krsek, Pavel, additional, Kudernatsch, Manfred, additional, Kudr, Martin, additional, Lamberink, Herm J, additional, Malmgren, Kristina, additional, Marusic, Petr, additional, Melikyan, Armen, additional, Menzler, Katja, additional, Noachtar, Soheyl, additional, Özkara, Çiğdem, additional, Pieper, Tom, additional, Pimentel, Jose, additional, Raicevic, Savo, additional, Rheims, Sylvain, additional, Ribeiro, Joana, additional, Rosenow, Felix, additional, Rössler, Karl, additional, Rydenhag, Bertil, additional, Sales, Francisco, additional, San Antonio-Arce, Victoria, additional, Schaller, Karl Lothar, additional, Schijns, Olaf, additional, Scholl, Theresa, additional, Schramm, Johannes, additional, Schulze-Bonhage, Andreas, additional, Sciot, Raf, additional, Seeck, Margitta, additional, Shishkina, Lyudmila, additional, Sokic, Dragoslav, additional, Specchio, Nicola, additional, Theys, Tom, additional, Thom, Maria, additional, Delgado, Rafael Toledano, additional, Toulouse, Joseph, additional, Uzan, Mustafa, additional, van Loon, Johannes, additional, Van Paesschen, Wim, additional, von Oertzen, Tim J, additional, Jansen, Floor, additional, Leijten, Frans, additional, van Rijen, Peter, additional, Spliet, Wim GM, additional, Mühlebner, Angelika, additional, Kasper, Burkhard S, additional, Fauser, Susanne, additional, Polster, Tilman, additional, Kalbhenn, Thilo, additional, Delev, Daniel, additional, McEvoy, Andrew, additional, Miserocchi, Anna, additional, Landré, Elisabeth, additional, Turak, Bares, additional, Varlet, Pascale, additional, Ferrand-Sorbets, Sarah, additional, Fohlen, Martine, additional, Bulteau, Christine, additional, Edelvik, Anna, additional, Shah, Mukesch J, additional, Scheiwe, Christian, additional, Delicado, Eva Gutierrez, additional, Tisdall, Martin, additional, Eltze, Christin, additional, Akkol, Serdar, additional, Deniz, Kaancan, additional, Oz, Buge, additional, Holthausen, Hans, additional, Hartlieb, Till, additional, Staudt, Martin, additional, Casciato, Sara, additional, Quarato, Pier P, additional, Giangaspero, Felice, additional, Streichenberger, Nathalie, additional, Guenot, Marc, additional, Isnard, Jean, additional, Valentijn, Antonio, additional, Chang, Amanda, additional, Mullatti, Nandini, additional, Zamecnik, Josef, additional, Zarubova, Jana, additional, Tomasek, Martin, additional, Immonen, Arto, additional, Saarela, Anni, additional, Rauramaa, Tuomas, additional, Lobrinus, Johannes A, additional, Egervari, Kristof, additional, Momjian, Shahan, additional, Harti, Elisabeth, additional, Lohr, Hannah, additional, Kroell, Judith, additional, Vermeulen, Lynn, additional, Cleeren, Evy, additional, Vlasov, Pavel, additional, Kozlova, Antonia, additional, Vorobyev, Alexey, additional, Goeppel, Gudrun, additional, Samueli, Sharon, additional, Czech, Thomas, additional, Hainfellner, Johannes, additional, Puttinger, Gertraud, additional, Schwarz, Gabriele, additional, Stefanits, Harald, additional, Weis, Serge, additional, Spreafico, Roberto, additional, Villani, Flavio, additional, Rossini, Laura, additional, Hermsen, Anke, additional, Knake, Susanne, additional, Nimsky, Christopher, additional, Carl, Barbara, additional, Belohlavkova, Anezka, additional, Benova, Barbora, additional, Bisschop, Jeroen, additional, Colon, Albert, additional, van Kranen-Mastenbroek, Vivianne, additional, Rouhl, Rob PW, additional, Hoogland, Govert, additional, Rumiá, Jordi, additional, Ramírez-Camacho, Alia, additional, Candela-Cantó, Santiago, additional, Ostrowsky-Coste, Karine, additional, Panagiotakaki, Eleni, additional, Montavont, Alexandra, additional, Kosal, Pascale Keo, additional, Gokce-Samar, Zeynep, additional, Milleret, Clara, additional, Buccoliero, Anna M, additional, Giordano, Flavio, additional, Sulentic, Vlatko, additional, Mrak, Goran, additional, Desnica, Andrej, additional, CarfíPavia, Giusy, additional, De Benedictis, Alessandro, additional, Marras, Carlo E, additional, Bascarevic, Vladimir, additional, Vojvodic, Nikola, additional, Ristic, Aleksandar, additional, Rebelo, Olinda, additional, Aledo-Serrano, Angel, additional, Garcia-Morales, Irene, additional, and Anciones, Carla, additional

Published
2020
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42. Brain-resident memory T cells generated early in life predispose to autoimmune disease in mice

Author

Steinbach, Karin, primary, Vincenti, Ilena, additional, Egervari, Kristof, additional, Kreutzfeldt, Mario, additional, van der Meer, Franziska, additional, Page, Nicolas, additional, Klimek, Bogna, additional, Rossitto-Borlat, Irène, additional, Di Liberto, Giovanni, additional, Muschaweckh, Andreas, additional, Wagner, Ingrid, additional, Hammad, Karim, additional, Stadelmann, Christine, additional, Korn, Thomas, additional, Hartley, Oliver, additional, Pinschewer, Daniel D., additional, and Merkler, Doron, additional

Published
2019
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47. Astrocytes Spatially Restrict VEGF Signaling by Polarized Secretion and Incorporation of VEGF into the Actively Assembling Extracellular Matrix

Author

Egervari, Kristof Levente, Potter, Gael, Guzman-Hernandez, Maria Luisa, Salmon, Patrick, Soto Ribeiro, Martinho, Kastberger, Birgit, Balla, Tamas, Wehrle-Haller, Bernhard, and Kiss, Jozsef Zoltan

Subjects
Cerebral Cortex, Neurons, Vascular Endothelial Growth Factor A, Microscopy, Confocal, Photobleaching, Time Factors, Green Fluorescent Proteins, Hydrazones, Cell Polarity, Transfection, Article, ddc:616.8, Extracellular Matrix, Rats, Soluble N-Ethylmaleimide-Sensitive Factor Attachment Proteins, Ki-67 Antigen, Astrocytes, Animals, Puromycin, Rats, Wistar, ddc:612, Cells, Cultured, Signal Transduction
Abstract

The spatial organization of vascular endothelial growth factor (VEGF) signaling is a key determinant of vascular patterning during development and tissue repair. How VEGF signaling becomes spatially restricted and the role of VEGF secreting astrocytes in this process remains poorly understood. Using a VEGF-GFP fusion protein and confocal time-lapse microscopy, we observed the intracellular routing, secretion and immobilization of VEGF in scratch-activated living astrocytes. We found VEGF to be directly transported to cell-extracellular matrix attachments where it is incorporated into fibronectin fibrils. VEGF accumulated at β1 integrin containing fibrillar adhesions and was translocated along the cell surface prior to internalization and degradation. We also found that only the astrocyte-derived, matrix-bound, and not soluble VEGF decreases β1 integrin turnover in fibrillar adhesions. We suggest that polarized VEGF release and ECM remodeling by VEGF secreting cells is key to control the local concentration and signaling of VEGF. Our findings highlight the importance of astrocytes in directing VEGF functions and identify these mechanisms as promising target for angiogenic approaches. GLIA 2016;64:440-456.

Published
2015

48. Concurrent <italic>IDH1</italic> and <italic>SMARCB1</italic> Mutations in Pediatric Medulloblastoma: A Case Report.

Author

El-Ayadi, Moatasem, Egervari, Kristof, Merkler, Doron, McKee, Thomas A., Gumy-Pause, Fabienne, Stichel, Damian, Capper, David, Pietsch, Torsten, Ansari, Marc, and von Bueren, André O.

Subjects
TUMORS in children, IMMUNOTHERAPY, CANCER treatment, GENETIC mutation, MEDULLOBLASTOMA
Abstract

Isocitrate Dehydrogenase-1 (IDH1) is a driver gene in several cancers including brain tumors such as low-grade and high-grade gliomas. Mutations of SMARCB1 were described in atypical teratoid rhabdoid tumors and to date have not been associated with the pathogenesis of medulloblastoma. We report concurrent IDH1 and SMARCB1 mutations in a medulloblastoma patient. We searched the catalog of somatic mutations in cancer (COSMIC) database and other mutation databases and -to our knowledge- this is the first reported case of medulloblastoma harboring both mutations together. Our patient is a 13-year-old male presenting with headache and vomiting at diagnosis. MRI revealed left cerebellar expansive lesion with no evidence of metastasis. A histopathological diagnosis of desmoplastic/nodular medulloblastoma was made after complete resection of the tumor. Immunophenotypic characterization and methylation profiling suggested a medulloblastoma with SHH activation. Next generation sequencing of a panel of 400 genes revealed heterozygous somatic IDH1(p.R132C), SMARCB1(p.R201Q), and CDH11(p.L625T) mutations. The patient was treated according to the HIT-SIOP PNET 4 protocol. He is in complete remission more than 2 years after diagnosis. In conclusion, increasing use of high throughput sequencing will certainly increase the frequency with which rare mutations or mutation combinations are identified. The exact frequency of this mutation combination and whether it has any particular therapeutic implications or prognostic relevance requires further investigation. [ABSTRACT FROM AUTHOR]

Published
2018
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