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001-es BibID:	BIBFORM040477
Első szerző:	Sturm, Dominik
Cím:	Hotspot mutations in H3F3A and IDH1 define distinct epigenetic and biological subgroups of glioblastoma / Dominik Sturm, Hendrik Witt, Volker Hovestadt, Dong-Anh Khuong-Quang, David T. W. Jones, Carolin Konermann, Elke Pfaff, Martje Tönjes, Martin Sill, Sebastian Bender, Marcel Kool, Marc Zapatka, Natalia Becker, Manuela Zucknick, Thomas Hielscher, Xiao-Yang Liu, Adam M. Fontebasso, Marina Ryzhova, Steffen Albrecht, Karine Jacob, Marietta Wolter, Martin Ebinger, Martin U. Schuhmann, Timothy van Meter, Michael C. Frühwald, Holger Hauch, Arnulf Pekrun, Bernhard Radlwimmer, Tim Niehues, Gregor von Komorowski, Matthias Dürken, Andreas E. Kulozik, Jenny Madden, Andrew Donson, Nicholas K. Foreman, Rachid Drissi, Maryam Fouladi, Wolfram Scheurlen, Andreas von Deimling, Camelia Monoranu, Wolfgang Roggendorf, Christel Herold-Mende, Andreas Unterberg, Christof M. Kramm, Jörg Felsberg, Christian Hartmann, Benedikt Wiestler, Wolfgang Wick, Till Milde, Olaf Witt, Anders M. Lindroth, Jeremy Schwartzentruber, Damien Faury, Adam Fleming, Magdalena Zakrzewska, Pawel P. Liberski, Krzysztof Zakrzewski, Peter Hauser, Miklos Garami, Almos Klekner, Laszlo Bognar, Sorana Morrissy, Florence Cavalli, Michael D. Taylor, Peter van Sluis, Jan Koster, Rogier Versteeg, Richard Volckmann, Tom Mikkelsen, Kenneth Aldape, Guido Reifenberger, V. Peter Collins, Jacek Majewski, Andrey Korshunov, Peter Lichter, Christoph Plass, Nada Jabado, Stefan M. Pfister
Dátum:	2012
ISSN:	1535-6108
Megjegyzések:	Glioblastoma (GBM) is a brain tumor that carries a dismal prognosis and displays considerable heterogeneity. We have recently identified recurrent H3F3A mutations affecting two critical amino acids (K27 and G34) of histone H3.3 in one-third of pediatric GBM. Here, we show that each H3F3A mutation defines an epigenetic subgroup of GBM with a distinct global methylation pattern, and that they are mutually exclusive with IDH1 mutations, which characterize a third mutation-defined subgroup. Three further epigenetic subgroups were enriched for hallmark genetic events of adult GBM and/or established transcriptomic signatures. We also demonstrate that the two H3F3A mutations give rise to GBMs in separate anatomic compartments, with differential regulation of transcription factors OLIG1, OLIG2, and FOXG1, possibly reflecting different cellular origins.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban külföldön készült közlemény
Megjelenés:	Cancer Cell. - 22 : 4 (2012), p. 425-437. -
További szerzők:	Witt, Hendrik Hovestadt, Volker Khuong-Quang, Dong-Anh Jones, David T. W. Konermann, Carolin Pfaff, Elke Tönjes, Martje Sill, Martin Bender, Sebastian Kool, Marcel Zapatka, Marc Becker, Natalia Zucknick, Manuela Hielscher, Thomas Liu, Xiao-Yang Fontebasso, Adam M. Ryzhova, Marina Albrecht, Stephen Jacob, Karine Wolter, Marietta Ebinger, Martin Schuhmann, Martin U. van Meter, Timothy E. Frühwald, Michael C. Hauch, Holger Pekrun, Arnulf Radlwimmer, Bernhard Niehues, Tim von Komorowski, Gregor Dürken, Matthias Kulozik, Andreas E. Madden, Jenny Donson, Andrew Foreman, Nicholas K. Drissi, Rachid Fouladi, Maryam Scheurlen, Wolfram von Deimling, Andreas Monoranu, Camelia Roggendorf, Wolfgang Herold-Mende, Christel Unterberg, Andreas Kramm, Christoph Felsberg, Jörg Hartmann, Christian Wiestler, Benedikt Wick, Wolfgang Milde, Till Witt, Olaf Lindroth, Anders Schwartzentruber, Jeremy Faury, Damien Fleming, Adam Zakrzewska, Magdalena Liberski, Pawel P. Zakrzewski, Krzystof Hauser Péter Garami Miklós Klekner Álmos (1970-) (idegsebész) Bognár László (1958-) (idegsebész, gyermekidegsebész) Morrissy, Sorana Cavalli, Florence Taylor, Michael D. van Sluis, Peter Koster, Jan Versteeg, Rogier Volckmann, Richard Mikkelsen, Tom Aldape, Kenneth Reifenberger, Guido Collins, V. Peter Majewski, Jacek Korshunov, Andrey Lichter, Peter Plass, Christoph Jabado, Nada Pfister, Stefan M.
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