TY  - JOUR
AU  - Johann, Pascal
AU  - Erkek, Serap
AU  - Zapatka, Marc
AU  - Kerl, Kornelius
AU  - Buchhalter, Ivo
AU  - Hovestadt, Volker
AU  - Jones, David
AU  - Sturm, Dominik
AU  - Hermann, Carl
AU  - Segura Wang, Maia
AU  - Korshunov, Andrey
AU  - Rhyzova, Marina
AU  - Gröbner, Susanne
AU  - Brabetz, Sebastian
AU  - Chavez, Lukas
AU  - Bens, Susanne
AU  - Gröschel, Stefan
AU  - Kratochwil, Fabian
AU  - Wittmann, Andrea
AU  - Sieber, Laura
AU  - Geörg, Christina
AU  - Wolf, Stefan
AU  - Beck, Katja
AU  - Oyen, Florian
AU  - Capper, David
AU  - van Sluis, Peter
AU  - Volckmann, Richard
AU  - Koster, Jan
AU  - Versteeg, Rogier
AU  - von Deimling, Andreas
AU  - Milde, Till
AU  - Witt, Olaf
AU  - Kulozik, Andreas E
AU  - Ebinger, Martin
AU  - Shalaby, Tarek
AU  - Grotzer, Michael
AU  - Sumerauer, David
AU  - Zamecnik, Josef
AU  - Mora, Jaume
AU  - Jabado, Nada
AU  - Taylor, Michael D
AU  - Huang, Annie
AU  - Aronica, Eleonora
AU  - Bertoni, Anna
AU  - Radlwimmer, Bernhard
AU  - Pietsch, Torsten
AU  - Schüller, Ulrich
AU  - Schneppenheim, Reinhard
AU  - Northcott, Paul A
AU  - Korbel, Jan O
AU  - Siebert, Reiner
AU  - Frühwald, Michael C
AU  - Lichter, Peter
AU  - Eils, Roland
AU  - Gajjar, Amar
AU  - Hasselblatt, Martin
AU  - Pfister, Stefan
AU  - Kool, Marcel
TI  - Atypical Teratoid/Rhabdoid Tumors Are Comprised of Three Epigenetic Subgroups with Distinct Enhancer Landscapes.
JO  - Cancer cell
VL  - 29
IS  - 3
SN  - 1535-6108
CY  - Cambridge, Mass.
PB  - Cell Press
M1  - DKFZ-2017-04858
SP  - 379 - 393
PY  - 2016
AB  - Atypical teratoid/rhabdoid tumor (ATRT) is one of the most common brain tumors in infants. Although the prognosis of ATRT patients is poor, some patients respond favorably to current treatments, suggesting molecular inter-tumor heterogeneity. To investigate this further, we genetically and epigenetically analyzed 192 ATRTs. Three distinct molecular subgroups of ATRTs, associated with differences in demographics, tumor location, and type of SMARCB1 alterations, were identified. Whole-genome DNA and RNA sequencing found no recurrent mutations in addition to SMARCB1 that would explain the differences between subgroups. Whole-genome bisulfite sequencing and H3K27Ac chromatin-immunoprecipitation sequencing of primary tumors, however, revealed clear differences, leading to the identification of subgroup-specific regulatory networks and potential therapeutic targets.
KW  - Chromosomal Proteins, Non-Histone (NLM Chemicals)
KW  - DNA-Binding Proteins (NLM Chemicals)
KW  - SMARCB1 Protein (NLM Chemicals)
KW  - SMARCB1 protein, human (NLM Chemicals)
KW  - Transcription Factors (NLM Chemicals)
LB  - PUB:(DE-HGF)16
C6  - pmid:26923874
DO  - DOI:10.1016/j.ccell.2016.02.001
UR  - https://inrepo02.dkfz.de/record/128845
ER  -