Atypical Teratoid/Rhabdoid Tumors Are Comprised of Three Epigenetic Subgroups with Distinct Enhancer Landscapes
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Atypical Teratoid/Rhabdoid Tumors Are Comprised of Three Epigenetic Subgroups with Distinct Enhancer Landscapes. / Johann, Pascal D; Erkek, Serap; Zapatka, Marc; Kerl, Kornelius; Buchhalter, Ivo; Hovestadt, Volker; Jones, David T W; Sturm, Dominik; Hermann, Carl; Segura Wang, Maia; Korshunov, Andrey; Rhyzova, Marina; Gröbner, Susanne; Brabetz, Sebastian; Chavez, Lukas; Bens, Susanne; Gröschel, Stefan; Kratochwil, Fabian; Wittmann, Andrea; Sieber, Laura; Geörg, Christina; Wolf, Stefan; Beck, Katja; Oyen, Florian; Capper, David; van Sluis, Peter; Volckmann, Richard; Koster, Jan; Versteeg, Rogier; von Deimling, Andreas; Milde, Till; Witt, Olaf; Kulozik, Andreas E; Ebinger, Martin; Shalaby, Tarek; Grotzer, Michael; Sumerauer, David; Zamecnik, Josef; Mora, Jaume; Jabado, Nada; Taylor, Michael D; Huang, Annie; Aronica, Eleonora; Bertoni, Anna; Radlwimmer, Bernhard; Pietsch, Torsten; Schüller, Ulrich; Schneppenheim, Reinhard; Northcott, Paul A; Korbel, Jan O; Siebert, Reiner; Frühwald, Michael C; Lichter, Peter; Eils, Roland; Gajjar, Amar; Hasselblatt, Martin; Pfister, Stefan M; Kool, Marcel.
In: CANCER CELL, Vol. 29, No. 3, 14.03.2016, p. 379-93.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Atypical Teratoid/Rhabdoid Tumors Are Comprised of Three Epigenetic Subgroups with Distinct Enhancer Landscapes
AU - Johann, Pascal D
AU - Erkek, Serap
AU - Zapatka, Marc
AU - Kerl, Kornelius
AU - Buchhalter, Ivo
AU - Hovestadt, Volker
AU - Jones, David T W
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 M
AU - Kool, Marcel
N1 - Copyright © 2016 Elsevier Inc. All rights reserved.
PY - 2016/3/14
Y1 - 2016/3/14
N2 - 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.
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.
U2 - 10.1016/j.ccell.2016.02.001
DO - 10.1016/j.ccell.2016.02.001
M3 - SCORING: Journal article
C2 - 26923874
VL - 29
SP - 379
EP - 393
JO - CANCER CELL
JF - CANCER CELL
SN - 1535-6108
IS - 3
ER -