H3-/IDH-wild type pediatric glioblastoma is comprised of molecularly and prognostically distinct subtypes with associated oncogenic drivers
Pediatric glioblastoma (pedGBM) is an extremely aggressive pediatric brain tumor, accounting for ~6% of all central nervous system neoplasms in children. Approximately half of pedGBM harbor recurrent somatic mutations in histone 3 variants or, infrequently, IDH1/2. The remaining subset of pedGBM is...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Korshunov, Andrey [verfasserIn] Schrimpf, Daniel - 1984- [verfasserIn] Sturm, Dominik - 1983- [verfasserIn] Hovestadt, Volker [verfasserIn] Habel, Antje [verfasserIn] Capper, David - 1979- [verfasserIn] Deimling, Andreas von - 1959- [verfasserIn] Pfister, Stefan - 1974- [verfasserIn] Jones, David T. W. [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
11 April 2017 |
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| Schlagwörter: |
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| Anmerkung: |
Gesehen am 25.10.2018 Im Titel ist die 3 in H3-/IDH tiefgestellt |
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| Umfang: |
10 |
| Übergeordnetes Werk: |
Enthalten in: Acta neuropathologica - Berlin : Springer, 1961, 134(2017), 3, Seite 507-516 |
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| Übergeordnetes Werk: |
volume:134 ; year:2017 ; number:3 ; pages:507-516 ; extent:10 |
| Links: |
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| DOI / URN: |
10.1007/s00401-017-1710-1 |
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| Katalog-ID: |
1582276145 |
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| 245 | 1 | 0 | |a H3-/IDH-wild type pediatric glioblastoma is comprised of molecularly and prognostically distinct subtypes with associated oncogenic drivers |c Andrey Korshunov, Daniel Schrimpf, Marina Ryzhova, Dominik Sturm, Lukas Chavez, Volker Hovestadt, Tanvi Sharma, Antje Habel, Anna Burford, Chris Jones, Olga Zheludkova, Ella Kumirova, Christof M. Kramm, Andrey Golanov, David Capper, Andreas von Deimling, Stefan M. Pfister, David T. W. Jones |
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| 500 | |a Im Titel ist die 3 in H3-/IDH tiefgestellt | ||
| 520 | |a Pediatric glioblastoma (pedGBM) is an extremely aggressive pediatric brain tumor, accounting for ~6% of all central nervous system neoplasms in children. Approximately half of pedGBM harbor recurrent somatic mutations in histone 3 variants or, infrequently, IDH1/2. The remaining subset of pedGBM is highly heterogeneous, and displays a variety of genomic and epigenetic features. In the current study, we aimed to further stratify an H3-/IDH-wild type (wt) pedGBM cohort assessed through genome-wide molecular profiling. As a result, we identified three molecular subtypes of these tumors, differing in their genomic and epigenetic signatures as well as in their clinical behavior. We designated these subtypes ‘pedGBM_MYCN’ (enriched for MYCN amplification), ‘pedGBM_RTK1’ (enriched for PDGFRA amplification) and ‘pedGBM_RTK2’ (enriched for EGFR amplification). These molecular subtypes were associated with significantly different outcomes, i.e. pedGBM_RTK2 tumors show a significantly longer survival time (median OS 44 months), pedGBM_MYCN display extremely poor outcomes (median OS 14 months), and pedGBM_RTK1 tumors harbor an intermediate prognosis. In addition, the various molecular subtypes of H3-/IDH-wt pedGBM were clearly distinguishable from their adult counterparts, underlining their biological distinctiveness. In conclusion, our study demonstrates significant molecular heterogeneity of H3-/IDH-wt pedGBM in terms of DNA methylation and cytogenetic alterations. The recognition of three molecular subtypes of H3-/IDH-wt pedGBM further revealed close correlations with biological parameters and clinical outcomes and may therefore, be predictive of response to standard treatment protocols, but could also be useful for stratification for novel, molecularly based therapies. | ||
| 650 | 4 | |a Brain tumor | |
| 650 | 4 | |a EGFR | |
| 650 | 4 | |a Glioblastoma | |
| 650 | 4 | |a Methylation | |
| 650 | 4 | |a MYCN | |
| 650 | 4 | |a PDGFRA | |
| 650 | 4 | |a Pediatric | |
| 650 | 4 | |a Prognostic | |
| 650 | 4 | |a RTK | |
| 650 | 4 | |a Subgroup | |
| 650 | 4 | |a Survival | |
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| 700 | 1 | |a Jones, David T. W. |e verfasserin |0 (DE-588)1058669672 |0 (DE-627)79739334X |0 (DE-576)414823583 |4 aut | |
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10.1007/s00401-017-1710-1 doi (DE-627)1582276145 (DE-576)512276145 (DE-599)BSZ512276145 (OCoLC)1341020375 DE-627 ger DE-627 rda eng Korshunov, Andrey verfasserin (DE-588)1043235361 (DE-627)770439365 (DE-576)394592093 aut H3-/IDH-wild type pediatric glioblastoma is comprised of molecularly and prognostically distinct subtypes with associated oncogenic drivers Andrey Korshunov, Daniel Schrimpf, Marina Ryzhova, Dominik Sturm, Lukas Chavez, Volker Hovestadt, Tanvi Sharma, Antje Habel, Anna Burford, Chris Jones, Olga Zheludkova, Ella Kumirova, Christof M. Kramm, Andrey Golanov, David Capper, Andreas von Deimling, Stefan M. Pfister, David T. W. Jones H 3 - / IDH 11 April 2017 10 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Gesehen am 25.10.2018 Im Titel ist die 3 in H3-/IDH tiefgestellt Pediatric glioblastoma (pedGBM) is an extremely aggressive pediatric brain tumor, accounting for ~6% of all central nervous system neoplasms in children. Approximately half of pedGBM harbor recurrent somatic mutations in histone 3 variants or, infrequently, IDH1/2. The remaining subset of pedGBM is highly heterogeneous, and displays a variety of genomic and epigenetic features. In the current study, we aimed to further stratify an H3-/IDH-wild type (wt) pedGBM cohort assessed through genome-wide molecular profiling. As a result, we identified three molecular subtypes of these tumors, differing in their genomic and epigenetic signatures as well as in their clinical behavior. We designated these subtypes ‘pedGBM_MYCN’ (enriched for MYCN amplification), ‘pedGBM_RTK1’ (enriched for PDGFRA amplification) and ‘pedGBM_RTK2’ (enriched for EGFR amplification). These molecular subtypes were associated with significantly different outcomes, i.e. pedGBM_RTK2 tumors show a significantly longer survival time (median OS 44 months), pedGBM_MYCN display extremely poor outcomes (median OS 14 months), and pedGBM_RTK1 tumors harbor an intermediate prognosis. In addition, the various molecular subtypes of H3-/IDH-wt pedGBM were clearly distinguishable from their adult counterparts, underlining their biological distinctiveness. In conclusion, our study demonstrates significant molecular heterogeneity of H3-/IDH-wt pedGBM in terms of DNA methylation and cytogenetic alterations. The recognition of three molecular subtypes of H3-/IDH-wt pedGBM further revealed close correlations with biological parameters and clinical outcomes and may therefore, be predictive of response to standard treatment protocols, but could also be useful for stratification for novel, molecularly based therapies. Brain tumor EGFR Glioblastoma Methylation MYCN PDGFRA Pediatric Prognostic RTK Subgroup Survival Schrimpf, Daniel 1984- verfasserin (DE-588)1063355044 (DE-627)812332032 (DE-576)422629529 aut Sturm, Dominik 1983- verfasserin (DE-588)1035550709 (DE-627)749549165 (DE-576)383282144 aut Hovestadt, Volker verfasserin (DE-588)1075291089 (DE-627)833134264 (DE-576)443370516 aut Habel, Antje verfasserin (DE-588)1052052592 (DE-627)787626570 (DE-576)407787186 aut Capper, David 1979- verfasserin (DE-588)133950751 (DE-627)558829902 (DE-576)300212402 aut Deimling, Andreas von 1959- verfasserin (DE-588)103034115X (DE-627)735093946 (DE-576)378138065 aut Pfister, Stefan 1974- verfasserin (DE-588)123850215 (DE-627)706450930 (DE-576)293908400 aut Jones, David T. W. verfasserin (DE-588)1058669672 (DE-627)79739334X (DE-576)414823583 aut Enthalten in Acta neuropathologica Berlin : Springer, 1961 134(2017), 3, Seite 507-516 Online-Ressource (DE-627)253389666 (DE-600)1458410-4 (DE-576)072283092 1432-0533 nnns volume:134 year:2017 number:3 pages:507-516 extent:10 http://dx.doi.org/10.1007/s00401-017-1710-1 Verlag Resolving-System Volltext https://doi.org/10.1007/s00401-017-1710-1 Verlag Volltext GBV_USEFLAG_U GBV_ILN_2013 ISIL_DE-16-250 SYSFLAG_1 GBV_KXP GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 134 2017 3 507-516 10 2013 01 DE-16-250 3029664384 00 --%%-- --%%-- --%%-- --%%-- l01 25-10-18 2013 01 DE-16-250 00 s hd2017 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_18 2013 01 DE-16-250 03 s s_10 2013 01 DE-16-250 04 p (DE-627)1464592632 Korshunov, Andrey 2013 01 DE-16-250 04 k (DE-627)1416740686 Klinikum der Universität Heidelberg 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_1 2013 01 DE-16-250 05 p (DE-627)1546527052 Schrimpf, Daniel 2013 01 DE-16-250 05 k (DE-627)1416741658 Pathologisches Institut 2013 01 DE-16-250 05 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 05 s pos_2 2013 01 DE-16-250 06 p (DE-627)1465968652 Sturm, Dominik 2013 01 DE-16-250 06 k (DE-627)1416740988 Zentrum für Kinder- und Jugendmedizin 2013 01 DE-16-250 06 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 06 s pos_4 2013 01 DE-16-250 07 p (DE-627)1515166457 Hovestadt, Volker 2013 01 DE-16-250 07 k (DE-627)1416822720 Extern 2013 01 DE-16-250 07 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 07 s pos_6 2013 01 DE-16-250 08 p (DE-627)1477787410 Habel, Antje 2013 01 DE-16-250 08 k (DE-627)1416741658 Pathologisches Institut 2013 01 DE-16-250 08 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 08 s pos_8 2013 01 DE-16-250 09 p (DE-627)1461348226 Capper, David 2013 01 DE-16-250 09 k (DE-627)1416822720 Extern 2013 01 DE-16-250 09 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 09 s pos_15 2013 01 DE-16-250 10 p (DE-627)1448137985 Deimling, Andreas von 2013 01 DE-16-250 10 k (DE-627)1416741658 Pathologisches Institut 2013 01 DE-16-250 10 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 10 s pos_16 2013 01 DE-16-250 11 p (DE-627)1464593051 Pfister, Stefan 2013 01 DE-16-250 11 k (DE-627)1416740988 Zentrum für Kinder- und Jugendmedizin 2013 01 DE-16-250 11 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 11 s pos_17 2013 01 DE-16-250 12 p (DE-627)1484823737 Jones, David T. W. 2013 01 DE-16-250 12 k (DE-627)1416466967 Medizinische Fakultät Heidelberg 2013 01 DE-16-250 12 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 12 s pos_18 |
| spelling |
10.1007/s00401-017-1710-1 doi (DE-627)1582276145 (DE-576)512276145 (DE-599)BSZ512276145 (OCoLC)1341020375 DE-627 ger DE-627 rda eng Korshunov, Andrey verfasserin (DE-588)1043235361 (DE-627)770439365 (DE-576)394592093 aut H3-/IDH-wild type pediatric glioblastoma is comprised of molecularly and prognostically distinct subtypes with associated oncogenic drivers Andrey Korshunov, Daniel Schrimpf, Marina Ryzhova, Dominik Sturm, Lukas Chavez, Volker Hovestadt, Tanvi Sharma, Antje Habel, Anna Burford, Chris Jones, Olga Zheludkova, Ella Kumirova, Christof M. Kramm, Andrey Golanov, David Capper, Andreas von Deimling, Stefan M. Pfister, David T. W. Jones H 3 - / IDH 11 April 2017 10 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Gesehen am 25.10.2018 Im Titel ist die 3 in H3-/IDH tiefgestellt Pediatric glioblastoma (pedGBM) is an extremely aggressive pediatric brain tumor, accounting for ~6% of all central nervous system neoplasms in children. Approximately half of pedGBM harbor recurrent somatic mutations in histone 3 variants or, infrequently, IDH1/2. The remaining subset of pedGBM is highly heterogeneous, and displays a variety of genomic and epigenetic features. In the current study, we aimed to further stratify an H3-/IDH-wild type (wt) pedGBM cohort assessed through genome-wide molecular profiling. As a result, we identified three molecular subtypes of these tumors, differing in their genomic and epigenetic signatures as well as in their clinical behavior. We designated these subtypes ‘pedGBM_MYCN’ (enriched for MYCN amplification), ‘pedGBM_RTK1’ (enriched for PDGFRA amplification) and ‘pedGBM_RTK2’ (enriched for EGFR amplification). These molecular subtypes were associated with significantly different outcomes, i.e. pedGBM_RTK2 tumors show a significantly longer survival time (median OS 44 months), pedGBM_MYCN display extremely poor outcomes (median OS 14 months), and pedGBM_RTK1 tumors harbor an intermediate prognosis. In addition, the various molecular subtypes of H3-/IDH-wt pedGBM were clearly distinguishable from their adult counterparts, underlining their biological distinctiveness. In conclusion, our study demonstrates significant molecular heterogeneity of H3-/IDH-wt pedGBM in terms of DNA methylation and cytogenetic alterations. The recognition of three molecular subtypes of H3-/IDH-wt pedGBM further revealed close correlations with biological parameters and clinical outcomes and may therefore, be predictive of response to standard treatment protocols, but could also be useful for stratification for novel, molecularly based therapies. Brain tumor EGFR Glioblastoma Methylation MYCN PDGFRA Pediatric Prognostic RTK Subgroup Survival Schrimpf, Daniel 1984- verfasserin (DE-588)1063355044 (DE-627)812332032 (DE-576)422629529 aut Sturm, Dominik 1983- verfasserin (DE-588)1035550709 (DE-627)749549165 (DE-576)383282144 aut Hovestadt, Volker verfasserin (DE-588)1075291089 (DE-627)833134264 (DE-576)443370516 aut Habel, Antje verfasserin (DE-588)1052052592 (DE-627)787626570 (DE-576)407787186 aut Capper, David 1979- verfasserin (DE-588)133950751 (DE-627)558829902 (DE-576)300212402 aut Deimling, Andreas von 1959- verfasserin (DE-588)103034115X (DE-627)735093946 (DE-576)378138065 aut Pfister, Stefan 1974- verfasserin (DE-588)123850215 (DE-627)706450930 (DE-576)293908400 aut Jones, David T. W. verfasserin (DE-588)1058669672 (DE-627)79739334X (DE-576)414823583 aut Enthalten in Acta neuropathologica Berlin : Springer, 1961 134(2017), 3, Seite 507-516 Online-Ressource (DE-627)253389666 (DE-600)1458410-4 (DE-576)072283092 1432-0533 nnns volume:134 year:2017 number:3 pages:507-516 extent:10 http://dx.doi.org/10.1007/s00401-017-1710-1 Verlag Resolving-System Volltext https://doi.org/10.1007/s00401-017-1710-1 Verlag Volltext GBV_USEFLAG_U GBV_ILN_2013 ISIL_DE-16-250 SYSFLAG_1 GBV_KXP GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 134 2017 3 507-516 10 2013 01 DE-16-250 3029664384 00 --%%-- --%%-- --%%-- --%%-- l01 25-10-18 2013 01 DE-16-250 00 s hd2017 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_18 2013 01 DE-16-250 03 s s_10 2013 01 DE-16-250 04 p (DE-627)1464592632 Korshunov, Andrey 2013 01 DE-16-250 04 k (DE-627)1416740686 Klinikum der Universität Heidelberg 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_1 2013 01 DE-16-250 05 p (DE-627)1546527052 Schrimpf, Daniel 2013 01 DE-16-250 05 k (DE-627)1416741658 Pathologisches Institut 2013 01 DE-16-250 05 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 05 s pos_2 2013 01 DE-16-250 06 p (DE-627)1465968652 Sturm, Dominik 2013 01 DE-16-250 06 k (DE-627)1416740988 Zentrum für Kinder- und Jugendmedizin 2013 01 DE-16-250 06 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 06 s pos_4 2013 01 DE-16-250 07 p (DE-627)1515166457 Hovestadt, Volker 2013 01 DE-16-250 07 k (DE-627)1416822720 Extern 2013 01 DE-16-250 07 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 07 s pos_6 2013 01 DE-16-250 08 p (DE-627)1477787410 Habel, Antje 2013 01 DE-16-250 08 k (DE-627)1416741658 Pathologisches Institut 2013 01 DE-16-250 08 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 08 s pos_8 2013 01 DE-16-250 09 p (DE-627)1461348226 Capper, David 2013 01 DE-16-250 09 k (DE-627)1416822720 Extern 2013 01 DE-16-250 09 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 09 s pos_15 2013 01 DE-16-250 10 p (DE-627)1448137985 Deimling, Andreas von 2013 01 DE-16-250 10 k (DE-627)1416741658 Pathologisches Institut 2013 01 DE-16-250 10 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 10 s pos_16 2013 01 DE-16-250 11 p (DE-627)1464593051 Pfister, Stefan 2013 01 DE-16-250 11 k (DE-627)1416740988 Zentrum für Kinder- und Jugendmedizin 2013 01 DE-16-250 11 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 11 s pos_17 2013 01 DE-16-250 12 p (DE-627)1484823737 Jones, David T. W. 2013 01 DE-16-250 12 k (DE-627)1416466967 Medizinische Fakultät Heidelberg 2013 01 DE-16-250 12 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 12 s pos_18 |
| allfields_unstemmed |
10.1007/s00401-017-1710-1 doi (DE-627)1582276145 (DE-576)512276145 (DE-599)BSZ512276145 (OCoLC)1341020375 DE-627 ger DE-627 rda eng Korshunov, Andrey verfasserin (DE-588)1043235361 (DE-627)770439365 (DE-576)394592093 aut H3-/IDH-wild type pediatric glioblastoma is comprised of molecularly and prognostically distinct subtypes with associated oncogenic drivers Andrey Korshunov, Daniel Schrimpf, Marina Ryzhova, Dominik Sturm, Lukas Chavez, Volker Hovestadt, Tanvi Sharma, Antje Habel, Anna Burford, Chris Jones, Olga Zheludkova, Ella Kumirova, Christof M. Kramm, Andrey Golanov, David Capper, Andreas von Deimling, Stefan M. Pfister, David T. W. Jones H 3 - / IDH 11 April 2017 10 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Gesehen am 25.10.2018 Im Titel ist die 3 in H3-/IDH tiefgestellt Pediatric glioblastoma (pedGBM) is an extremely aggressive pediatric brain tumor, accounting for ~6% of all central nervous system neoplasms in children. Approximately half of pedGBM harbor recurrent somatic mutations in histone 3 variants or, infrequently, IDH1/2. The remaining subset of pedGBM is highly heterogeneous, and displays a variety of genomic and epigenetic features. In the current study, we aimed to further stratify an H3-/IDH-wild type (wt) pedGBM cohort assessed through genome-wide molecular profiling. As a result, we identified three molecular subtypes of these tumors, differing in their genomic and epigenetic signatures as well as in their clinical behavior. We designated these subtypes ‘pedGBM_MYCN’ (enriched for MYCN amplification), ‘pedGBM_RTK1’ (enriched for PDGFRA amplification) and ‘pedGBM_RTK2’ (enriched for EGFR amplification). These molecular subtypes were associated with significantly different outcomes, i.e. pedGBM_RTK2 tumors show a significantly longer survival time (median OS 44 months), pedGBM_MYCN display extremely poor outcomes (median OS 14 months), and pedGBM_RTK1 tumors harbor an intermediate prognosis. In addition, the various molecular subtypes of H3-/IDH-wt pedGBM were clearly distinguishable from their adult counterparts, underlining their biological distinctiveness. In conclusion, our study demonstrates significant molecular heterogeneity of H3-/IDH-wt pedGBM in terms of DNA methylation and cytogenetic alterations. The recognition of three molecular subtypes of H3-/IDH-wt pedGBM further revealed close correlations with biological parameters and clinical outcomes and may therefore, be predictive of response to standard treatment protocols, but could also be useful for stratification for novel, molecularly based therapies. Brain tumor EGFR Glioblastoma Methylation MYCN PDGFRA Pediatric Prognostic RTK Subgroup Survival Schrimpf, Daniel 1984- verfasserin (DE-588)1063355044 (DE-627)812332032 (DE-576)422629529 aut Sturm, Dominik 1983- verfasserin (DE-588)1035550709 (DE-627)749549165 (DE-576)383282144 aut Hovestadt, Volker verfasserin (DE-588)1075291089 (DE-627)833134264 (DE-576)443370516 aut Habel, Antje verfasserin (DE-588)1052052592 (DE-627)787626570 (DE-576)407787186 aut Capper, David 1979- verfasserin (DE-588)133950751 (DE-627)558829902 (DE-576)300212402 aut Deimling, Andreas von 1959- verfasserin (DE-588)103034115X (DE-627)735093946 (DE-576)378138065 aut Pfister, Stefan 1974- verfasserin (DE-588)123850215 (DE-627)706450930 (DE-576)293908400 aut Jones, David T. W. verfasserin (DE-588)1058669672 (DE-627)79739334X (DE-576)414823583 aut Enthalten in Acta neuropathologica Berlin : Springer, 1961 134(2017), 3, Seite 507-516 Online-Ressource (DE-627)253389666 (DE-600)1458410-4 (DE-576)072283092 1432-0533 nnns volume:134 year:2017 number:3 pages:507-516 extent:10 http://dx.doi.org/10.1007/s00401-017-1710-1 Verlag Resolving-System Volltext https://doi.org/10.1007/s00401-017-1710-1 Verlag Volltext GBV_USEFLAG_U GBV_ILN_2013 ISIL_DE-16-250 SYSFLAG_1 GBV_KXP GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 134 2017 3 507-516 10 2013 01 DE-16-250 3029664384 00 --%%-- --%%-- --%%-- --%%-- l01 25-10-18 2013 01 DE-16-250 00 s hd2017 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_18 2013 01 DE-16-250 03 s s_10 2013 01 DE-16-250 04 p (DE-627)1464592632 Korshunov, Andrey 2013 01 DE-16-250 04 k (DE-627)1416740686 Klinikum der Universität Heidelberg 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_1 2013 01 DE-16-250 05 p (DE-627)1546527052 Schrimpf, Daniel 2013 01 DE-16-250 05 k (DE-627)1416741658 Pathologisches Institut 2013 01 DE-16-250 05 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 05 s pos_2 2013 01 DE-16-250 06 p (DE-627)1465968652 Sturm, Dominik 2013 01 DE-16-250 06 k (DE-627)1416740988 Zentrum für Kinder- und Jugendmedizin 2013 01 DE-16-250 06 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 06 s pos_4 2013 01 DE-16-250 07 p (DE-627)1515166457 Hovestadt, Volker 2013 01 DE-16-250 07 k (DE-627)1416822720 Extern 2013 01 DE-16-250 07 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 07 s pos_6 2013 01 DE-16-250 08 p (DE-627)1477787410 Habel, Antje 2013 01 DE-16-250 08 k (DE-627)1416741658 Pathologisches Institut 2013 01 DE-16-250 08 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 08 s pos_8 2013 01 DE-16-250 09 p (DE-627)1461348226 Capper, David 2013 01 DE-16-250 09 k (DE-627)1416822720 Extern 2013 01 DE-16-250 09 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 09 s pos_15 2013 01 DE-16-250 10 p (DE-627)1448137985 Deimling, Andreas von 2013 01 DE-16-250 10 k (DE-627)1416741658 Pathologisches Institut 2013 01 DE-16-250 10 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 10 s pos_16 2013 01 DE-16-250 11 p (DE-627)1464593051 Pfister, Stefan 2013 01 DE-16-250 11 k (DE-627)1416740988 Zentrum für Kinder- und Jugendmedizin 2013 01 DE-16-250 11 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 11 s pos_17 2013 01 DE-16-250 12 p (DE-627)1484823737 Jones, David T. W. 2013 01 DE-16-250 12 k (DE-627)1416466967 Medizinische Fakultät Heidelberg 2013 01 DE-16-250 12 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 12 s pos_18 |
| allfieldsGer |
10.1007/s00401-017-1710-1 doi (DE-627)1582276145 (DE-576)512276145 (DE-599)BSZ512276145 (OCoLC)1341020375 DE-627 ger DE-627 rda eng Korshunov, Andrey verfasserin (DE-588)1043235361 (DE-627)770439365 (DE-576)394592093 aut H3-/IDH-wild type pediatric glioblastoma is comprised of molecularly and prognostically distinct subtypes with associated oncogenic drivers Andrey Korshunov, Daniel Schrimpf, Marina Ryzhova, Dominik Sturm, Lukas Chavez, Volker Hovestadt, Tanvi Sharma, Antje Habel, Anna Burford, Chris Jones, Olga Zheludkova, Ella Kumirova, Christof M. Kramm, Andrey Golanov, David Capper, Andreas von Deimling, Stefan M. Pfister, David T. W. Jones H 3 - / IDH 11 April 2017 10 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Gesehen am 25.10.2018 Im Titel ist die 3 in H3-/IDH tiefgestellt Pediatric glioblastoma (pedGBM) is an extremely aggressive pediatric brain tumor, accounting for ~6% of all central nervous system neoplasms in children. Approximately half of pedGBM harbor recurrent somatic mutations in histone 3 variants or, infrequently, IDH1/2. The remaining subset of pedGBM is highly heterogeneous, and displays a variety of genomic and epigenetic features. In the current study, we aimed to further stratify an H3-/IDH-wild type (wt) pedGBM cohort assessed through genome-wide molecular profiling. As a result, we identified three molecular subtypes of these tumors, differing in their genomic and epigenetic signatures as well as in their clinical behavior. We designated these subtypes ‘pedGBM_MYCN’ (enriched for MYCN amplification), ‘pedGBM_RTK1’ (enriched for PDGFRA amplification) and ‘pedGBM_RTK2’ (enriched for EGFR amplification). These molecular subtypes were associated with significantly different outcomes, i.e. pedGBM_RTK2 tumors show a significantly longer survival time (median OS 44 months), pedGBM_MYCN display extremely poor outcomes (median OS 14 months), and pedGBM_RTK1 tumors harbor an intermediate prognosis. In addition, the various molecular subtypes of H3-/IDH-wt pedGBM were clearly distinguishable from their adult counterparts, underlining their biological distinctiveness. In conclusion, our study demonstrates significant molecular heterogeneity of H3-/IDH-wt pedGBM in terms of DNA methylation and cytogenetic alterations. The recognition of three molecular subtypes of H3-/IDH-wt pedGBM further revealed close correlations with biological parameters and clinical outcomes and may therefore, be predictive of response to standard treatment protocols, but could also be useful for stratification for novel, molecularly based therapies. Brain tumor EGFR Glioblastoma Methylation MYCN PDGFRA Pediatric Prognostic RTK Subgroup Survival Schrimpf, Daniel 1984- verfasserin (DE-588)1063355044 (DE-627)812332032 (DE-576)422629529 aut Sturm, Dominik 1983- verfasserin (DE-588)1035550709 (DE-627)749549165 (DE-576)383282144 aut Hovestadt, Volker verfasserin (DE-588)1075291089 (DE-627)833134264 (DE-576)443370516 aut Habel, Antje verfasserin (DE-588)1052052592 (DE-627)787626570 (DE-576)407787186 aut Capper, David 1979- verfasserin (DE-588)133950751 (DE-627)558829902 (DE-576)300212402 aut Deimling, Andreas von 1959- verfasserin (DE-588)103034115X (DE-627)735093946 (DE-576)378138065 aut Pfister, Stefan 1974- verfasserin (DE-588)123850215 (DE-627)706450930 (DE-576)293908400 aut Jones, David T. W. verfasserin (DE-588)1058669672 (DE-627)79739334X (DE-576)414823583 aut Enthalten in Acta neuropathologica Berlin : Springer, 1961 134(2017), 3, Seite 507-516 Online-Ressource (DE-627)253389666 (DE-600)1458410-4 (DE-576)072283092 1432-0533 nnns volume:134 year:2017 number:3 pages:507-516 extent:10 http://dx.doi.org/10.1007/s00401-017-1710-1 Verlag Resolving-System Volltext https://doi.org/10.1007/s00401-017-1710-1 Verlag Volltext GBV_USEFLAG_U GBV_ILN_2013 ISIL_DE-16-250 SYSFLAG_1 GBV_KXP GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 134 2017 3 507-516 10 2013 01 DE-16-250 3029664384 00 --%%-- --%%-- --%%-- --%%-- l01 25-10-18 2013 01 DE-16-250 00 s hd2017 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_18 2013 01 DE-16-250 03 s s_10 2013 01 DE-16-250 04 p (DE-627)1464592632 Korshunov, Andrey 2013 01 DE-16-250 04 k (DE-627)1416740686 Klinikum der Universität Heidelberg 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_1 2013 01 DE-16-250 05 p (DE-627)1546527052 Schrimpf, Daniel 2013 01 DE-16-250 05 k (DE-627)1416741658 Pathologisches Institut 2013 01 DE-16-250 05 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 05 s pos_2 2013 01 DE-16-250 06 p (DE-627)1465968652 Sturm, Dominik 2013 01 DE-16-250 06 k (DE-627)1416740988 Zentrum für Kinder- und Jugendmedizin 2013 01 DE-16-250 06 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 06 s pos_4 2013 01 DE-16-250 07 p (DE-627)1515166457 Hovestadt, Volker 2013 01 DE-16-250 07 k (DE-627)1416822720 Extern 2013 01 DE-16-250 07 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 07 s pos_6 2013 01 DE-16-250 08 p (DE-627)1477787410 Habel, Antje 2013 01 DE-16-250 08 k (DE-627)1416741658 Pathologisches Institut 2013 01 DE-16-250 08 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 08 s pos_8 2013 01 DE-16-250 09 p (DE-627)1461348226 Capper, David 2013 01 DE-16-250 09 k (DE-627)1416822720 Extern 2013 01 DE-16-250 09 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 09 s pos_15 2013 01 DE-16-250 10 p (DE-627)1448137985 Deimling, Andreas von 2013 01 DE-16-250 10 k (DE-627)1416741658 Pathologisches Institut 2013 01 DE-16-250 10 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 10 s pos_16 2013 01 DE-16-250 11 p (DE-627)1464593051 Pfister, Stefan 2013 01 DE-16-250 11 k (DE-627)1416740988 Zentrum für Kinder- und Jugendmedizin 2013 01 DE-16-250 11 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 11 s pos_17 2013 01 DE-16-250 12 p (DE-627)1484823737 Jones, David T. W. 2013 01 DE-16-250 12 k (DE-627)1416466967 Medizinische Fakultät Heidelberg 2013 01 DE-16-250 12 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 12 s pos_18 |
| allfieldsSound |
10.1007/s00401-017-1710-1 doi (DE-627)1582276145 (DE-576)512276145 (DE-599)BSZ512276145 (OCoLC)1341020375 DE-627 ger DE-627 rda eng Korshunov, Andrey verfasserin (DE-588)1043235361 (DE-627)770439365 (DE-576)394592093 aut H3-/IDH-wild type pediatric glioblastoma is comprised of molecularly and prognostically distinct subtypes with associated oncogenic drivers Andrey Korshunov, Daniel Schrimpf, Marina Ryzhova, Dominik Sturm, Lukas Chavez, Volker Hovestadt, Tanvi Sharma, Antje Habel, Anna Burford, Chris Jones, Olga Zheludkova, Ella Kumirova, Christof M. Kramm, Andrey Golanov, David Capper, Andreas von Deimling, Stefan M. Pfister, David T. W. Jones H 3 - / IDH 11 April 2017 10 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Gesehen am 25.10.2018 Im Titel ist die 3 in H3-/IDH tiefgestellt Pediatric glioblastoma (pedGBM) is an extremely aggressive pediatric brain tumor, accounting for ~6% of all central nervous system neoplasms in children. Approximately half of pedGBM harbor recurrent somatic mutations in histone 3 variants or, infrequently, IDH1/2. The remaining subset of pedGBM is highly heterogeneous, and displays a variety of genomic and epigenetic features. In the current study, we aimed to further stratify an H3-/IDH-wild type (wt) pedGBM cohort assessed through genome-wide molecular profiling. As a result, we identified three molecular subtypes of these tumors, differing in their genomic and epigenetic signatures as well as in their clinical behavior. We designated these subtypes ‘pedGBM_MYCN’ (enriched for MYCN amplification), ‘pedGBM_RTK1’ (enriched for PDGFRA amplification) and ‘pedGBM_RTK2’ (enriched for EGFR amplification). These molecular subtypes were associated with significantly different outcomes, i.e. pedGBM_RTK2 tumors show a significantly longer survival time (median OS 44 months), pedGBM_MYCN display extremely poor outcomes (median OS 14 months), and pedGBM_RTK1 tumors harbor an intermediate prognosis. In addition, the various molecular subtypes of H3-/IDH-wt pedGBM were clearly distinguishable from their adult counterparts, underlining their biological distinctiveness. In conclusion, our study demonstrates significant molecular heterogeneity of H3-/IDH-wt pedGBM in terms of DNA methylation and cytogenetic alterations. The recognition of three molecular subtypes of H3-/IDH-wt pedGBM further revealed close correlations with biological parameters and clinical outcomes and may therefore, be predictive of response to standard treatment protocols, but could also be useful for stratification for novel, molecularly based therapies. Brain tumor EGFR Glioblastoma Methylation MYCN PDGFRA Pediatric Prognostic RTK Subgroup Survival Schrimpf, Daniel 1984- verfasserin (DE-588)1063355044 (DE-627)812332032 (DE-576)422629529 aut Sturm, Dominik 1983- verfasserin (DE-588)1035550709 (DE-627)749549165 (DE-576)383282144 aut Hovestadt, Volker verfasserin (DE-588)1075291089 (DE-627)833134264 (DE-576)443370516 aut Habel, Antje verfasserin (DE-588)1052052592 (DE-627)787626570 (DE-576)407787186 aut Capper, David 1979- verfasserin (DE-588)133950751 (DE-627)558829902 (DE-576)300212402 aut Deimling, Andreas von 1959- verfasserin (DE-588)103034115X (DE-627)735093946 (DE-576)378138065 aut Pfister, Stefan 1974- verfasserin (DE-588)123850215 (DE-627)706450930 (DE-576)293908400 aut Jones, David T. 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Korshunov, Andrey @@aut@@ Schrimpf, Daniel @@aut@@ Sturm, Dominik @@aut@@ Hovestadt, Volker @@aut@@ Habel, Antje @@aut@@ Capper, David @@aut@@ Deimling, Andreas von @@aut@@ Pfister, Stefan @@aut@@ Jones, David T. W. @@aut@@ |
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H3-/IDH-wild type pediatric glioblastoma is comprised of molecularly and prognostically distinct subtypes with associated oncogenic drivers Andrey Korshunov, Daniel Schrimpf, Marina Ryzhova, Dominik Sturm, Lukas Chavez, Volker Hovestadt, Tanvi Sharma, Antje Habel, Anna Burford, Chris Jones, Olga Zheludkova, Ella Kumirova, Christof M. Kramm, Andrey Golanov, David Capper, Andreas von Deimling, Stefan M. Pfister, David T. W. Jones |
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h3-/idh-wild type pediatric glioblastoma is comprised of molecularly and prognostically distinct subtypes with associated oncogenic drivers |
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H3-/IDH-wild type pediatric glioblastoma is comprised of molecularly and prognostically distinct subtypes with associated oncogenic drivers |
| abstract |
Pediatric glioblastoma (pedGBM) is an extremely aggressive pediatric brain tumor, accounting for ~6% of all central nervous system neoplasms in children. Approximately half of pedGBM harbor recurrent somatic mutations in histone 3 variants or, infrequently, IDH1/2. The remaining subset of pedGBM is highly heterogeneous, and displays a variety of genomic and epigenetic features. In the current study, we aimed to further stratify an H3-/IDH-wild type (wt) pedGBM cohort assessed through genome-wide molecular profiling. As a result, we identified three molecular subtypes of these tumors, differing in their genomic and epigenetic signatures as well as in their clinical behavior. We designated these subtypes ‘pedGBM_MYCN’ (enriched for MYCN amplification), ‘pedGBM_RTK1’ (enriched for PDGFRA amplification) and ‘pedGBM_RTK2’ (enriched for EGFR amplification). These molecular subtypes were associated with significantly different outcomes, i.e. pedGBM_RTK2 tumors show a significantly longer survival time (median OS 44 months), pedGBM_MYCN display extremely poor outcomes (median OS 14 months), and pedGBM_RTK1 tumors harbor an intermediate prognosis. In addition, the various molecular subtypes of H3-/IDH-wt pedGBM were clearly distinguishable from their adult counterparts, underlining their biological distinctiveness. In conclusion, our study demonstrates significant molecular heterogeneity of H3-/IDH-wt pedGBM in terms of DNA methylation and cytogenetic alterations. The recognition of three molecular subtypes of H3-/IDH-wt pedGBM further revealed close correlations with biological parameters and clinical outcomes and may therefore, be predictive of response to standard treatment protocols, but could also be useful for stratification for novel, molecularly based therapies. Gesehen am 25.10.2018 Im Titel ist die 3 in H3-/IDH tiefgestellt |
| abstractGer |
Pediatric glioblastoma (pedGBM) is an extremely aggressive pediatric brain tumor, accounting for ~6% of all central nervous system neoplasms in children. Approximately half of pedGBM harbor recurrent somatic mutations in histone 3 variants or, infrequently, IDH1/2. The remaining subset of pedGBM is highly heterogeneous, and displays a variety of genomic and epigenetic features. In the current study, we aimed to further stratify an H3-/IDH-wild type (wt) pedGBM cohort assessed through genome-wide molecular profiling. As a result, we identified three molecular subtypes of these tumors, differing in their genomic and epigenetic signatures as well as in their clinical behavior. We designated these subtypes ‘pedGBM_MYCN’ (enriched for MYCN amplification), ‘pedGBM_RTK1’ (enriched for PDGFRA amplification) and ‘pedGBM_RTK2’ (enriched for EGFR amplification). These molecular subtypes were associated with significantly different outcomes, i.e. pedGBM_RTK2 tumors show a significantly longer survival time (median OS 44 months), pedGBM_MYCN display extremely poor outcomes (median OS 14 months), and pedGBM_RTK1 tumors harbor an intermediate prognosis. In addition, the various molecular subtypes of H3-/IDH-wt pedGBM were clearly distinguishable from their adult counterparts, underlining their biological distinctiveness. In conclusion, our study demonstrates significant molecular heterogeneity of H3-/IDH-wt pedGBM in terms of DNA methylation and cytogenetic alterations. The recognition of three molecular subtypes of H3-/IDH-wt pedGBM further revealed close correlations with biological parameters and clinical outcomes and may therefore, be predictive of response to standard treatment protocols, but could also be useful for stratification for novel, molecularly based therapies. Gesehen am 25.10.2018 Im Titel ist die 3 in H3-/IDH tiefgestellt |
| abstract_unstemmed |
Pediatric glioblastoma (pedGBM) is an extremely aggressive pediatric brain tumor, accounting for ~6% of all central nervous system neoplasms in children. Approximately half of pedGBM harbor recurrent somatic mutations in histone 3 variants or, infrequently, IDH1/2. The remaining subset of pedGBM is highly heterogeneous, and displays a variety of genomic and epigenetic features. In the current study, we aimed to further stratify an H3-/IDH-wild type (wt) pedGBM cohort assessed through genome-wide molecular profiling. As a result, we identified three molecular subtypes of these tumors, differing in their genomic and epigenetic signatures as well as in their clinical behavior. We designated these subtypes ‘pedGBM_MYCN’ (enriched for MYCN amplification), ‘pedGBM_RTK1’ (enriched for PDGFRA amplification) and ‘pedGBM_RTK2’ (enriched for EGFR amplification). These molecular subtypes were associated with significantly different outcomes, i.e. pedGBM_RTK2 tumors show a significantly longer survival time (median OS 44 months), pedGBM_MYCN display extremely poor outcomes (median OS 14 months), and pedGBM_RTK1 tumors harbor an intermediate prognosis. In addition, the various molecular subtypes of H3-/IDH-wt pedGBM were clearly distinguishable from their adult counterparts, underlining their biological distinctiveness. In conclusion, our study demonstrates significant molecular heterogeneity of H3-/IDH-wt pedGBM in terms of DNA methylation and cytogenetic alterations. The recognition of three molecular subtypes of H3-/IDH-wt pedGBM further revealed close correlations with biological parameters and clinical outcomes and may therefore, be predictive of response to standard treatment protocols, but could also be useful for stratification for novel, molecularly based therapies. Gesehen am 25.10.2018 Im Titel ist die 3 in H3-/IDH tiefgestellt |
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H3-/IDH-wild type pediatric glioblastoma is comprised of molecularly and prognostically distinct subtypes with associated oncogenic drivers |
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http://dx.doi.org/10.1007/s00401-017-1710-1 https://doi.org/10.1007/s00401-017-1710-1 |
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Schrimpf, Daniel 1984- Sturm, Dominik 1983- Hovestadt, Volker Habel, Antje Capper, David 1979- Deimling, Andreas von 1959- Pfister, Stefan 1974- Jones, David T. W. |
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Schrimpf, Daniel 1984- Sturm, Dominik 1983- Hovestadt, Volker Habel, Antje Capper, David 1979- Deimling, Andreas von 1959- Pfister, Stefan 1974- Jones, David T. W. |
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Korshunov, A. Korshunov, Andrey Schrimpf, D. Schrimpf, Daniel Sturm, Markus Dominik Sturm, Dominik Hovestadt, Volker Habel, Antje Capper, David Mark Capper, D. Capper, David Deimling, A. von Deimling, Andreas von Pfister, Stefan M. Pfister, Stefan Jones, David T. W. |
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Korshunov, A. Korshunov, Andrey Schrimpf, D. Schrimpf, Daniel Sturm, Markus Dominik Sturm, Dominik Hovestadt, Volker Habel, Antje Capper, David Mark Capper, D. Capper, David Deimling, A. von Deimling, Andreas von Pfister, Stefan M. Pfister, Stefan Jones, David T. W. |
| GND_txtF_mv |
Korshunov, A. Korshunov, Andrey Schrimpf, D. Schrimpf, Daniel Sturm, Markus Dominik Sturm, Dominik Hovestadt, Volker Habel, Antje Capper, David Mark Capper, D. Capper, David Deimling, A. von Deimling, Andreas von Pfister, Stefan M. Pfister, Stefan Jones, David T. W. |
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H 3 - / IDH |
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10.1007/s00401-017-1710-1 |
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2024-07-04T20:21:05.229Z |
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Approximately half of pedGBM harbor recurrent somatic mutations in histone 3 variants or, infrequently, IDH1/2. The remaining subset of pedGBM is highly heterogeneous, and displays a variety of genomic and epigenetic features. In the current study, we aimed to further stratify an H3-/IDH-wild type (wt) pedGBM cohort assessed through genome-wide molecular profiling. As a result, we identified three molecular subtypes of these tumors, differing in their genomic and epigenetic signatures as well as in their clinical behavior. We designated these subtypes ‘pedGBM_MYCN’ (enriched for MYCN amplification), ‘pedGBM_RTK1’ (enriched for PDGFRA amplification) and ‘pedGBM_RTK2’ (enriched for EGFR amplification). These molecular subtypes were associated with significantly different outcomes, i.e. pedGBM_RTK2 tumors show a significantly longer survival time (median OS 44 months), pedGBM_MYCN display extremely poor outcomes (median OS 14 months), and pedGBM_RTK1 tumors harbor an intermediate prognosis. In addition, the various molecular subtypes of H3-/IDH-wt pedGBM were clearly distinguishable from their adult counterparts, underlining their biological distinctiveness. In conclusion, our study demonstrates significant molecular heterogeneity of H3-/IDH-wt pedGBM in terms of DNA methylation and cytogenetic alterations. 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