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| 041 | _ | _ | |a English |
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| 245 | _ | _ | |a Diffuse pediatric high-grade glioma of methylation-based RTK2A and RTK2B subclasses present distinct radiological and histomolecular features including Gliomatosis cerebri phenotype. |
| 260 | _ | _ | |a London |c 2024 |b Biomed Central |
| 336 | 7 | _ | |a article |2 DRIVER |
| 336 | 7 | _ | |a Output Types/Journal article |2 DataCite |
| 336 | 7 | _ | |a Journal Article |b journal |m journal |0 PUB:(DE-HGF)16 |s 1732113853_5932 |2 PUB:(DE-HGF) |
| 336 | 7 | _ | |a ARTICLE |2 BibTeX |
| 336 | 7 | _ | |a JOURNAL_ARTICLE |2 ORCID |
| 336 | 7 | _ | |a Journal Article |0 0 |2 EndNote |
| 520 | _ | _ | |a Diffuse pediatric-type high-grade gliomas (pedHGG), H3- and IDH-wildtype, encompass three main DNA-methylation-based subtypes: pedHGG-MYCN, pedHGG-RTK1A/B/C, and pedHGG-RTK2A/B. Since their first description in 2017 tumors of pedHGG-RTK2A/B have not been comprehensively characterized and clinical correlates remain elusive. In a recent series of pedHGG with a Gliomatosis cerebri (GC) growth pattern, an increased incidence of pedHGG-RTK2A/B (n = 18) was observed. We added 14 epigenetically defined pedHGG-RTK2A/B tumors to this GC series and provided centrally reviewed radiological, histological, and molecular characterization. The final cohort of 32 pedHGG-RTK2A/B tumors consisted of 25 pedHGG-RTK2A (78%) and seven pedHGG-RTK2B (22%) cases. The median age was 11.6 years (range, 4-17) with a median overall survival of 16.0 months (range 10.9-28.2). Seven of 11 of the newly added cases with imaging available showed a GC phenotype at diagnosis or follow-up. PedHGG-RTK2B tumors exhibited frequent bithalamic involvement (6/7, 86%). Central neuropathology review confirmed a diffuse glial neoplasm in all tumors with prominent angiocentric features in both subclasses. Most tumors (24/27 with available data, 89%) diffusely expressed EGFR with focal angiocentric enhancement. PedHGG-RTK2A tumors lacked OLIG2 expression, whereas 43% (3/7) of pedHGG-RTK2B expressed this glial transcription factor. ATRX loss occurred in 3/6 pedHGG-RTK2B samples with available data (50%). DNA sequencing (pedHGG-RTK2A: n = 18, pedHGG-RTK2B: n = 5) found EGFR alterations (15/23, 65%; predominantly point mutations) in both subclasses. Mutations in BCOR (14/18, 78%), SETD2 (7/18, 39%), and the hTERT promoter (7/19, 37%) occurred exclusively in pedHGG-RTK2A tumors, while pedHGG-RTK2B tumors were enriched for TP53 alterations (4/5, 80%). In conclusion, pedHGG-RTK2A/B tumors are characterized by highly diffuse-infiltrating growth patterns and specific radiological and histo-molecular features. By comprehensively characterizing methylation-based tumors, the chance to develop specific and effective therapy concepts for these detrimental tumors increases. |
| 536 | _ | _ | |a 312 - Funktionelle und strukturelle Genomforschung (POF4-312) |0 G:(DE-HGF)POF4-312 |c POF4-312 |f POF IV |x 0 |
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| 650 | _ | 7 | |a Gliomatosis cerebri |2 Other |
| 650 | _ | 7 | |a Methylation |2 Other |
| 650 | _ | 7 | |a Pediatric high-grade glioma |2 Other |
| 650 | _ | 7 | |a RTK2A |2 Other |
| 650 | _ | 7 | |a RTK2B |2 Other |
| 650 | _ | 7 | |a Receptor tyrosine kinase |2 Other |
| 650 | _ | 7 | |a pedHGG |2 Other |
| 650 | _ | 2 | |a Humans |2 MeSH |
| 650 | _ | 2 | |a Child |2 MeSH |
| 650 | _ | 2 | |a Male |2 MeSH |
| 650 | _ | 2 | |a Female |2 MeSH |
| 650 | _ | 2 | |a Brain Neoplasms: genetics |2 MeSH |
| 650 | _ | 2 | |a Brain Neoplasms: pathology |2 MeSH |
| 650 | _ | 2 | |a Brain Neoplasms: diagnostic imaging |2 MeSH |
| 650 | _ | 2 | |a Adolescent |2 MeSH |
| 650 | _ | 2 | |a Child, Preschool |2 MeSH |
| 650 | _ | 2 | |a Neoplasms, Neuroepithelial: genetics |2 MeSH |
| 650 | _ | 2 | |a Neoplasms, Neuroepithelial: pathology |2 MeSH |
| 650 | _ | 2 | |a Neoplasms, Neuroepithelial: diagnostic imaging |2 MeSH |
| 650 | _ | 2 | |a DNA Methylation |2 MeSH |
| 650 | _ | 2 | |a Glioma: genetics |2 MeSH |
| 650 | _ | 2 | |a Glioma: pathology |2 MeSH |
| 650 | _ | 2 | |a Glioma: diagnostic imaging |2 MeSH |
| 650 | _ | 2 | |a Phenotype |2 MeSH |
| 700 | 1 | _ | |a Friker, Lea L |b 1 |
| 700 | 1 | _ | |a Nussbaumer, Gunther |b 2 |
| 700 | 1 | _ | |a Bison, Brigitte |b 3 |
| 700 | 1 | _ | |a Dangouloff-Ros, Volodia |b 4 |
| 700 | 1 | _ | |a Métais, Alice |b 5 |
| 700 | 1 | _ | |a Sumerauer, David |b 6 |
| 700 | 1 | _ | |a Zamecnik, Josef |b 7 |
| 700 | 1 | _ | |a Benesch, Martin |b 8 |
| 700 | 1 | _ | |a Perwein, Thomas |b 9 |
| 700 | 1 | _ | |a van Vuurden, Dannis |b 10 |
| 700 | 1 | _ | |a Wesseling, Pieter |b 11 |
| 700 | 1 | _ | |a La Madrid, Andrés Morales |b 12 |
| 700 | 1 | _ | |a Garrè, Maria Luisa |b 13 |
| 700 | 1 | _ | |a Antonelli, Manila |b 14 |
| 700 | 1 | _ | |a Giangaspero, Felice |b 15 |
| 700 | 1 | _ | |a Pietsch, Torsten |b 16 |
| 700 | 1 | _ | |a Sturm, Dominik |0 P:(DE-He78)a46a5b2a871859c8e2d63d2f8c666807 |b 17 |u dkfz |
| 700 | 1 | _ | |a Jones, David T W |0 P:(DE-He78)551bb92841f634070997aa168d818492 |b 18 |u dkfz |
| 700 | 1 | _ | |a Pfister, Stefan M |0 P:(DE-He78)f746aa965c4e1af518b016de3aaff5d9 |b 19 |u dkfz |
| 700 | 1 | _ | |a Grabovska, Yura |b 20 |
| 700 | 1 | _ | |a Mackay, Alan |b 21 |
| 700 | 1 | _ | |a Jones, Chris |b 22 |
| 700 | 1 | _ | |a Grill, Jacques |b 23 |
| 700 | 1 | _ | |a Ajlil, Yassine |b 24 |
| 700 | 1 | _ | |a von Bueren, André O |b 25 |
| 700 | 1 | _ | |a Karremann, Michael |b 26 |
| 700 | 1 | _ | |a Hoffmann, Marion |b 27 |
| 700 | 1 | _ | |a Kramm, Christof M |b 28 |
| 700 | 1 | _ | |a Kwiecien, Robert |b 29 |
| 700 | 1 | _ | |a Castel, David |b 30 |
| 700 | 1 | _ | |a Gielen, Gerrit H |b 31 |
| 700 | 1 | _ | |a Varlet, Pascale |b 32 |
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