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| Home > Publications database > A subset of pediatric-type thalamic gliomas share a distinct DNA methylation profile, H3K27me3 loss and frequent alteration of EGFR. > print |
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| 100 | 1 | _ | |a Sievers, Philipp |0 P:(DE-He78)8aad075b17d93a5636a34942bdbd7ee6 |b 0 |e First author |
| 245 | _ | _ | |a A subset of pediatric-type thalamic gliomas share a distinct DNA methylation profile, H3K27me3 loss and frequent alteration of EGFR. |
| 260 | _ | _ | |a Oxford |c 2021 |b Oxford Univ. Press |
| 336 | 7 | _ | |a article |2 DRIVER |
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| 336 | 7 | _ | |a Journal Article |b journal |m journal |0 PUB:(DE-HGF)16 |s 1641315506_11028 |2 PUB:(DE-HGF) |
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| 336 | 7 | _ | |a Journal Article |0 0 |2 EndNote |
| 500 | _ | _ | |a 2021 Jan 30;23(1):34-43 #EA:B360#LA:B300# |
| 520 | _ | _ | |a Malignant astrocytic gliomas in children show a remarkable biological and clinical diversity. Small in-frame insertions or missense mutations in the EGFR gene have recently been identified in a distinct subset of pediatric-type bithalamic gliomas with a unique DNA methylation pattern.Here, we investigated an epigenetically homogeneous cohort of malignant gliomas (n=58) distinct from other subtypes and enriched for pediatric cases and thalamic location, in comparison with this recently identified subtype of pediatric bithalamic gliomas.EGFR gene amplification was detected in 16/58 (27%) tumors, and missense mutations or small in-frame insertions in EGFR were found in 20/30 tumors with available sequencing data (67%; five of them co-occurring with EGFR amplification). Additionally, eight of the 30 tumors (27%) harbored an H3.1 or H3.3 K27M mutation (six of them with a concomitant EGFR alteration). All tumors tested showed loss of H3K27me3 staining, with evidence of EZHIP overexpression in the H3 wildtype cases. Although some tumors indeed showed a bithalamic growth pattern, a significant proportion of tumors occurred in the unilateral thalamus or in other (predominantly midline) locations.Our findings present a distinct molecular class of pediatric-type malignant gliomas largely overlapping with the recently reported bithalamic gliomas characterized by EGFR alteration, but additionally showing a broader spectrum of EGFR alterations and tumor localization. Global H3K27me3 loss in this group appears to be mediated by either H3 K27 mutation or EZHIP overexpression. EGFR inhibition may represent a potential therapeutic strategy in these highly aggressive gliomas. |
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| 773 | _ | _ | |a 10.1093/neuonc/noaa251 |g p. noaa251 |0 PERI:(DE-600)2094060-9 |n 1 |p 34-43 |t Neuro-Oncology |v 23 |y 2021 |x 1523-5866 |
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