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000164298 1001_ $$0P:(DE-He78)8aad075b17d93a5636a34942bdbd7ee6$$aSievers, Philipp$$b0$$eFirst author
000164298 245__ $$aA subset of pediatric-type thalamic gliomas share a distinct DNA methylation profile, H3K27me3 loss and frequent alteration of EGFR.
000164298 260__ $$aOxford$$bOxford Univ. Press$$c2021
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000164298 520__ $$aMalignant astrocytic gliomas in children show a remarkable biological and clinical diversity. Small in-frame insertions or missense mutations in the EGFR gene have recently been identified in a distinct subset of pediatric-type bithalamic gliomas with a unique DNA methylation pattern.Here, we investigated an epigenetically homogeneous cohort of malignant gliomas (n=58) distinct from other subtypes and enriched for pediatric cases and thalamic location, in comparison with this recently identified subtype of pediatric bithalamic gliomas.EGFR gene amplification was detected in 16/58 (27%) tumors, and missense mutations or small in-frame insertions in EGFR were found in 20/30 tumors with available sequencing data (67%; five of them co-occurring with EGFR amplification). Additionally, eight of the 30 tumors (27%) harbored an H3.1 or H3.3 K27M mutation (six of them with a concomitant EGFR alteration). All tumors tested showed loss of H3K27me3 staining, with evidence of EZHIP overexpression in the H3 wildtype cases. Although some tumors indeed showed a bithalamic growth pattern, a significant proportion of tumors occurred in the unilateral thalamus or in other (predominantly midline) locations.Our findings present a distinct molecular class of pediatric-type malignant gliomas largely overlapping with the recently reported bithalamic gliomas characterized by EGFR alteration, but additionally showing a broader spectrum of EGFR alterations and tumor localization. Global H3K27me3 loss in this group appears to be mediated by either H3 K27 mutation or EZHIP overexpression. EGFR inhibition may represent a potential therapeutic strategy in these highly aggressive gliomas.
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000164298 7001_ $$0P:(DE-He78)d20d08adc992abdb6ccffa1686f1ba17$$aStichel, Damian$$b3
000164298 7001_ $$0P:(DE-He78)d5149ffd74f42a2fa87a086d66645aaa$$aReuß, David$$b4
000164298 7001_ $$0P:(DE-He78)a46a5b2a871859c8e2d63d2f8c666807$$aSturm, Dominik$$b5
000164298 7001_ $$aHench, Jürgen$$b6
000164298 7001_ $$aFrank, Stephan$$b7
000164298 7001_ $$aKrskova, Lenka$$b8
000164298 7001_ $$aVicha, Ales$$b9
000164298 7001_ $$aZapotocky, Michal$$b10
000164298 7001_ $$aBison, Brigitte$$b11
000164298 7001_ $$aCastel, David$$b12
000164298 7001_ $$aGrill, Jacques$$b13
000164298 7001_ $$0P:(DE-HGF)0$$aDebily, Marie-Anne$$b14
000164298 7001_ $$0P:(DE-HGF)0$$aHarter, Patrick N$$b15
000164298 7001_ $$aSnuderl, Matija$$b16
000164298 7001_ $$aKramm, Christof M$$b17
000164298 7001_ $$0P:(DE-HGF)0$$aReifenberger, Guido$$b18
000164298 7001_ $$0P:(DE-He78)8d9c904a6cea14d4c99c78ba46e41f93$$aKorshunov, Andrey$$b19
000164298 7001_ $$aJabado, Nada$$b20
000164298 7001_ $$aWesseling, Pieter$$b21
000164298 7001_ $$0P:(DE-He78)92e9783ca7025f36ce14e12cd348d2ee$$aWick, Wolfgang$$b22
000164298 7001_ $$aSolomon, David A$$b23
000164298 7001_ $$aPerry, Arie$$b24
000164298 7001_ $$aJacques, Thomas S$$b25
000164298 7001_ $$aJones, Chris$$b26
000164298 7001_ $$0P:(DE-He78)143af26de9d57bf624771616318aaf7c$$aWitt, Olaf$$b27
000164298 7001_ $$0P:(DE-He78)f746aa965c4e1af518b016de3aaff5d9$$aPfister, Stefan$$b28
000164298 7001_ $$0P:(DE-He78)a8a10626a848d31e70cfd96a133cc144$$avon Deimling, Andreas$$b29
000164298 7001_ $$0P:(DE-He78)551bb92841f634070997aa168d818492$$aJones, David$$b30$$eLast author
000164298 7001_ $$0P:(DE-He78)a1f4b408b9155beb2a8f7cba4d04fe88$$aSahm, Felix$$b31$$eLast author
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