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. 2020 Apr 23;8:57. doi: 10.1186/s40478-020-00930-9

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© The Author(s) 2020

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 3 — Histopathologic findings of atypical DIPG (aDIPG). A wide range of disease entities was identified in aDIPG (a). Only slightly more than half of the diffuse aDIPG harbored a histone H3 K27M mutation (b). Tissue sections immunostained for histone H3 K27M–mutant protein and trimethylation of the H3 K27 residue are shown in (c) and (d), respectively. The remaining panels are representative images of identified entities, including angiocentric glioma (AG) (e); diffuse astrocytoma (DA) (f); anaplastic astrocytoma (AA) (g); glioblastoma (GBM) (h); pilocytic astrocytoma (PA) (i); ganglioglioma (GG) (j); C19MC-altered embryonal tumor with multilayered rosettes (ETMR) (k); and CNS embryonal tumor, not otherwise specified (ET, NOS) (l)