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. 2021 Jun 15;12:3621. doi: 10.1038/s41467-021-23922-2

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© The Author(s) 2021, corrected publication 2021

Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — Freshly resected glioma specimens were acquired from patients representing major glioma malignancy groups: pilocytic astrocytomas (WHO grade I, PA, n = 11), diffuse astrocytomas (WHO grade II and III, DA, n = 7) and glioblastomas (WHO grade IV, GBM, n = 15). Clinical data about each patient was collected. Glioma tissues were homogenized to a single cell suspension and experimentally defined numbers of cells were split into portions that were processed for RNA-seq, ATAC-seq, ChIP-seq, or DNA methylation experiments. Differential analysis of epigenomic and transciptomic profiles across glioma grades was performed, followed by identification of related regulatory mechanisms. Results from all genome-wide experiments were made available in a genome browser (http://regulomics.mimuw.edu.pl/GliomaAtlas/).