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. 2024 Feb 7;25:45. doi: 10.1186/s13059-024-03172-3

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© The Author(s) 2024

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 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. 6 — A The distribution of average promoter DNA methylation for all genes, JARID2 binding site (JBS)genes, LE50 and LE70 genes in primary (P) and recurrent (R) GBM tumors from all patients (top) and once separated into Down (middle) and Up (bottom) responders. B The proportion of differentially methylated promoters (DMP) between primary and matched recurrent GBM. C The average change in methylation between primary and matched recurrent tumors for the DMP from panel B. D The proportion of single GBM cell promoters that have different methylation status. E The proportion of promoters with the H3K27me3 mark in nine patient GBMs. F The proportion of JBSgene promoters that had EZH2 bound according to ChIPseq of paired patient samples from an Up and a Down responder. G The proportion of promoters with a specific change in EZH2 occupancy that belonged to each gene set