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. 2022 Feb 28;8:91. doi: 10.1038/s41420-022-00883-z

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© The Author(s) 2022

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. 2 — A–G Expression levels of EIF4EBP1 mRNA in glioblastoma patient samples plotted against the mRNA expression levels of (A) MYBL2, (B) FOXM1, (C) ETS1, (D) HIF-1A, (E) JUN, (F) E2F1 or (G) E2F6 in the REMBRANDT cohort (n = 228 patients) [26]. Co-expression levels were quantified by calculating the Pearson correlation coefficient. H ChIP peak locations within the human EIF4EBP1 promoter, exon 1 and part of intron 1 (−1500 to +1000; hg38; Chr8: 38,029,034–38,031,534) from ChIP-sequencing data for histone H3K27 acetylation (H3K27ac) and H3K4 trimethylation (H3K4me3), ETS1, FOXM1, JUN, E2F1, and E2F6 (Encode consortium, Encyclopedia of DNA Elements at UCSC; [41, 42]), HIF-1A (accession code GSE39089; name GSM955978; run SRR518265 [43]) and MYBL2 (accession code GSE119972; name GSM3389599 [44]).