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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. 1 — A Expression levels of EIF4EBP1 in non-neoplastic brain tissue (NNBT) and glioblastoma tissues from the REMBRANDT [26] and SUN [27] cohorts. B Expression levels of EIF4EBP1 in 172 NNBT samples (BERCHTOLD [67]) and according to EIF4EBP1 copy number variation in 507 malignant gliomas of CNS WHO grade 4 of TCGA cohort [32] categorized as EIF4EBP1 copy number loss (hemizygous deletion [loss]), EIF4EBP1 balanced copy number (balanced), or EIF4EBP1 low-level copy number gain (gain). C DNA methylation levels of 12 CpG sites located within the EIF4EBP1 promoter region (hg19; Chr8: 37,886,520–37,889,020) using the datasets GSE112179 and GSE156374 for NNBT (n = 13) and GSE119774 for malignant glioma (M. glioma) tissues (n = 40) with 0 representing unmethylated and 1 representing fully methylated CpG sites. Note identical methylation patterns in normal brain tissue and the glioblastoma samples. Significance in A, B was calculated using an unpaired and two-tailed parametric t test (*p < 0.05, **p < 0.01, ****p < 0.0001).