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Fig. 1 | Genome Biology

Fig. 1

From: Cancer-specific CTCF binding facilitates oncogenic transcriptional dysregulation

Fig. 1

Identification of cancer-specific CTCF binding patterns in the human genome. a Distribution of coefficient of variation of chromatin accessibility at different genomic features, calculated using DNase-seq data from over 60 cell lines from ENCODE. b Distribution of occupancy score for all 688,429 union CTCF binding sites (blue), and percentage of CTCF sites that contain a CTCF motif at each occupancy score (orange). c Distribution of CTCF binding occupancy score in 8 ChIP-seq datasets for T-ALL cell lines (y-axis) and the occupancy frequency score in the other 763 ChIP-seq datasets (x-axis). Color density in each unit represents the number of CTCF binding sites with designated scores. d CTCF ChIP-seq signals at a 2-kb region surrounding T-ALLlost (top) and T-ALLgained (bottom) binding sites in normal CD4+ T cells and the T-ALL cell lines Jurkat and CUTLL1, and SMC3 signals at the same regions in CUTLL1. e Example of CTCF ChIP-seq signals around a T-ALL-specific lost CTCF binding site. f Example of CTCF ChIP-seq signals around a T-ALL-specific gained CTCF binding site. g Number of identified gained (left) and lost (right) CTCF binding sites in each of the 6 cancer types and number of shared sites between each pair of cancer types. Color density of each element represents the level of similarity measured by Jaccard index. h Genomic distribution of identified lost (left) and gained (right) CTCF binding sites in the 6 cancer types. Promoter regions are defined as ± 2 kb from any TSS in the genome. i Differential chromatin accessibility (ATAC-seq) in TCGA patient samples at identified cancer-specific lost (blue), gained (red), and constitutive (gray) CTCF binding sites in each of the 4 cancer types compared to all other TCGA samples. *, p < 0.05, **, p < 0.001, by two-tailed unpaired Student’s t test

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