Fig. 1
Tumor regression upon MYC inactivation in T-ALL is associated with genome-wide changes in DNA (hydroxy)methylation. MeDIP- and hMeDIP-seq analysis of T-ALL cells (6780) derived from EµSRα-tTAα;tet-o-MYC mice before and upon MYC inactivation through treatment with 20 ng/mL DOX for 2 days. a Genomic distribution of DMRs and hDMRs is displayed as chromosome-based circular plot. Cutoff: log2FC ≥ 1 with a P value of ≤ 10−4. b Hypo- or hypermethylated DMRs and hDMRs are shown annotated for their association with mRNAs, enhancers, super-enhancers, small noncoding RNAs, and long noncoding RNAs. c Hypo- or hypermethylated DMRs and hDMRs associated with mRNAs are shown annotated for cis-regulatory elements: CpG islands, exons, introns, 5′-/3′-UTRs, and sequences 2 kbp upstream or downstream of the nearest gene. Heatmap showing hierarchical clustering of d DMRs and e hDMRs associated with protein-coding genes. Gene names are listed in Additional file 3. f Gene ontology analysis (DAVID) indicating biological processes associated with DMRs and hDMRs