Fig. 5

Partially hypermethylated UMRs were accompanied by local changes of key histone modifications contributed to oncogene activation. A The barplot displays the overlap between up-regulated phUMR-related genes and oncogenes. p-value was computed using Fisher’s exact test. The specific numbers of overlapping genes between phUMRs/fhUMRs related differentially expressed genes and cancer genes are displayed on the bars. B The Boxplot shows fold changes of average histone modification signals at partial Hyper, flanking UMR and downstream regions of up-regulated oncogenes. Partial Hyper and flanking UMR was determined by the border of hypermethylated CpGs in IDH mutant gliomas, and downstream represent the region from the border of phUMR to TES of oncogene. C Genome Browser tracks depict DNA methylation, gene transcription and histone modification changes across CCND1 in IDH mutant glioma (red) and normal brain tissue (blue). D Boxplot compared methylation level changes (left) or gene expression (right) of CCND1 among IDH mutant glioma and normal brain tissues. CGI, methylation level was quantified as mean methylation level of CpG sites in promoter CpG island of CCND1. phUMR: methylation level was quantified as mean methylation level of CpG sites in hypermethylated regions on phUMRs of CCND1. E Hypothesis model of oncogene activation accompanied by partial methylation erosion and chromatin reprogramming