Analysis of promoter capture Hi-C libraries from IDH-mutated and IDH-wildtype glioma cell-lines provides insight into the DNA regulatory landscape of glioma tumours.. Promoter Capture Hi-C (PCHi-C) in three glioma cell lines

Adult gliomas are a cancer of unmet clinical need, and while rare at an incidence of ~4 per 100,000 in the European population, they comprise the vast majority of malignant brain tumours. Gliomas can be classified as low-grade (WHO grade II/III) and high-grade (WHO grade IV/GBM).Gain of function driver mutations in IDH1 or IDH2 (from now on referred to as IDH-mutations) occur in ~80% of low-grade gliomas. IDH mutations have been shown to cause metabolic changes in glioma tumours as well as large-scale changes in methylation patterns. A recent study showed that IDH mutated gliomas are hypermethylated at CTCF binding sites, causing aberrant gene expression and disrupting topological associated domains (TADs), suggesting they may alter chromosome topology relative to IDH-wildtype tumours. To further investigate this we report on a study in which we carried out Promoter Hi-C in IDH-mutant and IDH-wildtype glioma cell-lines.