EPCO-44. HOXD13 GENE PLAYS A ROLE AS A PUTATIVE MASTER EPIGENETIC REGULATOR IN GLIOMA RECURRENCE AND PROGRESSION

Abstract BACKGROUND Adult diffuse glioma is a heterogenous brain tumor group that has malignant potential and recurring properties. Glioma CpG island methylator phenotype (G-CIMP) associated with chromatin remodeling encompasses two different methylation degrees: G-CIMP-high G-CIMP-low have high levels of DNA loss methylation, respectively. confers more favorable prognosis better predictive values by altering transcriptional dynamics the gene expression. METHODS We performed Chromatin Immunoprecipitation Sequencing (ChIP-Seq) on extracted from fresh frozen primary tissues (G-CIMP-high G-CIMP-low). processed sequencing data using FastQC (v.:0.11.5), bwa-mem (v.:0.7.15) picard tool (v.:2.7.1). The ChIP-seq peaks differentially bound were obtained MACS2 (v.:2.1.1) DiffBind (v.:3.4.11), also integrated transcriptomic, epigenomic genomic data. RESULTS Initial results showed H3K27ac H3K4me3 peak gains losses are located mainly in intronic intergenic regions. integration between epigenetic transcriptomic revealed promoter HOXD13 upregulated GCIMP-low presents an active regulatory region enriched sites. able to identify GCIMP-low, addition presenting downregulated genes than GCIMP-high, greater affinity peaks. In we identified regions highly presence marks. CONCLUSION mapped enrichment histone modifications TSS expressed identifying both susceptibility GIMP-low interact fact progression GCIMP-high can be explained association gain downregulation. Also, predicted as putative master regulator G-CIMP demethylation process and, consequently, recurrence progression, over time.