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Fig. 1 | BMC Cancer

Fig. 1

From: A role for SETD2 loss in tumorigenesis through DNA methylation dysregulation

Fig. 1

Performing a differential methylation analysis comparing SETD2 cases and SETD2 control cancer samples in (A) clear cell renal cell carcinoma and (B) lung adenocarcinoma shows a large number of differentially methylated CpGs. The top 10% of differentially methylated CpG sites, i.e. CpGs with the greatest ∆β values are shown in the heatmap. Unsupervised hierarchical clustering was carried out using complete-linkage clustering and distance measure is given by the Euclidean distance. Hypomethylated CpGs in both (C) papillary renal cell carcinoma and (D) lung adenocarcinoma show strong enrichment in gene bodies (p < 0.05) whereas in comparison, hypermethylated CpGs in papillary renal cell carcinoma and lung adenocarcinoma are more enriched in promoter regions and transcription start sites; Illumina array shows the distribution of CpGs in the entire 450k methylation array; β-value represents level of methylation; 3’UTR: 3’ untranslated region, 5’UTR: 5’ untranslated region; TSS1500: 1500 bp upstream of transcription start site, TSS200: 200 bp upstream of transcription start site.

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