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Figure 1 | Clinical Epigenetics

Figure 1

From: High-frequency aberrantly methylated targets in pancreatic adenocarcinoma identified via global DNA methylation analysis using methylCap-seq

Figure 1

Data mining of MethylCap-seq libraries. (A) Experimental strategy to evaluate differential DNA methylation in PC compared with PN. (B) Chromosomal view of genome-wide distribution of hypermethylated DNA in PC compared with PN. Red bar, hypermethylation in PC; green bar, hypermethylation in PN. (C) Hypermethylated peaks around the TSS site in PC compared with those in PN. Peaks were surveyed in a broad region (from 5 kb downstream to 5 kb upstream of the TSS). (D) Mapping peaks and differently methylated regions (DMRs) that were specific for PC and PN. The DMRs are shown according to their inclusion in different gene structure context, such as refGene or CpG island (CGI) definitions. Note that the y-axis is interrupted to show whole dataset. (E) Genomic distribution of DMRs with PC and PN in transcription start sites (TSSs), intragenic regions, and intergenic regions. The total number of DMRs is presented at the top of each graph. (F) DMR distribution over the various gene structures based on sole refGene involvement versus both CGI and refGene involvement in PC-specific and PN-specific DMRs. The genomic context is defined as that found in the UCSC database. (G) PC- and PN-selective DMR distribution over orphan CGIs versus refGene-related CGIs, and over CGI-containing promoters vs. no-CGI promoters. (H) DMRs (and their related genes) in PC and PN, considering the involvement of various CGI features (CGI, CGI shore, or both). CGI, CpG island; DMR, differently methylated regions. PC, pancreatic cancer; PN, adjacent non-tumor tissue; TSS, transcription start site.

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