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. 2018 Apr 27;12(6):814–829. doi: 10.1002/1878-0261.12191

Figure 2.

Figure 2

DNA methylation alterations in CP‐CML cells. (A) Heatmaps of differentially methylated probes in CP‐CML and HD CD34+ CD15− (left panel) and CD34− CD15+ (right panel) cells. Hypo‐ and hypermethylated probes are shown on the upper and lower panels, respectively, and their number is indicated. The CpG‐island status and genomic features of the probes are indicated by color codes. (B) Distribution of hyper‐ and hypomethylated probes in CP‐CML cells, AML CD34+ cells, and eight types of solid tumors. For each solid tumor type, CpG‐island methylator phenotype (CIMP)‐positive (+) and CIMP‐negative (−) samples were analyzed separately. BLCA, bladder urothelial carcinoma; BRCA, breast invasive carcinoma; COAD, colon adenocarcinoma; HNSC, head–neck squamous cell carcinoma; KIRP, kidney renal papillary cell carcinoma; LIHC, liver hepatocellular carcinoma; LUSC, lung squamous cell carcinoma; LUAD, lung adenocarcinoma. (C) Circular karyotype showing the position of hyper‐ (in red) and hypomethylated (in blue) DMRs in CP‐CML CD34+ CD15− (inner circle) and CD34− CD15+ (outer circle) cells. Some hotspot regions are named. (D) Detail of the WT1 locus showing a cluster of hypermethylated probes in the two promoter regions in CP‐CML CD34+ CD15− and CD34− CD15+ cells compared with HD cells.