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. 2009 Sep 13;31(1):27–36. doi: 10.1093/carcin/bgp220

Fig. 2.

Fig. 2.

DNA methylation changes in cancer. In normal cells, CpG island promoters are generally unmethylated and when active, as in the case of tumor suppressor genes, are accompanied by active histone marks such as acetylation and H3K4 methylation (green circles, 4) allowing for a transcriptionally active open chromatin structure. However, repetitive regions, transposons, CpG poor intergenic regions and imprinted gene promoters are heavily methylated and accompanied by repressive histone marks such as H3K9 methylation (red circles, 9) that together form a silent chromatin state. During tumorigenesis, tumor suppressor gene promoters with CpG islands become methylated, resulting in the formation of silent chromatin structure and aberrant silencing (indicated by the red arrow). In contrast, the repetitive sequences, transposons and imprinted gene promoters become hypomethylated resulting in their aberrant activation (indicated by the green arrow).