Changes in the pattern of DNA methylation are commonly seen in human tumors. Both genome wide hypomethylation (insufficient methylation) and region-specific hypermethylation (excessive methylation) have been suggested to play a role in carcinogenesis2. A common cause of the loss of tumor-suppressor miRNAs in cancer is the silencing of primary transcripts by CpG island promoter by hypermethylation3. DNA hypomethylation also contributes to cancer development via three major mechanisms, such as: an increase in genomic instability, reactivation of transposable elements and loss of imprinting
