ABSTRACT
In recent years, great strides have been taken toward understanding the establishment of aberrant epigenetic patterns in human cancers. For DNA methylation, it is known that two apparently contrasting phenomena coexist in the cancer cell: hypomethylation and hypermethylation. It has been shown that a profound loss of global 5-methylcytosine genomic content occurs in cancer cells with discrete areas of dense hypermethylation [1-3] occurring in the CpG islands located in the promoters of certain tumor-suppressor genes, such as p16INK4a, BRCA1, or hMLH, leading to gene silencing [1,3]. In contrast, for cancer cells overall hypomethylation takes place predominantly in DNA repetitive sequences and has been linked to chromosomal instability [2,3].
