Abstract

Changes in DNA methylation patterns is a prominent characteristic of human tumors. Tumor cells display reduced levels of genomic DNA methylation and site-specific CpG island hypermethylation. Methylation of CpG dinucleotides is catalyzed by the enzyme family of DNA methyltransferases (DNMTs). In this review, the role of DNA methylation and DNMTs as key determinants of carcinogenesis is further elucidated. The chromatin modifying proteins that are known to interact with DNMTs are also described. Finally, the role of DNMTs as potential therapeutic targets is addressed.

Keywords: Biomarkers, cancer, chromatin modification, CpG methylation, DNMTs, epigenetic therapy, oncogenes, tumor suppressor genes, DNA cytosine-5 methyltransferases, DNA methyltransferases, Aberrant methylation, histone proteins, histone acetyltransferases (HATs), histone methyltransferases, retinoblastoma-associated histone-binding proteins, lymphoid-specific helicase, estrogenreceptor, restriction landmark genomic scanning, RLGS, methylation-specific PCR, heterochromatin, 5-aza-2'-deoxycytidine, Polycomb Repressive Complex 2, PRC2, 5-azacytidine (Vidaza), 5-aza-2'-deoxycytidine (Decitabine), myelodysplastic syndromes, MDS