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. Author manuscript; available in PMC: 2012 Oct 4.
Published in final edited form as: Semin Oncol. 2008 Aug;35(4):378–387. doi: 10.1053/j.seminoncol.2008.04.008

Figure 1.

Figure 1

Mechanism of reactivation of silenced genes in cancer using azanucleosides and HDAC (histone deacetylase) inhibitors. Aberrant silencing of tumor-suppressor genes is maintained by factors that control chromatin states. DNMT (DNA methyltransferase) and HDAC enzymes cooperatively work to methylate DNA and deacetylate histones, respectively. Treatment with azanucleosides reduces DNMT activity and thus promotes net DNA demethylation (occurring during DNA replication or by active processes), while HDAC inhibitors promote a net gain of histone acetylation. In combination, these two therapies work synergistically to promote and maintain active chromatin states. HAT, histone acetyltransferase.