The reciprocal relationships between metabolism and epigenetic regulation are attractive opportunities for targeted cancer therapy. Multiple drug candidates targeting epigenetic mechanisms are currently in trials for breast cancer. Among those with published promising results are the HDAC inhibitors SAHA (Vorinostat) (109–111), entinostat (112), valproate (113), and romidepsin (114). Romidepsin and vorinostat have been FDA approved for treatment of T-cell lymphomas (115, 116). An inhibitor of a DNA methyltransferase, 5-aza-2′-deoxycytidine (5azaC), causes DNA hypomethylation, is FDA approved for treatment of myelodysplastic syndrome (117, 118), and has early promise for breast cancer (119, 120). The great promise of these drugs should drive the search for other epigenetic targets in cancer therapy.
