Clinical activity has been observed in a number of hematologic tumors, and vorinostat is currently approved by the Food and Drug Administrations (FDA) for use in patients with refractory cutaneous T-cell lymphoma ( 18).īortezomib (Velcade, PS-341, Millennium, Cambridge, MA) is a modified dipeptidyl boronic acid that reversibly inhibits the 26S proteasome, a large protease complex that degrades ubiquinated proteins. Vorinostat (suberoylanilide hydroxamic acid (SAHA) or MK-0683, Zolinza®, Merck, Whitehouse Station, NJ) is a small molecule inhibitor of class I and II HDAC enzymes that promotes cell cycle arrest and apoptosis in a wide variety of human hematopoietic cells ( 4– 11) and carcinoma cell lines ( 12– 17). In tumor cells, HDACs also target many non-histone proteins such as tumor suppressor genes and proteins that control proliferation, migration, death and angiogenesis ( 4) and provide a unique mechanistic approach for anti-cancer therapy. HATs promote transcriptional activity by catalyzing the acetylation of N-terminal histone lysine residues ( 1, 2), while HDAC activity results in chromatin condensation and silencing of various genes, including those involved in cell survival, proliferation, differentiation, and apoptosis ( 3). The dynamic equilibrium between histone acetylation and deacetylation is regulated by histone acetyltransferases (HATs) and histone deacetylases (HDACs). DNA that is wrapped around condensed, non-acetylated histones is transcriptionally inactive, whereas acetylation of N-terminal histone lysine residues exposes DNA to important transcription factors that promote transcriptional activity ( 1, 2). Gene expression is influenced by chromatin structure. Kemper, Jr.Histone deacetylation plays a key role in the epigenetic regulation of gene expression and has been implicated in the development and progression of cancer. Neighborhood Tourism Development Fund, City of Kansas City, MO Stern Foundation for the Arts – Commerce Bank, Trustee Muriel McBrien Kauffman Family Foundation
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