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Alterations or changes in epigenetic processes permit changes in gene transcription and are associated with cancer.8,9 Overexpressed or sustained HDAC activity, occurring in some cancer cells, results in deacetylation of the histone tails or histone hypoacetylation. Histone hypoacetylation results in a more closed or tightly packaged chromatin structure in which certain genes may become inaccessible to transcription factors and not get transcribed. This is thought to be a mechanism for limiting or silencing tumor suppressor genes, such as p53, and cyclin-dependent kinase inhibitors, such as p21.9,10 These dysfunctional events can play a role in the risk of cancer development.11
