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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 do 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 p21.7,10 These dysfunctional events play a role in the risk of cancer development.11
