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Access to genes in DNA is controlled by how tightly DNA is packed in the cell.1,2 Modification of histones, the proteins around which DNA is wrapped, regulate whether the DNA is accessible to polymerases, allowing the genes to be transcribed, or inaccessible, restricting transcription of genes.1,2
This epigenetic code is dynamically written, erased, and read by families of enzymes.3 Histone acetyltransferases are writers that add acetyl groups, causing the DNA to become transcriptionally active.2,3 Histone deacetylases (HDACs) are erasers that remove acetyl groups from histones, resulting in tighter histone-DNA interactions that block gene transcription.2,3 Readers recognize and bind to modified histones and can recruit transcriptional machinery to certain genes.3
Altered expression, dysregulation, and mutations of HDAC genes leading to alterations in the acetylation state of histones have been implicated in tumor development in various cancers.2,4,5 Targeting the epigenetic code with molecules such as HDAC inhibitors is a therapeutic approach under active investigation.1,3