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Currently, you can access the following clinical trials being conducted worldwide:

342,868 studies
in
216 countries
Clinical trial information and results are updated daily from ClinicalTrials.gov. The latest data update was conducted on 08/04/2020.
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Clinical trial information and results are updated daily from ClinicalTrials.gov. The latest data update was conducted on 08/04/2020.
  • Histone Modification

    The safety and efficacy of the agents and/or uses under investigation have not been established. There is no guarantee that the agents will receive health authority approval or become commercially available in any country for the uses being investigated.

     

    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

    View Related Molecules

    References

    1. Oronsky B, et al. Transl Oncol. 2014;7:626-631. PMID: 25389457
    2. Ververis K, et al. Biologics. 2013;7:47-60. PMID: 3459471
    3. Tarakhovsky A. Nat Immunol. 2010;11:565-568. PMID: 20562839
    4. New M, et al. Mol Oncol. 2012;6:637-656. PMID: 23141799
    5. Marsoni S, et al. Epigenetics. 2008;3:164-171. PMID: 18487953