Encyclopedia of Cancer

Living Edition
| Editors: Manfred Schwab

Epigenetic Therapy

  • Debby Hellebrekers
  • Manon van Engeland
Living reference work entry
DOI: https://doi.org/10.1007/978-3-642-27841-9_1948-2

Definition

Epigenetic therapy refers to therapy using inhibitors of DNA methylation and histone deacetylation, which reverse these epigenetic modifications. These compounds inhibit tumor growth in vitro and in vivo, which is thought to be due to reactivation of epigenetically silenced tumor suppressor genes by inhibition of promoter DNA methylation and histone deacetylation of these genes.

Characteristics

DNA Methylation and Histone Deacetylation

Epigenetic modifications regulate heritable changes in gene expression without changing the primary DNA sequence. The best-studied epigenetic mechanisms are DNA methylation and posttranslational histone modifications. DNA methylation is the covalent addition of a methyl group to the DNA, predominantly to the base cytosine 5′ to guanine, also called a CpG dinucleotide. CpG dinucleotides are clustered in small stretches of DNA called CpG islands, often located in or near the promoter region of approximately half of all human genes. Methylation...

Keywords

Acute Myeloid Leukemia Valproic Acid Histone Acetylation HDAC Inhibitor Histone Deacetylation 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
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References

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  3. Hellebrekers DM, Griffioen AW, van Engeland M (2007) Dual targeting of epigenetic therapy in cancer. Biochim Biophys Acta 1775:76–91PubMedGoogle Scholar
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See Also

  1. (2012) Anti-Angiogenic Drugs. In: Schwab M (ed) Encyclopedia of Cancer, 3rd edn. Springer Berlin Heidelberg, pp 207–208. doi: 10.1007/978-3-642-16483-5_302Google Scholar
  2. (2012) Chimeric Oncoproteins. In: Schwab M (ed) Encyclopedia of Cancer, 3rd edn. Springer Berlin Heidelberg, p 811. doi: 10.1007/978-3-642-16483-5_1095Google Scholar
  3. (2012) Chromatin. In: Schwab M (ed) Encyclopedia of Cancer, 3rd edn. Springer Berlin Heidelberg, p 825. doi: 10.1007/978-3-642-16483-5_1125Google Scholar
  4. (2012) DNA Methyltransferases. In: Schwab M (ed) Encyclopedia of Cancer, 3rd edn. Springer Berlin Heidelberg, p 1140. doi: 10.1007/978-3-642-16483-5_6997Google Scholar
  5. (2012) FDA. In: Schwab M (ed) Encyclopedia of Cancer, 3rd edn. Springer Berlin Heidelberg, p 1386. doi: 10.1007/978-3-642-16483-5_2136Google Scholar
  6. (2012) Histone Deacetylation. In: Schwab M (ed) Encyclopedia of Cancer, 3rd edn. Springer Berlin Heidelberg, p 1702. doi: 10.1007/978-3-642-16483-5_2753Google Scholar
  7. (2012) Histone Proteins. In: Schwab M (ed) Encyclopedia of Cancer, 3rd edn. Springer Berlin Heidelberg, p 1706. doi: 10.1007/978-3-642-16483-5_2761Google Scholar
  8. (2012) Nucleoside Analogs. In: Schwab M (ed) Encyclopedia of Cancer, 3rd edn. Springer Berlin Heidelberg, p 2577. doi: 10.1007/978-3-642-16483-5_4164Google Scholar
  9. (2012) PML-RARa. In: Schwab M (ed) Encyclopedia of Cancer, 3rd edn. Springer Berlin Heidelberg, p 2931. doi: 10.1007/978-3-642-16483-5_4645Google Scholar
  10. (2012) Tumor Endothelial Cell. In: Schwab M (ed) Encyclopedia of Cancer, 3rd edn. Springer Berlin Heidelberg, p 3795. doi: 10.1007/978-3-642-16483-5_6026Google Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 2015

Authors and Affiliations

  1. 1.Department of Pathology, GROW-School for Oncology and Developmental BiologyMaastricht University HospitalMaastrichtThe Netherlands