Epigenetics in Cancer
More Information »Dysregulation of epigenetic modifications has been shown to result in oncogenesis and cancer progression. Unlike genetic mutations, epigenetic alterations are considered to be reversible, and thus make a promising therapeutic target.
Epigenetics in Cancer Product Areas
(Taken from Epigenetics in Cancer, Cancer Research Product Guide Edition 3, 2015)Enlarge »
Figure 1:The fundamental unit of chromatin is the nucleosome, which consists of an octamer of the histone proteins H2A, H2B, H3 and H4 (two of each) tightly bound by DNA. Alterations in chromatin structure by post-translational modifications can regulate gene expression through the formation of heterochromatin or euchromatin, which usually repress or activate gene transcription, respectively.
Post-translational modifications include DNA methylation and the covalent methylation (Me) and acetylation (Ac) of histone tails. DNA methylation represses transcription by blocking the binding of transcription complexes to the gene promoter. The acetylation of histone tails usually loosens the DNA from around the nucleosomes, increasing the accessibility of gene promoters to transcription complexes, therefore promoting transcription. Alternatively histone tail methylation can repress or promote gene expression, depending on the site and extent of methylation, as well as the presence of other histone modifications in the vicinity. The pattern of these post-translational modifications on a nucleosome determines the transcriptional profile of nearby genes. Dysregulation of post-translational modifications can result in aberrant gene expression, which causes oncogenesis and cancer progression.
Abbreviations: BRD: bromodomains, DNMT: DNA methyltransferases, DUB: deubiquitinating enzymes, HAT: histone acetyltransferases, HDAC: histone deacetylases, KDM: histone demethylases, KMT/PRMT: lysine methyltransferases/protein arginine methyltransferases.
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October 30 - November 3, 2016
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