Epigenomics and epigenetic therapy of cancer.
Epigenetic inactivation of genes that are crucial for the control of normal cell growth is a hallmark of cancer cells. These epigenetic mechanisms include crosstalk between DNA methylation, histone modification and other components of chromatin higher-order structure, and lead to the regulation of gene transcription. Re-expression of genes epigenetically inactivated can result in the suppression of tumour growth or sensitization to other anticancer therapies. Small molecules that reverse epigenetic inactivation are now undergoing clinical trials in cancer patients. This, together with epigenomic analysis of chromatin alterations such as DNA methylation and histone acetylation, opens up the potential both to define epigenetic patterns of gene inactivation in tumours and to use drugs that target epigenetic silencing.
Brown
Robert
R
Cancer Research UK Dept of Medical Oncology, Beatson Laboratories, Glasgow University, Glasgow, UK G61 1BD. r.brown@beatson.gla.ac.uk
Strathdee
Gordon
G
D002843:Chromatin / Q000235:genetics*; D019175:DNA Methylation; D015972:Gene Expression Regulation, Neoplastic; D020868:Gene Silencing; D015316:Genetic Therapy; D023281:Genomics; D056572:Histone Deacetylase Inhibitors; D006801:Humans; D008780:Methyltransferases / Q000378:metabolism; D009369:Neoplasms / Q000235:genetics / Q000628:therapy*; D011401:Promoter Regions, Genetic
D002843:Chromatin; D056572:Histone Deacetylase Inhibitors; D008780:Methyltransferases