| Literature DB >> 11927287 |
Robert Brown1, Gordon Strathdee.
Abstract
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.Entities:
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Year: 2002 PMID: 11927287 DOI: 10.1016/s1471-4914(02)02314-6
Source DB: PubMed Journal: Trends Mol Med ISSN: 1471-4914 Impact factor: 11.951