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The Role of DNA Methylation in the Pathogenesis and Treatment of Cancer

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DNA methylation is a major epigenetic mechanism that leads to inhibition of gene transcription and is known to be involved in the pathogenesis of cancer. The effectors of DNA methylation are DNA methyltransferases (DNMTs) that catalyze either de novo or maintenance methylation of hemimethylated DNA after DNA replication. DNA methylation patterns in cancer are distorted, with three ways by which DNA methylation contributes to cancer: hypomethylation of the cancer genome, focal hypermethylation of the promoters of tumour suppressor genes, and direct mutagenesis. Drugs that inhibit DNMTs are proving to be useful in the treatment of cancer with a few such drugs approved for clinical use. These drugs include nucleoside inhibitors, non-nucleoside inhibitors, oligonucleotides, and noncoding RNAs that target messenger RNAs of genes encoding DNMTs. The major value of DNMT inhibitors could be that at low doses they can induce the re-expression of aberrantly silenced tumour suppressor genes, allowing cancer cells to revert to a normal phenotype and/or reacquire cellular pathways needed for cell cycle regulation and apoptosis induction. They could also be useful in combination with other anticancer drugs.

Keywords: Cancer Genome; Chemotherapy; DNA; Focal Hypermethylation; Hypomethylation; Tumour; cancer; methylation; pathogenesis; treatment

Document Type: Research Article


Publication date: 2012-11-01

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  • Current Clinical Pharmacology publishes frontier reviews on all the latest advances in clinical pharmacology. The journal's aim is to publish the highest quality review articles in the field. Topics covered include: pharmacokinetics; therapeutic trials; adverse drug reactions; drug interactions; drug metabolism; pharmacoepidemiology; and drug development. The journal is essential reading for all researchers in clinical pharmacology.
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