Effects of 5-azacytidine and its 2′-deoxyderivative on cell differentiation and DNA methylation

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      This usually occurs during the S phase of cell cycle in rapidly proliferating cells whereby 5-AzaCR is incorporated into the DNA. It remains covalently bound with the DNMT and DNA, causing the enzyme functions to be blocked and loss of methylation in the daughter cells after replication (Jones, 1985; Tanaka et al., 1980). This therefore leads to a change in the epigenetic restriction and subsequent reactivation of genes that are relevant to the acquisition of higher stem cell potential (Christman, 2002).

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      As described here, encouraging data from clinical trials, azacitidine treatment registries, and retrospective analyses, suggest that azacitidine has wide therapeutic application in AML. Azacitidine is a cytidine analog DNA methyltransferase inhibitor and hypomethylating agent (HMA) (Jones, 1985a,b; Jones et al., 1983). Azacitidine is phosphorylated by uridine-cytidine kinase to a monophosphate derivative and then further to diphosphate and triphosphate forms.

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      In 1984 it was shown that 5-azacytidine acts as a non-competitive inhibitor of DNA (cytosine-5)-methyltransferase and can cause hypomethylation of DNA in mammalian cells [5]. The ability of 5-azacytidine to act, following its incorporation into DNA, to inhibit DNA methyltransferase resulting in new cytosine methylation patterns (hypomethylation) leading to altered gene expression and differentiation was first reviewed in a comprehensive fashion in 1985 [6]. Thus, as it has become apparent that epigenetic mechanisms underlie differentiation and specify the phenotype of cells it is not unexpected to see that the number of publications and interest in this area of science have increased at a stunning rate in recent years.

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