5-azacytidine


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5-azacytidine

A chemical analogue of the nucleoside cytidine which cells incorporate into DNA during replication and RNA during transcription; it inhibits methyltransferase resulting in demethylation of the sequence, affecting the binding of cell regulatory proteins to the DNA/RNA substrate. It is used to manage myelodysplastic syndromes.
 
Adverse effects
Anaemia, nausea, vomiting, diarrhoea, decreased blood pressure, liver defects, pulmonary oedema.
References in periodicals archive ?
Effects of 5-azacytidine and butyrate on differentiation and apoptosis of hepatic cancer cell lines.
The technique involves extracting adult human fat cells and treating them with the compound 5-Azacytidine (AZA), along with platelet-derived growth factor-AB (PDGF-AB) for approximately two days.
Bernstein and his colleagues tested their hypothesis by growing glioma cells in petri dishes and adding a rarely used first-generation chemotherapy drug, 5-Azacytidine, that dissolves methyl groups.
Several of these newly discovered mutations raise the possibility of targeting subpopulations of JMML cases with existing drugs: Janus kinase (JAK) inhibitors, currently used to treat certain other bone marrow and blood cancers such as polycythemia vera, might inhibit signaling through a hyperactive JAK-STAT pathway identified in some patients, while other agents such as 5-azacytidine, most commonly used as a treatment for a blood disorder known as myelodysplastic syndrome, could be used to reduce excessive epigenetic DNA methylation seen in others.
The impact of 5-azacytidine on placental weight, glycoprotein pattern and proliferating cell nuclear antigen expression in rat placenta.
Van de Walle evaluated the drug 5-Azacytidine, marketed under the name Vidaza and already used in the treatment of certain human cancers.
Myogenic cells derived from rat bone marrow mesenchymal stem cells exposed to 5-azacytidine.
Delivery of 5-azacytidine to human cancer cells by elaidic acid esterification increases therapeutic drug efficacy.
ESA use may have been affected during the study period by the market entry and diffusion of two new types of disease modifying agents, hypomethylating agents (HMA; 5-azacytidine or decitabine, approved by the FDA in 2004 and 2006, respectively) and lenalidomide, approved in late 2005.
Furthermore, demethylation induced by 5-azacytidine resulted in gene reactivation in PTPRO-methylated and -silenced breast cancer cell lines.
11) Transdifferentiation can also be achieved by the administration of some chemicals, as has been shown by studies that report the transdifferentiation of mesenchymal stem cells into cardiomyocytes by exposure to 5-Azacytidine.

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