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<p> <span style="font-size:10pt;font-family:Arial;">There is growing evidence revolving around ‘trio of events’ viz., human diseases, genetic alternations and acquired epigenetic abnormalities.<span> </span>Much has been discussed in earlier sections highlighting the significance of promoter CpG island methylation and gene silencing.<span> </span>As shown by Harikrishnan et al., (26) that the methylated DNA binding protein (MeCP2) is associated with Brahma (<em>Brm</em>), a catalytic component of SW1/SNF chromatin-remodeling complex.<span> </span>Thus, it is clear that the cytosine methylation is mediated by MeCP2.<span> </span>Further, there is a potential link between cytosine methylation and chromatin silencing - one of the crux events for the initiation of tumor and it is hypothesized to constitute a distinct phenotype viz., ‘CpG island methylation phenotype’ (CIMP).<span> </span>Histone modification, such as, loss of acetylation at lysine 16 and trimethylation at lysine 20 of histone H4 are the epigenetic events prone to human cancer.<span> </span>Besides, there is another interesting polycomb repressor complex (PRC 2) in the initiation of genome silencing.<span> </span>This contains histone methyltransferases which possibly translocate methyl groups to lysine residues 9 and 27 of histone H3 (27).<span> </span>It is reported by Peter and Stephen (28) that the polycomb gene (BMI1), a component of PRC1 is unusually over expressed in several human cancers.<span> </span>In addition, transcription of a number of tumor suppressor genes such as p16, BRCA1, p53, hMLH-1 has now been shown to be inhibited due to the hypermethylation of their corresponding promoter sites (29). <span> </span></span> </p> <p> <span style="font-size:10pt;font-family:Arial;"> </span> </p> <p> <span style="font-size:10pt;font-family:Arial;">Another side of the coin in gene silencing is that the methylation of CpG dinucleotides prevents transcription factors such as <em>c-Myc</em> to recognize their foot-prints on DNA (30).<span> </span>The above accumulated experimental evidences strongly indicate that the entire methylated epigenome is customarily dysregulated causing cancer to develop.<span> </span>These epigenetic dictums in cancer have led to the development of an entirely new therapeutic approach in which the focus is to reverse gene (tumor suppressor gene) silencing (28).<span> </span>Thus, the drugs inhibiting DNA methyl transferase enzyme such as azanucleoside (31), 5-fluoro-2’-deoxycytidine (32) and Zebularine (33) are under active consideration of FDA, USA for treatment of cancer. </span> </p>
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