الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
The field of epigenetics has witnessed a recent explosion in our knowledge on the importance of epigenetic events in the control of both normal cellular processes and abnormal events associated with disease. Advances in the field of cancer epigenetics and epigenomics have turned academic, medical, and public attention to the potential application of epigenetics in cancer control.
Cancer research has generated a body of evidence that link changes to the genome with the carcinogenic process. These changes and in particular modifications in the DNA methylation machinery, have been hypothesized to serve as excellent candidates for the association between environmental exposure and cancer development. Epigenetic changes have been strongly implicated in every step during tumor development and progression. These discoveries have resulted in an increasingly accepted view that epigenetics play a fundamental role in carcinogenesis.
Much attention has been recently directed towards elucidating the connection between DNA methylation and cancer development. In fact, it is believed that aberrant DNA methylation patterns may serve as powerful detection, diagnostic and risk assessment biomarkers. Evidence suggests that hyper methylation of GC-rich DNA regions (CpG islands) plays a major causal role in cancer development primarily through its ability to inactivate and thus silence tumor suppressor genes. Under normal conditions, such CpG islands are unmethylated and their hyper methylation, during carcinogenesis, is hypothesized to have profound effects in mammalian gene expression and it has been estimated that aberrant methylation of cytosine residues, within these CpG islands, is the single most common lesion in cancer cells even when compared to the overall rate of both mutations and cytogenetic abnormalities. Based on extensive findings of aberrant DNA methylation in malignancy, inhibitors of DNA methyltransferases (DNMTIs) have been examined as a means of inducing re-expression of tumor suppressor genes and reversal of malignant phenotypes.