Abstract
It is now well established that, in addition to genetic changes that may include germ line and somatic DNA alterations, cancers can also arise as a result of a series of epigenetic DNA mutations (1). In mammals, DNA is methylated at cytosine residues in the 5′ position of CpG dinucleotides. The genomic methylation pattern is established in the early embryo before implantation and is then stably maintained throughout differentiation (2). However, in cancer the methylation pattern of the cell is altered, with repeated DNA regions often undergoing hypomethylation and CpG island promoter regions undergoing hypermethylation (3). Hypomethylation of DNA is thought to be involved in the expression of previously dormant proto-ongogenes, and hypermethylation of the promoter regions is associated with gene silencing. Hypermethylation of tumor suppressor genes and other CpG island genes, such as p15, p16, estrogen receptor, E-cadherin, VHL, HIC-1, and retinoblastoma and corresponding transcriptional silencing have been demonstrated in many different forms of cancer (1). However, each cancer appears to have a specific subset of genes that are susceptible to methylation (4). Therefore, detection of the methylation of these genes could provide a useful diagnostic tool to identify the cancer cell and monitor the cancer during therapy.
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Clark, S.J., Millar, D.S., Molloy, P. (2003). Bisulfite Methylation Analysis of Tumor Suppressor Genes in Prostate Cancer from Fresh and Archival Tissue Samples. In: Russell, P.J., Jackson, P., Kingsley, E.A. (eds) Prostate Cancer Methods and Protocols. Methods in Molecular Medicine™, vol 81. Springer, Totowa, NJ. https://doi.org/10.1385/1-59259-372-0:219
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DOI: https://doi.org/10.1385/1-59259-372-0:219
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