DNA methylation and gene silencing in cancer

By S. Baylin. Nature Clinical Practice Oncology, 2005

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Epigenetics and gene expression (2010, background): “CpG islands themselves are unevenly distributed throughout the genome and were initially thought to be concentrated in promoter regions of genes (Doerfler, 1981; Baylin, 2005; Miranda and Jones, 2007; Shen et al., 2007).”
Epigenetics in cancer. (2010, background): “Since the initial discovery of CpG island hypermethylation of the Rb promoter (a tumor suppressor gene associated with retinoblastoma) [77], various other tumor suppressor genes including p16, MLH1 and BRCA1, have also been shown to undergo tumor-specific silencing by hypermethylation [3,4,78].”
Oxidative stress, DNA methylation and carcinogenesis. (2008, background): “[25] S.”
An epigenetic switch involving NF-κB, Lin28, let-7 microRNA, and IL6 links inflammation to cell transformation (2009, neutral): “In addition to genetic changes, tumor suppressor genes can be inactivated by epigenetic silencing through DNA methylation (Baylin, 2005), and this can occur through an elaborate pathway triggered by an oncoprotein (Gazin et al.”
Molecular mechanisms of alcohol-mediated carcinogenesis (2007, background): “Therefore, DNA methylation or demethylation is an effective mechanism to suppress or activate gene transcriptio”
DNA hypomethylation and human diseases. (2007, neutral): “carcinogenesis [4–6].”