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Epigenetics in Lung Cancer*: Focus on Progression and Early Lesions

James G. Herman, MD
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*From the Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Johns Hopkins University, Baltimore, MD.

Correspondence to: James G. Herman, MD, Johns Hopkins University, Bunting Blaustein Cancer Research Bldg, 1650 Orleans St, Suite 541, Baltimore, MD 21231; e-mail: bendeka@jhmi.edu



Chest. 2004;125(5_suppl):119S-122S. doi:10.1378/chest.125.5_suppl.119S
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Genetic alterations are a hallmark of human cancer. Changes in DNA methylation, an epigenetic modification that is present in mammalian cells, are also characteristic of human cancer. The CpG dinucleotide, which is usually underrepresented in the genome, is clustered in the promoter regions of some genes. These promoter regions have been termed CpG islands. CpG islands are protected from methylation in normal cells, with the exception of genes on the inactive X chromosome and imprinted genes.1 This protection is critical, since the methylation of promoter region CpG islands is associated with a loss of expression of these genes. The following three different alterations in DNA methylation are common in human cancer: (1) global hypomethylation, often seen within the body of genes; (2) dysregulation of DNA methyltransferase I, the enzyme involved in maintaining methylation patterns, and potentially other methyltransferases; and (3) regional hypermethylation in normally ummethylated CpG islands.

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