PMID: 9659578Jul 11, 1998Paper

Role of the cytosine DNA-methyltransferase and p16INK4a genes in the development of mouse lung tumors

Experimental Lung Research
Steven A Belinsky

Abstract

CpG island methylation is an epigenetic modification of DNA associated with the silencing of gene transcription. The p16INK4a (p16) tumor suppressor gene is inactivated in human non-small cell lung cancers (NSCLCs) by either homozygous deletion or aberrant methylation. Inactivation of tumor suppressor genes by methylation has been linked in part to altered activity of the cytosine DNA-methyltransferase (DNA-MTase), the enzyme that catalyzes DNA methylation at CpG sites. The purpose of these studies was to define the role of DNA-MTase and p16 in the development of murine lung cancer. DNA-MTase activity was determined in alveolar type II and Clara cells from A/J and C3H mice that exhibit high and low susceptibility, respectively, for lung tumor formation. Increased DNA-MTase activity leading to an increase in overall DNA methylation was found only in alveolar type II cells, the target for murine adenocarcinomas. Both DNA-MTase and DNA methylation changes were detected 7 days after carcinogen exposure and, thus, were early events in neoplastic evolution. In addition, enzyme activity increased incrementally during lung cancer progression. Expression of p16 was detected in all primary lung tumors from A/J mice; however, levels of ex...Continue Reading

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Jan 8, 2008·Journal of Toxicology and Environmental Health. Part B, Critical Reviews·Neelam AzadVal Vallyathan
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Jan 1, 2013·International Journal of Chronic Diseases·Mann Ying Lim, Paul S Thomas

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