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Effects of Budesonide on Overall 5-Methylcytosine Levels and Specific Methylation and Messenger RNA Expression of the Insulin-Like Growth Factor II Gene in Mouse Lung Tumors*

Ronald Lubet, PhD; Lianhui Tao; Wei Wang; Paula Kramer; Michael Perreira
Author and Funding Information

*From the Chemopreventive Agent Development Research Group-Division of Cancer Prevention (Dr. Lubet), National Cancer Institute, Rockville, MD; and the Department of Pathology (Drs. Tao, Wang, Kramer, and Perreira), Medical College of Ohio, Toledo, OH.

Correspondence to: Ronald A. Lubet, PhD, Program Director, NCI-DCP, Rm 2110, 6130 Executive Dr, Rockville, MD 20852; e-mail: rl57q@nih.gov



Chest. 2004;125(5_suppl):157S. doi:10.1378/chest.125.5_suppl.157S
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The effects of limited treatment with budesonide, an effective chemopreventive agent, on 5-methylcytosine (5MC) levels, and on the specific hypomethylation and expression of the insulin-like growth factor (IGF) II gene in mouse lung tumors was determined. Female strain A mice were administered two weekly doses of vinylcarbamate intraperitoneally. Thirty-four weeks later, mice were administered dietary budesonide (2.4 or 0.6 ppm in diet) or vehicle control for a period of 7 days and then were killed. We found that the level of 5MC in lung tumors, measured immunologically, was reduced roughly 60% when compared with normal lung parenchyma, which is in agreement with generalized hypomethylation in many tumors. In contrast, tumors treated with budesonide for 7 days exhibited a dose-dependent increase in 5MC, with the higher dose giving 5MC levels similar to control lung parenchyma.

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