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* National Institutes of Health, National Cancer Institute, Nutritional Sciences Research Group, Rockville, Maryland 20892–7328; and United States Department of Agriculture, Grand Forks Human Nutrition Research Center, Grand Forks, North Dakota 58202–9034
To whom requests for reprints should be addressed at 1 Nutritional Sciences Research Group, Division of Cancer Prevention, National Cancer Institute, 6130 Executive Boulevard, Suite 3159, Rockville, MD 20892–7328. E-mail: davisci{at}mail.nih.gov
DNA methylation is an important epigenetic mechanism of transcriptional control. DNA methylation plays an essential role in maintaining cellular function, and changes in methylation patterns may contribute to the development of cancer. Aberrant methylation of DNA (global hypomethylation accompanied by region-specific hypermethylation) is frequently found in tumor cells. Global hypomethylation can result in chromosome instability, and hypermethylation has been associated with the inaction of tumor suppressor genes. Preclinical and clinical studies suggest that part of the cancer-protective effects associated with several bioactive food components may relate to DNA methylation patterns. Dietary factors that are involved in one-carbon metabolism provide the most compelling data for the interaction of nutrients and DNA methylation because they influence the supply of methyl groups, and therefore the biochemical pathways of methylation processes. These nutrients include folate, vitamin B12, vitamin B6, methionine, and choline. However, looking at individual nutrients may be too simplistic. Dietary methyl (folate, choline, and methionine) deficiency in combination causes decreased tissue S-adeno-sylmethionine, global DNA hypomethylation, hepatic steatosis, cirrhosis, and ultimately hepatic tumorigenesis in rodents in the absence of carcinogen treatment. Other dietary components such as vitamin B12, alcohol, and selenium may modify the response to inadequate dietary folate.
Key Words: DNA methylation • cancer • folate • selenium • epigenetics
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