![]() |
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Nutritional Sciences Research Group, Division of Cancer Prevention, National Cancer Institute, Department of Health and Human Services, Rockville, MD 20852
2To whom correspondence should be addressed. E-mail: milnerj{at}mail.nih.gov.
Mounting evidence points to dietary habits as an important determinant of cancer risk and tumor behavior. Although the linkages with diet are intriguing, the literature is also laden with inconsistencies. The reasons for these inconsistencies are likely multi-factorial, but probably reflect variations in the ability of bioactive constituents to reach or affect critical molecular targets. Fluctuations in the foods consumed not only influence the intake of particular bioactive components, but may alter metabolism and potentially influence the sites of action of both essential and nonessential nutrients. Genetic polymorphisms are increasingly recognized as another factor that can alter the response to dietary components (nutritional transcriptomic effect) by influencing the absorption, metabolism, or sites of action. Likewise, variation in DNA methylation patterns and other epigenetic events that influence overall gene expression can be influenced by dietary intakes. Furthermore, variation in the ability of food components to increase or depress gene expression (nutrigenomic effect) may account for some of the observed inconsistencies in the response to dietary change. Because a host of food components are recognized to influence phosphorylation and other posttranslational events, it is also likely that these and other proteomic modifications account for at least part of the response and variation that is reported in the literature. Collectively, it is clear that bioactive food components can influence a number of key molecular events that are involved in health and disease resistance. As the era of molecular nutrition unfolds, a greater understanding of how these foods and components influence cancer will surely arise. Such information will be critical in the development of effective tailored strategies for reducing cancer burden. Just as important, however, is that as this information unfolds it is utilized within a responsible bioethical framework.
KEY WORDS: bioactive nutrigenomics nutrigenetics proteomics metabolomics
This article has been cited by other articles:
![]() |
N. Matsuura, Y. Miyamae, K. Yamane, Y. Nagao, Y. Hamada, N. Kawaguchi, T. Katsuki, K. Hirata, S.-I. Sumi, and H. Ishikawa Aged Garlic Extract Inhibits Angiogenesis and Proliferation of Colorectal Carcinoma Cells J. Nutr., March 1, 2006; 136(3): 842S - 846S. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. R. Martin Targeting Apoptosis with Dietary Bioactive Agents Experimental Biology and Medicine, February 1, 2006; 231(2): 117 - 129. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. Uauy and N. Solomons Diet, Nutrition, and the Life-Course Approach to Cancer Prevention J. Nutr., December 1, 2005; 135(12): 2934S - 2945S. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. L. Rock, S. W. Flatt, L. Natarajan, C. A. Thomson, W. A. Bardwell, V. A. Newman, K. A. Hollenbach, L. Jones, B. J. Caan, and J. P. Pierce Plasma Carotenoids and Recurrence-Free Survival in Women With a History of Breast Cancer J. Clin. Oncol., September 20, 2005; 23(27): 6631 - 6638. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. Zaina, M. W. Lindholm, and G. Lund Nutrition and Aberrant DNA Methylation Patterns in Atherosclerosis: More than Just Hyperhomocysteinemia? J. Nutr., January 1, 2005; 135(1): 5 - 8. [Abstract] [Full Text] [PDF] |
||||