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Evidence continues to mount that dietary components are important determinants of cancer risk and tumor behavior Although these linkages are fascinating, numerous inconsistencies are also evident in the literature. Although multifactorial, these discrepancies likely reflect variation in the ability of food constituents to reach and/or modify critical molecular targets. Genetic polymorphisms can alter the response to dietary components (nutrigenetic effect) by influencing the absorption, metabolism, or site of action. Like-wise, variation in DNA methylation patterns and other epigenomic events that influence overall gene expression can influence the biological response to food components and vice versa. Fluctuations in the ability of food components to increase or depress gene expression (nutritional transcriptomic effect) may also account for some of the inconsistencies in the response to foods. Functional proteomic studies that capture all of the proteins produced by a species and link them to physiological significance within the cell will be fundamental to understanding the relationship between dietary interventions, proteome changes, and cancer Although a bioactive food component may influence a number of key molecular events that are involved with cancer prevention, to do so it must achieve an effective concentration within the target site, be in the correct metabolic form, and bring about a change in one or more small molecular weight signals in the cellular milleau (metabolomic effects). Fundamental to assessing and evaluating the significance of the interrelationships among bioactive food components with nutrigenetics, nutritional epigenomics, nutritional transcriptomics, proteomics, and metabolomics is knowledge about the appropriate tissue/cell or surrogate to evaluate and validated biomarkers that reflect changes in each. As the era of molecular nutrition grows, a greater understanding about the role of foods and their components on cancer risk and tumor behavior will surely unfold. Such information will be critical in the development of effective preemptive approaches to reduce the cancer burden. [ABSTRACT FROM AUTHOR]

Dietary nutrients can influence cancer risk by inhibiting or enhancing carcinogenesis through diverse mechanisms of action. The identification and elucidation of their sites of action have been a focus of nutrition and cancer research for more than four decades. Transforming nutrition and cancer research from a predominantly observational to a molecular approach offers exciting opportunities for truly identifying those who will and will not benefit from dietary intervention strategies. The emerging field of nutritional genomics, defined here as the study of any genetic or epigenetic interaction with a nutrient, will be key to this evolution. Unraveling which genetic upregulation or downregulation leads to subsequent phenotype changes will not be easy. There is evidence that genetic polymorphisms can influence the dynamics between nutrients and molecular targets and, thus, contribute to variation in response among individuals. Because many molecular targets will likely be identified, it may be necessary to credential nutrients, that is, to determine which specific nutrient-related genetic and epigenetic changes bring about phenotypic changes, to establish which interactions are the most important and under what circumstances. Vitamin D, calcium, folate, selenium, genistein, and resveratrol are highlighted, because they represent specific classes of nutrients and illustrate the need to credential various nutrients to understand their physiological significance in cancer prevention. As the science of nutrition unfolds, a clearer understanding will emerge about how nutrients can modulate cancer risk through molecular interactions and how foods might be changed by agronomic approaches and/or biotechnology. Undeniably, embracing new genomic technologies offers exciting opportunities for advances in the broad area of nutrition, especially those related to cancer prevention. [ABSTRACT FROM AUTHOR]

Discoveries about molecular targets for nutrients will unquestionably provide important clues into how best to optimize nutrition for an individual. The 'Credentialing' of nutrients in terms of their influence on genetic and epigenetic events that bring about a desired phenotypic change is surely within the future of nutrition science. [ABSTRACT FROM AUTHOR]

Knowledge gaps persist about the efficacy of cancer prevention strategies based on dietary food components. Adaptations to nutrient supply are executed through tuning of multiple protein networks that include transcription factors, histones, modifying enzymes, translation factors, membrane and nuclear receptors, and secreted proteins. However, the simultaneous quantitative and qualitative measurement of all proteins that regulate cancer processes is not practical using traditional protein methodologies. Proteomics offers an attractive opportunity to fill this knowledge gap and unravel the effects of dietary components on protein networks that impinge on cancer. The articles presented in this supplement are from talks proffered in the "Nutrition Proteomics and Cancer Prevention" session at the American Institute for Cancer Research Annual Research Conference on Food, Nutrition, Physical Activity and Cancer held in Washington, DC on October 21 and 22, 2010. Recent advances in MS technologies suggest that studies in nutrition and cancer prevention may benefit from the adoption of proteomic tools to elucidate the impact on biological processes that govern the transition from normal to malignant phenotype; to identify protein changes that determine both positive and negative responses to food components; to assess how protein networks mediate dose-, time-, and tissue-dependent responses to food components; and, finally, for predicting responders and nonresponders. However, both the limited accessibility to proteomic technologies and research funding appear to be hampering the routine adoption of proteomic tools in nutrition and cancer prevention research. [ABSTRACT FROM AUTHOR]