Cancer is a genetic disease resulting from multiple genetic defects caused by exposure to environmental, dietary, and infectious agents as well as other lifestyle factors. Figure 2.2 presents a conceptual framework for these relationships, showing the molecular mechanisms of dietary constituents in the carcinogenesis pathway, from activation of procarcinogens to the initiation and promotion stages of carcinogenesis, and to tissue invasion and metastasis.20
The implications of our broadening knowledge of the biology of cancer and the impact of nutrient intake is that we can hope to utilize nutritional interventions to slow the progression of tumor development in the intraepithelial hyperplasia phase before tumor size becomes large enough for diagnosis and probability of metastasis increases (Figure 2.3).110 Opportunity exists to stretch this prevention phase so that symptom-free life of the future patient with cancer is prolonged. Because the median age of cancer diagnosis in the U.S. is 70 years, and the average life expectancies are 74 years for men and 79 years for women, cancer delay may result in total prevention for many people.111
In the postgenomic era, new opportunities are arising from advances in nutrition sciences to understand the integrative biology of living organisms. The complexities of the interactions among genotype, diet, and environment are unraveling, and personalized nutrition recommendations for individuals will become feasible. Nutritional genomics, proteomics, and metabolic profiling use high throughput technologies that enable researchers to analyze thousands of genes and their interactions simultaneously. Nutritional genomics refers to the interface of plant biochemistry, genomics, and human nutrition for the purpose of understanding and manipulating nutrient reactions and interactions at the molecular or genomic level.8 One mechanism involves gene-nutrient interactions in relation to specific gene polymorphisms among individuals have already been identified. The example of broccoli intake in relation to colon cancer risk in GSTM1-null genotype individuals was reviewed earlier. Another example involves certain polymorphisms in the methylenetetrahydrofolate reductase gene, a key enzyme in one-carbon metabolism, that have been associated with a lower risk of developing colorectal cancer, but only in persons with adequate folate status.112
The resulting data facilitate molecular analysis of bioactive food components and identification of appropriate biomarkers that target individuals who are at risk and predisposed to cancer. Ever-increasing evidence, including that presented in this volume, substantiate the beneficial effects of certain nutrients and interactions between nutrients in the carcinogenesis pathway, paving the way for modification of nutritional requirements as a cancer prevention strategy. In the future, diet, nutrition, and cancer prevention will be included in public health programs that target cancer risk management in the population at large, and on individual programs that focus on particular cancer risk profiles. Concomitantly, agricultural sciences will continue to develop improved plants through both traditional breeding techniques and genetic modification and food industries will provide functional foods enriched with beneficial nutrients.920 Targeting cancer prevention with specific foods and/or bioactive components is a relatively nontoxic and cost-effective strategy for reducing cancer burden. However, the complexity of the human diet coupled with individual variation in the carcinogenesis process will make continued research in the area of diet and cancer prevention mandatory.46
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Learning About 10 Ways Fight Off Cancer Can Have Amazing Benefits For Your Life The Best Tips On How To Keep This Killer At Bay Discovering that you or a loved one has cancer can be utterly terrifying. All the same, once you comprehend the causes of cancer and learn how to reverse those causes, you or your loved one may have more than a fighting chance of beating out cancer.