This book provides researchers and practitioners with a unique collection of current research on the role of vitamins and micronutrients in cancer prevention and treatment. New theories are discussed, including a hypothesis that dietary factors may protect against genetically predisposed cancers. Mechanisms by which different vitamins and minerals appear to inhibit carcinogenesis or cell transformation are described, including vitamins A, C, E, and selenium protection against oxidative stress by induction of enzymes as catalase and dismutase or inteference with free radical mechanisms; organosulfur compound inhibition of P450 activation enzymes or enhancement of detoxification enzymes; metal ion effects in the modulation of gene expression by site-specific binding of Zn-finger loop domains; B-carotene metabolite up-regulation of gap junctional communication between cells; and vitamin D3 elimination of amplified oncogenes or drug resistant genes. The book also reviews literature implicating a possible relationship between potassium and the control of cancer. Other information presented includes a discussion of contemporary technologies and data associating lipotrope deficiencies with alterations in xenobiotic metabolism, nucleic acid methylation, purine and pyrimidine synthesis, signal transduction, and chromosome anomalies.

The fifth of the annual research conferences of the American Institute for Cancer Research was held September l-2, 1994, at the L'Enfant Plaza Hotel in Washington, DC. Appropriately, in view of current directions in research, the theme was "Diet and Cancer: Molecular Mechanisms of Interactions". This proceedings volume contains chapters from the platform presentations and abstracts from the poster session held on the end of the first day. The subtopics for the tl;rree sessions held were "Retinoids, Vitamins A and Din Cancer Prevention and Therapy," "Choline and Lipids: Signal Transduction, Gene Expression and Growth Regulation," and "Dietary Factors and Regulation of Oncogenes, Growth and Differentiation. " A general overview on vitamins A and D emphasized that A and D, in addition to their established roles in vision, reproduction, and bone mineral homeostasis, may play significant roles in regulating cell function. Vitamin A metabolites, trans-retinoic acid and 9-cis-retinoic acid, regulate growth and differentiation. Furthermore, vitamin A deprived animals were more susceptible to both spontaneous and carcinogen-induced tumors. Epidemiological studies showed a correlation between low A intake and higher incidences of certain types of human cancers. Conversely, all-trans retinoic acid is useful in treatment and control of certain types of cancer. Physiologically, Vitamin D is converted to the active form, l ,25-dihydroxyvitamin D (VD). VD regulates hormone production and secretion, myocardial contractility, vascu 3 3 3 lar tone, and growth inhibition and differentiation.

The American Institute for Cancer Research (AICR) sponsored its third annual confer ence on nutrition and cancer. The theme was "Diet and Cancer: Markers, Prevention, and Treatment. " The conference was held October 29-30, 1992 at the Ritz Carlton Hotel in McLean, Virginia. This proceedings contains chapters from the platform presentations and abstracts from the poster presentations. Several chapters address each of four session topics: Retinoids as Differentiation Agents in Cancer Therapy, Biological Markers of Cancer Risk, Chemoprevention of Cancer by Non-Nutrients in Foods, and Nutritional Problems and Support in the Treatment of Cancer. The first three chapters discuss in detail different mechanisms by which retinoids influence differentiation and provide evidence to support their use in cancer therapy. In vivo and in vitro studies show the effects of retinoic acid (RA) on tumorigenicity and cellu lar/molecular events. A synopsis of data showing the involvement of the retinoblastoma (RB) gene in HL-60 cell differentiation induced by RA and 1,2S-dihydroxy vitamin D3 (VD) is presented. In SCID (severe combined immunodeficiency) mice injected with HL-60 3 human leukemia cells and gavaged daily with RA, the number of tumor sites and number of mice with tumors are reduced. All trans-RA induces myeloid differentiation in HL-60 cells. Similarly, VD3 induces HL-60 monocytic differentiation. In both cases an early down regulation of retinoblastoma (RB) gene expression precedes the differentiation.

The fifth of the annual research conferences of the American Institute for Cancer Research was held September l-2, 1994, at the L'Enfant Plaza Hotel in Washington, DC. Appropriately, in view of current directions in research, the theme was "Diet and Cancer: Molecular Mechanisms of Interactions." This proceedings volume contains chapters from the platform presentations and abstracts from the poster session held on the end of the first day. The subtopics for the tl;rree sessions held were "Retinoids, Vitamins A and Din Cancer Prevention and Therapy," "Choline and Lipids: Signal Transduction, Gene Expression and Growth Regulation," and "Dietary Factors and Regulation of Oncogenes, Growth and Differentiation. " A general overview on vitamins A and D emphasized that A and D, in addition to their established roles in vision, reproduction, and bone mineral homeostasis, may play significant roles in regulating cell function. Vitamin A metabolites, trans-retinoic acid and 9-cis-retinoic acid, regulate growth and differentiation. Furthermore, vitamin A deprived animals were more susceptible to both spontaneous and carcinogen-induced tumors. Epidemiological studies showed a correlation between low A intake and higher incidences of certain types of human cancers. Conversely, all-trans retinoic acid is useful in treatment and control of certain types of cancer. Physiologically, Vitamin D is converted to the active form, l,25-dihydroxyvitamin D (VD). VD regulates hormone production and secretion, myocardial contractility, vascu 3 3 3 lar tone, and growth inhibition and differentiation."

The American Institute for Cancer Research (AICR) sponsored its third annual confer ence on nutrition and cancer. The theme was "Diet and Cancer: Markers, Prevention, and Treatment. " The conference was held October 29-30, 1992 at the Ritz Carlton Hotel in McLean, Virginia. This proceedings contains chapters from the platform presentations and abstracts from the poster presentations. Several chapters address each of four session topics: Retinoids as Differentiation Agents in Cancer Therapy, Biological Markers of Cancer Risk, Chemoprevention of Cancer by Non-Nutrients in Foods, and Nutritional Problems and Support in the Treatment of Cancer. The first three chapters discuss in detail different mechanisms by which retinoids influence differentiation and provide evidence to support their use in cancer therapy. In vivo and in vitro studies show the effects of retinoic acid (RA) on tumorigenicity and cellu lar/molecular events. A synopsis of data showing the involvement of the retinoblastoma (RB) gene in HL-60 cell differentiation induced by RA and 1,2S-dihydroxy vitamin D3 (VD) is presented. In SCID (severe combined immunodeficiency) mice injected with HL-60 3 human leukemia cells and gavaged daily with RA, the number of tumor sites and number of mice with tumors are reduced. All trans-RA induces myeloid differentiation in HL-60 cells. Similarly, VD3 induces HL-60 monocytic differentiation. In both cases an early down regulation of retinoblastoma (RB) gene expression precedes the differentiation."

The American Institute for Cancer Research (AICR) sponsored its second annual conference on nutrition and cancer. The theme was "Exercise, Calories, Fat, and Cancer" and the conference was held September 4-5, 1991 at the Ritz Carlton Hotel in Pentagon City, Virginia. This proceedings volume contains chapters from the platform presentations and abstracts from each poster presentation. Relationships among physical activity, calorie consumption, energy expenditure, dietary fat, and cancer are described in the context of epidemiologic, animal, and in vitro studies. Dietary recommendations to lower cancer risk are based on expanding evidence relating nutrition and cancer. Identification of the precise dietary contribution to disease is complicated by the concurrent genetic and environmental contributions, in addition to the inherent difficulties in gathering and interpreting epidemiologic data. Individual variations in cancer risk are the result of differences in genetic and environmental factors including sources and amounts of calories consumed, metabolism, and energy expenditure. Human and animal studies describing independent and combined influences of exercise, calorie restriction, and dietary fat on carcinogenesis are reported in this volume.