Dietary Fats, Lipids, Hormones, and Tumorigenesis New Horizons in Basic Research

This book was inspired by a gatheringofscientists in Los Angeles in 1994 under the auspices of the UCLA Clinical Nutrition Research Unit which is funded by the National Cancer Institute to promote new research into nutrition and cancer prevention. This unit supports research integrating basic and me...

Full description

Bibliographic Details
Other Authors: Heber, David (Editor), Kritchevsky, David (Editor)
Format: eBook
Language:English
Published: New York, NY Springer US 1996, 1996
Edition:1st ed. 1996
Series:Advances in Experimental Medicine and Biology
Subjects:
Online Access:
Collection: Springer Book Archives -2004 - Collection details see MPG.ReNa
LEADER 03605nmm a2200361 u 4500
001 EB000621378
003 EBX01000000000000000474460
005 00000000000000.0
007 cr|||||||||||||||||||||
008 140122 ||| eng
020 |a 9781461311515 
100 1 |a Heber, David  |e [editor] 
245 0 0 |a Dietary Fats, Lipids, Hormones, and Tumorigenesis  |h Elektronische Ressource  |b New Horizons in Basic Research  |c edited by David Heber, David Kritchevsky 
250 |a 1st ed. 1996 
260 |a New York, NY  |b Springer US  |c 1996, 1996 
300 |a X, 186 p  |b online resource 
505 0 |a 1. Overview of Fat and Calories in Tumorigenesis -- 2. Interrelationships of High Fat Diets, Obesity, Hormones, and Cancer -- 3. Nutritional, Hormonal, and Environmental Mechanisms in Breast Tumorigenesis -- 4. Stromal-Epithelial Cell Interactions in Breast Cancer -- 5. 20-EPI-Vitamin D3 Analogs: Potent Modulators of Proliferation and Differentiation of Breast Cancer Cell Lines in Vitro -- 6. Novel Lipids and Cancer: Isoprenoids and Other Phytochemicals -- 7. Metabolism of Exogenous and Endogenous Arachidonic Acid in Cancer -- 8. Stable Isotopes and Mass Isotopomer Study of Fatty Acid and Cholesterol Synthesis: A Review of the MIDA Approach -- 9. Lipid Biomarkers of Adherence to Low Fat Diets -- 10. Choline: A Nutrient that is Involved in the Regulation of Cell Proliferation, Cell Death, and Cell Transformation -- 11. The Role of Folate, Choline, and Methionine in Carcinogenesis Induced by Methyl-Deficient Diets -- 12. Dietary Fat and Colon Cancer -- 13. High Fat Diet, Lipid Peroxidation, and Pancreatic Carcinogenesis -- 14. Nutritional Approaches to the Prevention of Prostate Cancer Progression 
653 |a Animal Anatomy 
653 |a Anatomy, Comparative 
653 |a Nutrition    
653 |a Botany 
653 |a Immunology 
653 |a Nutrition 
653 |a Plant Science 
653 |a Oncology 
700 1 |a Kritchevsky, David  |e [editor] 
041 0 7 |a eng  |2 ISO 639-2 
989 |b SBA  |a Springer Book Archives -2004 
490 0 |a Advances in Experimental Medicine and Biology 
028 5 0 |a 10.1007/978-1-4613-1151-5 
856 4 0 |u https://doi.org/10.1007/978-1-4613-1151-5?nosfx=y  |x Verlag  |3 Volltext 
082 0 |a 616.994 
520 |a This book was inspired by a gatheringofscientists in Los Angeles in 1994 under the auspices of the UCLA Clinical Nutrition Research Unit which is funded by the National Cancer Institute to promote new research into nutrition and cancer prevention. This unit supports research integrating basic and metabolic/clinical investigations which examine observations from epidemiologic studies and their application to the prevention ofcommon forms ofcancer through nutritional intervention. There is a great deal ofinformation from epidemiologic, experimental and metabolic studies implicating elements ofthe diet as important in the development and progression of common forms ofcancer including breast cancer, colon cancer, prostate cancer, and uterine cancer. When these forms ofcancerareexaminedcarefully, it isclearthat they share anumber ofcommon etiologic factors related to dietary fat, lipids, and hormones. A human cancer is usually discovered at a point where it has formed a detectable mass. For many forms of cancer, this may require 10 to 15 years from the time when the cancer is first initiated. Nutritional efforts at prevention may delay the progression ofcancer to a detectable mass resulting in reduced incidence and may retard the clinical progression and metastatic spread ofcancer after its primary treatment