By Peter Greenwald (auth.), Vincenzo Zappia, Fulvio Della Ragione, Alfonso Barbarisi, Gian Luigi Russo, Rossano Dello Iacovo (eds.)
This quantity comprises contributions awarded on the moment foreign Sym posium on meals and melanoma, held in Naples, Italy, in October 1998 on the nationwide Tumor Institute "Fondazione Pascale." through the convention, specialists from various disciplines mentioned pivotal and well timed matters at the interactions among human foodstuff and the advance of malignancies. evaluating the subjects of this assembly with these mentioned on the First Sympo sium in 1992, the foremost clinical developments definitely derive from the vast use of molecular techniques to accomplish learn in meals. furthermore, the elemental remark of R. Doll and R. Peto (1981), which recommended that not less than 35% of all cancers (with huge variations between varied tumors) may be avoided through nutritional regimens, has been definitively proven through epidemiological experiences. nevertheless, the relationships among nutrition and melanoma are really elaborate and complicated; it's tricky, and while no longer methodologically right, to minimize them to uncomplicated phrases. Metabolic and hormonal components, contaminants and organic brokers, and deficiency of particular protecting meals are all items of a similar puzzle.
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Extra info for Advances in Nutrition and Cancer 2
Nutritional Factors in Human Cancers 41 84. G. Folate status and adenomatous colonic polyps. A colonoscopieally controlled study. Dis Colon Rectum. 1995; 38:64-68. 85. D. Vegetables, fruit, and cancer. II. Mechanisms. Cancer Causes Control. 1991;2:427-442. 86. A. Prooxidant states and tumor promotion. Science. 1985;227:375-381. 87. Wiseman H. and Halliwell B. Damage to DNA by reactive oxygen and nitrogen species: role in inflammatory disease and progression to cancer. Biochem 1. 1996;313:17-29.
The transfer of the methyl group from 5-methyl tetrahydrofolate to homocysteine forms methionine, a reaction also requiring cobalamin. If compensatory production of methionine is hindered by insufficient 5-methyl tetrahydrofolate level, and possibly cobalmine levels, the methyl supply for DNA methylation may be inadequate. Because these processes would appear to be important for cell types in general, it is possible that folate deficiency could be a risk factor for numerous cancer types. In fact, some supportive though inconclusive evidence exists for various cancer sites.
DNA synthesis and repair processes are dependent on various nutritional factors, including folic acid. 5,10-methylene tetrahydrofolate is the cellular form of folate required for synthesis of thymidine. 60-62 Recently, Blount et a1. 63 demonstrated that folate deficiency caused massive incorporation of uracil into human DNA and to increased frequency of chromosomal breaks. These were reversed when folate-deficient individuals were treated with folic acid supplementation. The methylation of DNA cytosine at specific cytosine-phospho-guanine (epG) sites inhibits gene transcription and, thus, has a role in the regulation of gene expression.