Download Diet and Cancer: Molecular Mechanisms of Interactions by R. M. Niles (auth.) PDF

By R. M. Niles (auth.)

The 5th of the yearly learn meetings of the yankee Institute for melanoma examine was once held September l-2, 1994, on the L'Enfant Plaza resort in Washington, DC. thoroughly, in view of present instructions in examine, the subject matter was once "Diet and melanoma: Molecular Mechanisms of Interactions". This lawsuits quantity includes chapters from the platform shows and abstracts from the poster consultation hung on the tip of the 1st day. The subtopics for the tl;rree classes held have been "Retinoids, supplementations A and Din melanoma Prevention and Therapy," "Choline and Lipids: sign Transduction, Gene Expression and development Regulation," and "Dietary elements and law of Oncogenes, progress and Differentiation. " A basic review on supplementations A and D emphasised and D, as well as their confirmed roles in imaginative and prescient, copy, and bone mineral homeostasis, may possibly play major roles in regulating cellphone functionality. nutrition A metabolites, trans-retinoic acid and 9-cis-retinoic acid, keep watch over development and differentiation. additionally, diet A­ disadvantaged animals have been extra prone to either spontaneous and carcinogen-induced tumors. Epidemiological stories confirmed a correlation among low A consumption and better incidences of specific sorts of human cancers. Conversely, all-trans retinoic acid comes in handy in remedy and keep an eye on of particular types of melanoma. Physiologically, diet D is switched over to the lively shape, l ,25-dihydroxyvitamin D (VD). VD regulates hormone creation and secretion, myocardial contractility, vascu­ three three three lar tone, and development inhibition and differentiation.

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At first, the reason for this shift was not clear; however, we realized that the serum in our culture medium contained retinoids. In normal cervical cells, cytokeratin expression is retinoid responsive; however, the retinoid levels present in the culture medium are not high enough to influence keratin gene expression. The dramatic shift in the pattern ofkeratin gene expression in the HPV 16-immortalized cells could be explained if the cells had become sensitized to the effects ofretinoids. To test this hypothesis, we grew ECE16-l cells in retinoid-free medium or in medium supplemented with various natural or synthetic retinoids and monitored the effects on keratin gene expression (28).

Abnormal bronchial airway histology was very common. All subjects had basal cell hyperplasia on at least one biopsy (Figure lA). Eight of 13 (62%) subjects had squamous metaplasia with keratinization, the most severe pathologic change on at least 1 biopsy (Figure 1C, Table 3). These findings are consistent with our earlier studies, and suggest that airway metaplasia may be an appropriate biomarker of airway injury and I or increased risk for lung cancer in these subjects. D. 3 ug/dl) were determined as described above (Table 3).

1994. 6. , Itri LM. Retinods and human cancer, in "The Retinoids: Biology, Chemistry, and Medicine, Sporn MB, Roberts AB, eds. 1994. 7. Doll R, Peto R. The causes of cancer: Quantitative estimates of avoidable risks of cancer in the United States today, J Nat/ Cancer Inst 66:1192-1308 (1981). 8. Gazdar AF. The molecular and cellular basis of human lung cancer, Anticancer Res 13:261-268 (1994). 9. Minna JD. The molecular biology of lung cancer pathogenesis, Chest 103:445S-56S (1993). 10. Ames BN, Gold LS.

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