| Sign In to gain access to subscriptions and/or personal tools. |
Nutrition and Tumor Promotion: In Vivo Methods for Measurement of Cellular Proliferation and Protein MetabolismNutrition/Infection Laboratory, Cancer Research Institute, New England Deaconess Hospital, Harvard Medical School, Boston
Nutrition/Infection Laboratory, Cancer Research Institute, New England Deaconess Hospital, Harvard Medical School, Boston
Nutrition/Infection Laboratory, Cancer Research Institute, New England Deaconess Hospital, Harvard Medical School, Boston
The notion that tumors act as "nitrogen traps" has led to the belief that nutrition support of the cancer-bearing patient can enhance tumor growth. Proponents of this theory consider the provision of energy and essential nutrients as well as the influence of hormones and growth factors as responsible for this effect. On the other hand, nutrition administration in the debilitated cancer patient may improve antitumor host defense mechanisms and reduce tumor growth. This paper reviews methodologic issues related to the study of nutrition and cancer growth with emphasis on in vivo methods for measuring tumor protein turnover and cytokinetics. Using this combined approach, we previously demonstrated that dietary fat may significantly regulate tumor growth during chronic feeding as well as with short-term intravenous nutrition support in experimental models. Although the mechanism of this effect remains unclear, we have reasoned that by altering arachidonic acid metabolism and prostaglandin synthesis,
Journal of Parenteral and Enteral Nutrition, Vol. 16, No. 6 Suppl,
76S-82S (1992) This article has been cited by other articles:
|
|
|||||||||||||||
 |
|
|
 |
|
Sign In to gain access to subscriptions and/or personal tools.
-3 fatty acids could change tumor protein breakdown rates and inhibit the proliferation potential of these tumors. Acknowledging alternative hypotheses, we now present cytokinetic evidence that intracellular protein degradation may regulate tumor cell proliferation. Additional studies relating dietary fat, tumor protein metabolism and tumor proliferation potential are currently in progress. We propose that the effect of nutrition administration on tumor growth is complex and involves several regulatory systems. Thus, based on available evidence, an a priori tumor-enhancing effect for nutrition support is clearly not warranted. Intracellular protein breakdown and host defense mechanisms, both of which are energy dependent, are important loci at which nutrition and tumor growth regulation could interact. Results from experimental tumor models have indicated that specific dietary fats, such as fish oil and structured lipids, may be used favorably in the nutrition support of the cancer patient. (Journal of Parenteral and Enteral Nutrition 16:76S-82S, 1992) 
