title: Nutrition and tumor promotion: in vivo methods for measurement of cellular proliferation and protein metabolism.
abstract: 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, omega-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.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Nutrition/Infection Laboratory, New England Deaconess Hospital, Harvard Medical School, Boston, MA 02115.
authors.forename: N W
authors.initials: NW
authors.lastname: Istfan
authors.forename: J M
authors.initials: JM
authors.lastname: Wan
authors.forename: B R
authors.initials: BR
authors.lastname: Bistrian
mesh_terms: D000818:Animals; D002455:Cell Division; D004032:Diet / Q000009:adverse effects*; D004041:Dietary Fats / Q000009:adverse effects; D006801:Humans; D009363:Neoplasm Proteins / Q000378:metabolism*; D009369:Neoplasms / Q000378:metabolism / Q000473:pathology*; D009374:Neoplasms, Experimental / Q000473:pathology; D010289:Parenteral Nutrition, Total / Q000009:adverse effects*
chemical_list: D004041:Dietary Fats; D009363:Neoplasm Proteins