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Conference Paper: Nutrition and tumor promotion: In vivo methods for measurement of cellular proliferation and protein metabolism

TitleNutrition and tumor promotion: In vivo methods for measurement of cellular proliferation and protein metabolism
Authors
Issue Date1992
PublisherSage Publications, Inc.. The Journal's web site is located at http://pen.sagepub.com
Citation
Journal Of Parenteral And Enteral Nutrition, 1992, v. 16 n. 6 SUPPL., p. 76S-82S How to Cite?
AbstractThe 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, ω-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.
Persistent Identifierhttp://hdl.handle.net/10722/179571
ISSN
2015 Impact Factor: 3.517
2015 SCImago Journal Rankings: 1.149
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorIstfan, NWen_US
dc.contributor.authorWan, JMen_US
dc.contributor.authorBistrian, BRen_US
dc.date.accessioned2012-12-19T09:59:54Z-
dc.date.available2012-12-19T09:59:54Z-
dc.date.issued1992en_US
dc.identifier.citationJournal Of Parenteral And Enteral Nutrition, 1992, v. 16 n. 6 SUPPL., p. 76S-82Sen_US
dc.identifier.issn0148-6071en_US
dc.identifier.urihttp://hdl.handle.net/10722/179571-
dc.description.abstractThe 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, ω-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.en_US
dc.languageengen_US
dc.publisherSage Publications, Inc.. The Journal's web site is located at http://pen.sagepub.comen_US
dc.relation.ispartofJournal of Parenteral and Enteral Nutritionen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCell Divisionen_US
dc.subject.meshDiet - Adverse Effectsen_US
dc.subject.meshDietary Fats - Adverse Effectsen_US
dc.subject.meshHumansen_US
dc.subject.meshNeoplasm Proteins - Metabolismen_US
dc.subject.meshNeoplasms - Metabolism - Pathologyen_US
dc.subject.meshNeoplasms, Experimental - Pathologyen_US
dc.subject.meshParenteral Nutrition, Total - Adverse Effectsen_US
dc.titleNutrition and tumor promotion: In vivo methods for measurement of cellular proliferation and protein metabolismen_US
dc.typeConference_Paperen_US
dc.identifier.emailWan, JM: jmfwan@hku.hken_US
dc.identifier.authorityWan, JM=rp00798en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1177/014860719201600608-
dc.identifier.pmid1287229-
dc.identifier.scopuseid_2-s2.0-0026482506en_US
dc.identifier.volume16en_US
dc.identifier.issue6 SUPPL.en_US
dc.identifier.spage76Sen_US
dc.identifier.epage82Sen_US
dc.identifier.isiWOS:A1992JY96400008-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridIstfan, NW=7003819779en_US
dc.identifier.scopusauthoridWan, JM=8930305000en_US
dc.identifier.scopusauthoridBistrian, BR=35463916700en_US

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