Pathophysiology of cancer cachexia: Much more than host-tumour interaction?

被引：121

作者：

Skipworth, Richard J. E. ^{[1
]}

Stewarta, Grant D. ^{[1
]}

Dejong, Cornelis H. C. ^{[2
,3
]}

Preston, Tom ^{[4
]}

Fearon, Kenneth C. H. ^{[1
]}

机构：

[1] Univ Edinburgh, Royal Infirm, Sch Clin Sci & Community Hlth, Edinburgh EH16 4SA, Midlothian, Scotland

[2] Univ Maastricht, Dept Surg, NL-6202AZ Maastricht, Netherlands

[3] NUTRIM, NL-6202AZ Maastricht, Netherlands

[4] Univ Glasgow, Scottish Univ Environm Res Ctr, Glasgow G75 0QF, Lanark, Scotland

来源：

CLINICAL NUTRITION | 2007年 / 26卷 / 06期

关键词：

cancer; pathophysiology; protein metabolism; elderly; physical activity;

D O I：

10.1016/j.clnu.2007.03.011

中图分类号：

R15 [营养卫生、食品卫生]; TS201 [基础科学];

学科分类号：

100403 ;

摘要：

Cancer cachexia is a syndrome of progressive nutritional depletion which causes significant morbidity and mortality in cancer patients. One of the main pathogenetic mechanisms underlying cancer cachexia. is a complex interaction between the host and the tumour. Tumour cells interact with host cells within the tumour mass resulting in the production of catabolic mediators which degrade host tissue. In addition, the host may mount an aberrant metabolic response to the tumour. However, in recent years, it has also been understood that patient factors, including age and levels of physical activity, and the specific mechanics of protein metabolism in cancer patients may also have a significant impact. In this review article, we not only summarise previous knowledge surrounding host-tumour interaction, but we also discuss these broader concepts in the pathogenesis of cancer cachexia. Clinicians should consider such concepts in the design of an effective multimodal therapy for cachexia. (C) 2007 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.

引用

页码：667 / 676

页数：10

共 65 条

[1] Modulation of the liver export protein synthetic response to feeding by an n-3 fatty-acid-enriched nutritional supplement is associated with anabolism in cachectic cancer patients [J].