This Article  • References  • Full text PDF  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citation map  • Citing articles on HighWire  • Contact me when this article is cited  Related Content  • Similar articles in this journal  Social Bookmarking   What's this?

Mark C. Stovroff, MD; Douglas L. Fraker, MD; Jeffrey A. Norton, MD

Arch Surg. 1989;124(1):94-99.

Abstract
• Cachectin/tumor necrosis factor has been postulated to be a possible mediator of cancer cachexia. Using a sensitive bioassay, we attempted to detect circulating cachectin activity in the serum of sarcoma-bearing rats and to correlate levels with measurements of cachexia and the extent of disease. In addition, we resected the tumor to determine the time course of reversal of cachexia and the disappearance of cachectin activity in the serum. Circulating cachectin activity was not detectable in the serum of non–tumor-bearing rats or in tumorbearing rats until 28 days after implantation. With evidence of food intake and body weight decline, cachectin activity became detectable in the serum and levels increased as cachexia and tumor burden increased. Serum cachectin activity levels correlated directly with tumor burden and inversely with food intake and body weight change. After resection of the tumor, food intake and body weight increased and serum cachectin activity became undetectable. Serum triglyceride levels were higher in cachectic tumor-bearing rats than in pair-fed non–tumor-bearing controls, and levels decreased after tumor resection as cachectin activity decreased. The results suggest that cachectin is a humoral mediator of cachexia in this rattumor model.

(Arch Surg 1989;124:94-99)

Author Affiliations
From the Surgical Metabolism Section, Surgery Branch, National Cancer Institute, Bethesda, Md.

Footnotes
Accepted for publication July 11, 1988.

Read before the Annual Meeting of the Society of Surgical Oncology, New Orleans, May 23, 1988.

Reprint requests to Surgical Metabolism Section, Surgery Branch, National Cancer Institute, Bethesda, MD 20892 (Dr Norton).

CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter     What's this?

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Leptin and Tumor Necrosis Factor-{{alpha}} Induce the Tyrosine Phosphorylation of Signal Transducer and Activator of Transcription Proteins in the Hypothalamus of Normal Rats In Vivo
Rizk et al.
Endocrinology 2001;142:3027-3032.
ABSTRACT | FULL TEXT  

Hepatic Metastasis Alters the Immune Function of Murine Liver Nonparenchymal Cells
Johnkoski et al.
Arch Surg 1992;127:1325-1329.
ABSTRACT  

The Role of Cytokines in Cancer Cachexia
Moldawer et al.
JPEN J Parenter Enteral Nutr 1992;16:43S-49S.
ABSTRACT