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Research Article Free access | 10.1172/JCI113216

Protein synthesis in hepatocytes isolated from patients with gastrointestinal malignancy.

H F Starnes Jr, R S Warren, and M F Brennan

Memorial Sloan-Kettering Cancer Center, New York, New York 10021.

Find articles by Starnes, H. in: JCI | PubMed | Google Scholar

Memorial Sloan-Kettering Cancer Center, New York, New York 10021.

Find articles by Warren, R. in: JCI | PubMed | Google Scholar

Memorial Sloan-Kettering Cancer Center, New York, New York 10021.

Find articles by Brennan, M. in: JCI | PubMed | Google Scholar

Published November 1, 1987 - More info

Published in Volume 80, Issue 5 on November 1, 1987
J Clin Invest. 1987;80(5):1384–1390. https://doi.org/10.1172/JCI113216.
© 1987 The American Society for Clinical Investigation
Published November 1, 1987 - Version history
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Abstract

To investigate the effect of remote and proximate cancer on hepatic protein metabolism, we determined rates of total protein synthesis by hepatocytes (HPS) isolated from 31 patients undergoing liver wedge biopsy: 7 patients with benign disease, 14 with gastric cancer, and 10 with colorectal cancer (5 of whom had liver metastases). Patients with malignant disease without weight loss had a threefold higher rate of total HPS (4,980 +/- 814 pmol/h per 10(5) viable cells) than patients with benign disease without weight loss (1,278 +/- 318 pmol/h per 10(5) viable cells, P less than 0.001). Among the patients with gastric cancer, eight with preoperative weight loss had lower rates of HPS (380 +/- 90 pmol/h per 10(5) viable cells) than those without weight loss (4,061 +/- 401 pmol/h per 10(5) viable cells, P less than 0.002). The highest rates of HPS were seen in patients with colorectal cancer with liver metastases (8,005 +/- 1,975 pmol/h per 10(5) viable cells) vs. colorectal cancer patients without liver metastases (3,060 +/- 575 pmol/h per 10(5) viable cells, P less than 0.03). These data indicate that modulation of hepatic protein synthesis occurs in malignancy in man. However, the stimulatory influence of the tumor-bearing state may be overridden by the inhibitory effects of cachexia.

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