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Plasma Protein Synthesis in Experimental Cancer Compared to Paraneoplastic Conditions, Including Monokine Administration¹

Department of Surgery, Sahlgrenska Hospital, University of Gothenburg, S-413 45 Gotherburg, Sweden

During tumor growth, there are characteristic alterations in the concentration and synthesis of various plasma proteins. The purpose of this study was to evaluate whether these changes are unique to a tumor-bearing state, or rather, they represent a generalized response to a paraneoplastic state mediated by the release of monokines or proteincalorie malnutrition. Plasma protein synthesis and concentrations in mice bearing a transplantable fibrosarcoma were compared to animals receiving either a terpentine abscess, Corynebacterium parvum administration, calorie-protein depletion, or administration of the recombinant-derived monokines, murine interleukin 1 or human tumor necrosis factor-.

Tumor-bearing animals showed a significant increase in total plasma protein synthesis that was similar in magnitude to the increase seen following a terpentine abscess or after administration of interleukin 1 or tumor necrosis factor-. Similarly, the pattern of protein synthesis and concentration, as determined by isoelectric focusing or sodium dodecyl sulphate-polyacrylamide gel electrophoresis, were similar, albeit not identical, among tumor-bearing animals and those receiving either a terpentine abscess, C. parvum and monokine administration. Serum amyloid P concentrations were markedly elevated in tumor-bearing animals, as they were in animals after a sterile abscess and following interleukin 1 administration, as well as to a lesser extent tumor necrosis factor- administration.

We can therefore conclude that the majority of changes in plasma protein concentration and synthesis seen in this tumor-bearing model are similar to those seen during an acute inflammation and can be reproduced to a large extent by the administration of the monokines, interleukin 1 or tumor necrosis factor-.

¹ Supported in part by grants from the Swedish Cancer Society (project 2147-B87-01V, project 93), the Swedish Medical Research Council (project 536), and the Assar Gabrielsson Foundation.

² Received additional support from the Center for Nutritional Research, Charitable Trust, Boston, MA 02215.

³ To whom requests for reprints should be addressed, at Department of Surgery, Sahlgrenska sjukhuset, S-413 45 Göteborg, Sweden.

Received 7/14/86. Revised 1/27/87. Accepted 7/30/87.

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