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Experimental Cancer Cachexia Induced by Transplantable Colon 26 Adenocarcinoma in Mice

Nippon Roche Research Center, Kamakura [Y. T., H. E., T. T., T. U., T. I., I. H., H. I.]; Cancer Chemotherapy Center, Japanese Foundation for Cancer Research, Tokyo [T. K.]; and Osaka University, the Hospital of Microbial Diseases, Osaka [T. T.], Japan

The present study investigates a tumor model for cachectic mice. Among various murine transplantable tumors, used for assessing cytostatics, we identified colon 26 adenocarcinoma (colon 26) as capable of causing cachexia. Fifteen days after inoculation, the tumor grew to about 6% of the body weight causing substantial carcass weight loss of 3.4 g (14.5% of the carcass weight). When the tumor size was 2.7 g at 3 weeks after the inoculation, the carcass weight was 12 g less than the age-matched control. The tumor continued to grow while the mice maintained this weight, surviving for an average of 45 days. This extensive weight loss was essentially the wasting of adipose and muscle tissues. Hypoglycemia and hypercorticism occurred during the time of the weight loss. In addition, the colon 26 caused disorders of hepatic functions: the concentration of acute phase proteins in serum increased; the number of hepatic glucocorticoid-cytosol receptors decreased; and activities of hepatic catalase and drug-metabolizing enzymes decreased. On the other hand, noncachectic mice with Meth A fibrosarcoma gained weight, which was somewhat less than the control, and had neither hypoglycemia nor hypercorticism, although some mild disorders of hepatic functions were found. Mice bearing colon 26 is an appropriate model for elucidating the mechanism that causes cachexia.

¹ To whom requests for reprints should be addressed.

Received 5/16/89. Accepted 12/19/89.

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