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Experimental Studies of Factors Influencing Development of Hepatic Metastases

XVII. Role of Thyroid¹

Department of Pathology and Department of Surgery, Laboratory of Surgical Research, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania

Hypothyroidism induced by the administration of propylthiouracil or thyroidectomy and verified by measurements of RBC uptake of triiodothyronine-1-¹³¹I (TRIT) failed to alter the incidence, size, or extent of hepatic metastases from that observed in controls. Effective administration of thyroid stimulating hormone (TSH) or sodium d-thyroxine as evidenced by TRIT and histology of thyroid glands resulted in an increase in size and extent but only a slight, relatively insignificant increase in incidence of such lesions. The administration of these agents also produced comparable findings in thyroidectomized members receiving tumor cell inoculation, indicating that this effect was not related to their effect on thyroid function per se. The cogent possibility that this augmentation might be related to hepatic damage induced by these agents was also negated by observing normal hepatic structure and serum transaminase activities. Further, no difference in histologic appearance of thyroids or TRIT was noted in rats receiving injections of Walker tumor cells that subsequently developed hepatic tumors and those in which tumor growth did not occur. Although the actual mechanism of action of sodium d-thyroxine and TSH on the growth of artificially induced hepatic metastases was not evident, the results minimize any significant thyroidal effect on metastases, at least in the model utilized.

¹ Supported by USPHS Grants CA-05949 and CA-06670 and American Cancer Society Grant P-142.

Received 1/28/66. Accepted 5/24/66.