Rats bearing transplantable thyroid tumors representing two different stages of progression were used to study the incorporation of 131I into monoiodotyrosine, diiodotyrosine, diiodothyronine, triiodothyronine, and thyroxine by the host thyroid glands and the tumors. The tissues were simultaneously used for assaying iodide peroxidase activity. Both the less progressed “transitional” and the more advanced “autonomous” tumors lowered the incorporation of 131I by the host thyroid. The tumors themselves showed extremely low incorporation, although thyroidectomy of the host significantly increased the incorporation in the tumors. However, results of incorporation experiments do not distinguish the transitional from the autonomous tumors.

Tumor growth also caused iodide peroxidase activity in the host thyroid to decline. The enzyme activity in the transitional tumor approached the activity in normal thyroid. Thyroidectomy of the host, however, greatly reduced the enzyme activity in the tumor. By contrast, the autonomous tumor had no measurable peroxidase activity. Apparently, no correlation exists between the incorporation and the enzyme activity in the tumor, although both biochemical parameters are subject to the influence of the host thyroid. However, the results indicate that iodide peroxidase activity can serve as a more sensitive gauge to measure the progression of the thyroid tumor from a transitional to an autonomous stage than can 131I incorporation.

A parallel cytogenetic analysis of the tumors used in the biochemical studies shows that the percentage of aneuploidy in the cells of the transitional tumors was lower than that in the cells of the autonomous tumors. Nearly all cells of the autonomous tumors had altered karyotypes. Furthermore, most of the 41-chromosome cells of the transitional tumors had one chromosome of the metacentric group missing, but a high percentage of all cells of the autonomous tumors lost this chromosome.


This work was supported in part by a grant from the University of Michigan Cancer Research Institute and by a grant from the Office of Research Administration, The University of Michigan, and in part by the Marie Williams Memorial Grant for Cancer Research from the American Cancer Society (Grant P-484).

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