Summary and Conclusions
The relationship of growth of TSH-secreting pituitary tumors to thyroid function was studied by destroying or depressing the thyroid gland of mice with graded doses of I131, grafting tumors on such animals, and correlating tumor growth with thyroid function. The results indicate that proliferation of grafted TSH-secreting pituitary tumor cells depends on the secretion of TH.
Near complete or complete destruction of the thyroid follows administration of a single dose of 200 or more µc. of I131. This provides the maximum stimulus to pituitary growth. A lower dose, about 75 µc., produces a lasting depression of the thyroid, some follicles of which, although normal in appearance, are incapable of undergoing fully compensating hyperplasia. In most mice 25 µc. interferes little, if at all, with the thyroid function, with ability of this gland to be stimulated by TSH, and with its capacity to inhibit the growth of pituitary tumors. The inverse relationship between thyroid function, as indicated by its ability to take up I131, and stimulation of the pituitary tumor grafts is almost quantitative.
Cells of thyroid glands which escaped destruction by large doses of I131 do not have the ability to undergo a fully compensating hyperplasia. This may be due in part to the stenosing “radiation arteritis” and diffuse fibrosis in the thyroid region caused by I131.
Radiothyroidectomy causes an increased total-body retention (or diminished elimination) of I131 during the first 24 hours following injection. Pituitary tumor grafts secreting TSH further enhance total-body retention of I131. The sites of this I131 are not precisely known. In radiothyroidectomized mice (with and without tumor) the elimination of the retained I131 is rapid. In normal mice bearing grafted tumors most of the retained radioiodine is in the thyroid, and its retention is lasting.
Work performed under Contract No. W-7405-eng-26 for the Atomic Energy Commission.