- 18 - Endogenous Thyroid Stimulating Hgrmone (TSH) Neoplasm Formation Following 131] Radiation in In one of the more recent rat experiments using small doses of 131 I and periods of observation of almost 2 years, we have succeeded in obtaining negplasms in almost 75% of the rat thyroids. The yield has become sufficiently high in]this model so that it has been possible to test the factors which inhibit or stimulate|the induction and growth of such lesions. | TSH has been theoretically implicated in the development of thyroid neoplasms. Observations that tumors were produced by the use of chronic iodine |deficient diet or by the chronic use of goitrogenic substances supported the belief by radioiodines might operate in a similar fashion. t the damage caus Just as the la€k of iodine to mak thyroid hormone, or the block of the synthesis of hormone a deficiegcy of thyroid hormone With a campensatory increase in the output of TSH,so radiatign damage to the cellular mechanism for hormone production may work in a Simijar way. Lindsay, Furth and Doniach have independently suggested that there may be a le mechanisn responsible for the radiation induced neoplasms, i.e., that radiati Might initiate the neoplasm and TSH pramote its growth. hypertrophy (increase in cell height} had been given t 31; The principal investigatoy in the thyroid of some of first noted cellu e's chicks that (1948). ‘This has been observed by many investigators and has beer considered a manifestation of the stimulus from TSH, but assays for]TSH, until the las few years, have not been sufficiently sensitive to detect reliably elevations of TSH unless there was major damage to the gland. fhe very slight We Plasms develop mich more consistently following surprisingly small than large ones. We also have learned that when there is histologi¢ evidence of damg fron 11, the incidence of neoplasms is mich decreased. In studie} published under our former AEC contracts, we have shown that radiation fron 131) caksed intrinsic dama that might impair the capacity for cellular replication without se hormone production. Thus, if damage is sufficient to cause a rise ously hampering TSH to significa