damage, inhibiting the hypertrophy that results from thiouracil and leavifig cel2s which survive but are incapable of replication. It now appears that for fiypersZastic glands with doses of 2.5 to 5 uc per aninal (yielding tissue doses of 10,00 to 20,000 rads) and for normal glands with doses of 10 to 20 uc (yielding thE same amount of radiation) result in the greatest probability of neoplasm formafFion. This radiation causes little change in thyroid weight for the first six to twellve month provided no rapid growth of a neoplasm cecurs. However, after about fivejmonths the expected increase in thyroid weight, when an antithyroid drug is given, cEnnot be preduced as in the non-radiated controls. Following a tissue dose of about 8000 rads animals whose thyroids chronically stimulated display thyroid weights which are slightly below non-radiated controls. Furthermore, their response to an antithyroid druk _is greatly reduced. A full response is usually not displayed where dose rads has been delivered. It should be emphasized that these are very prefli conclusions and may be modified when additional material now in preparati and further analysis is made. By sacrificing animals and testing the mitotic activity that is oce chronic stimulation or that may be produced by acute five day stimulatio antithyroid drugs, it has been possible to judge the temporary inhibitio resulting from the initial radiation insult. Depending on the dose th with the passage of time. The initial temporary reduction in mitotic re be significant, but brief for doses as low as 2000 rads. After a short period and after all1311 is gone, there my be only partial recovery of depacity for mitotic activity at somewhat higher doses. At the same time, chronic stifuileticn with antithyroid drugs seem to 9 produce appreciable degrees of hypertrophy of the gland. After long. pericds following 1 I, some degree of mitotic activity may induced by acute administration of the drug, but in many cases the gland cannot made to increase in weight. . The technique for acutely challenging a crippled thyroid by giving drug is a unique and roughly quantitative means of testing capacity for activity. antithyroid itotic t the cells As time passes following the dose of 131], some recovery inability to undergo mitotic activity cecurs. After 12 to 15 months, such thyroid show scme n chellenced areas of variability with respect to follicle size and cell size. When with the antithyroid drug, the labelling of nuclei is not uniformly disp there may be no discretely encapsulated groups of cells which are cleari a neorlasn, the tendency for cell division seems more prevalent in some areas than i others. The non-uniform distribution of labelling with tritiated thymidine presumably relates to the nodularity that evolves when these glands are stimulated to hypertroghy. Ultimately if such glands are chronically challenged in most cases they are found tq@ contain lesions whose histologic appearance, degree of encapsulation and discret@ly different tendency for mitotic activity are quite evident. A variety of thyroid neoplesms have new been observed in these animdls. _of the lesions are papillary in pattern. Mest Many show single layers of epifhelium in very simple configurations. Others show papillary structure with active[proliferative activity that trends into solid cellular patterns composed of pleomorphi forms . Some thyroid lobes are completely replaced by what appears to be a benigg lesicn. . Other. lesions which appear malignant are found invading the thyroid capsie and the fat nearby. In some cases, the trachea has been invaded and malignant c@lis are seen within the trachea as well as musculature of the neck. Autoradiographs pith i3ly, when satisfactory , have so far shown less 191z in such neoplasms than infthe normal thems A 3 aca rm nano at all Thene anneara ta he non sioni ficant diffepence in