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EXTENSIVE evidence indicates that thyrotropin stimulates the growth and function of differentiated thyroid carcinomas.1 These responses evidently reflect the presence in thyroid cancer cells of functioning thyrotropin receptors, which, on binding thyrotropin, mediate an increase in the cellular concentration of cyclic AMP, the second messenger for most actions of thyrotropin.2 3 4 The circulating thyroid-stimulating immunoglobulins characteristic of Graves' disease are antibodies against the thyrotropin receptor; like thyrotropin, they activate thyroid adenylate cyclase and cause the development in the intrinsically normal thyroid of the hyperfunction and hyperplasia characteristic of this disease.5 6 7 Therefore, it is of interest that according to clinical and laboratory . . .
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Filetti et al. (1988) studied this question.
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