The objective of these studies was to elucidate further the mechanisms of the thyroid dependency of Morris Hepatoma 44. In vivo experiments indicated that while exogenous thyroxine (8 pg per kg) reversed the hypothyroid-mediated inhibition of primary hepatoma growth, no such effect was noted with the administration of ovine prolactin (100 pg per kg s.c.) and bovine growth hormone (LOO pg per kg, s.c.). In contrast, ovine prolactin significantly stimulated tumor growth in euthyroid animals. We have documented the presence of nuclear triiodothyronine (T3) receptors in Morris Hepatoma 44. The dissociation constant Kd (4.38 f 0.84 nM) and binding capacity (2.16 2 0.84 pmoles per mg DNA) of these receptors was significantly greater than those of host liver tissue (1.48 f 0.41 N a n d 0.93 k 0.32 pmole per mg DNA, respectively). The binding capacity of hepatoma nuclear T3 receptors was markedly reduced in the hypothyroid state, while liver nuclear receptor capacity was not significantly changed. In addition, the binding of T3 to cytoplasmic proteins was greater in hepatomas relative to host liver. Analogous to the observations with nuclear receptors, the binding of T3 to hepatoma cytosol was significantly reduced in the hypothyroid state, while the binding activity of liver cytosol was unchanged. These results are consistent with 8 possible role for nuclear receptors and/or cytoplasmic binding proteins for T3 in mediating the dlrect Influence of thyroid hormones on the growth of Morris Hepatoma 44. Our results, however, do not preclude a role for other hormones (i.e., pituitary hormones acting via the hypothalamo-hypophyseal axis)

22 patients with hyperplasia and adenomas of the parathyroid glands were studied and reviewed. They form the basis of this report, which emphasizes the idiosyncracies and vagaries of this disease. The diagnosis of hyperparathyroidism is reported in context with the clinical picture, and the overall relationship of this condition to multiple endocrine adenomatosis is explored in some depth. A specific patient review is made which illustrates the odd clinical behavior of parathyroid hyperfunction; 3 patients with cancers are studied in detail. Surgical management is discussed and concentrates on the more vexing aspects of parathyroid identification, adenomas vs. hyperplasia, recurrent disease and cancer.

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