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Epidermal Growth Factor Receptors on Cultured Neoplastic Human Thyroid Cells and Effects of Epidermal Growth Factor and Thyroid-stimulating Hormone on Their Growth¹

Second Division of Internal Medicine, Kyoto University School of Medicine, 54 Kawaharacho, Shogoin, Sakyoku, Kyoto 606 [M. M., H. S., T. M., K. H., H. I.], and Kuma Hospital, 8-2-35, Shimoyamate Street, Chuoku, Kobe 650 [K. K.], Japan

Epidermal growth factor (EGF) receptors on primary-cultured human thyroid cells from 27 neoplasias (nine adenomas and 18 differentiated carcinomas) were analyzed and compared with those on the cultured nonneoplastic part of human thyroid cells. Total binding of ¹²⁵I-EGF to the nonneoplastic part, adenoma, and carcinoma cells did not differ significantly. Scatchard analysis showed that the neoplastic human thyroid cells, like their adjacent nonneoplastic counterparts, consistently possessed EGF receptors with two components. In a paired study of five patients, the association constant of the carcinoma cells' high-affinity component (Ka1) was found to be significantly lower than that of adjacent nonneoplastic thyroid cells (P < 0.05). Furthermore, a study of the cells from 18 carcinomas revealed that overall their Ka1s (4.15 ± 0.82 x 10⁹ M^-1, mean ± SEM) were significantly lower than those of adenoma cells (10.34 ± 1.51 x 10⁹ M^-1, n = 9) and of nonneoplastic cells adjacent to them (8.32 ± 0.84 x 10⁹ M^-1, n = 23). The difference in Ka1s for adenoma and nonneoplastic thyroid cells was not statistically significant. The number of receptor sites (Cmax) per cell was not significantly different in any of the three.

Incorporation of [³H]thymidine (dThd) increased significantly in all kinds of thyroid cells examined following the addition of 10 nM EGF, and the paired study showed that the size of this increase was not significantly different in neoplastic and adjacent nonneoplastic cells. The addition of 300 microunits/ml of thyroid-stimulating hormone caused a significant increase in dThd incorporation by adenoma cells but not by carcinoma or nonneoplastic cells. Furthermore, combined treatment with EGF and thyroid-stimulating hormone additively promoted adenoma cell growth only.

A close inverse relationship was observed between Ka1 and the stimulatory effect of EGF on the dThd uptake in both nonneoplastic thyroid cells and adenoma cells. Carcinoma cells also showed similar profiles, but Ka1 relative to dThd increases were much smaller than the other two.

¹ This work was partly supported by grants-in-aid from the Ministry of Education (Nos. 62614513 and 62480252) and the Japan Society for the Promotion of Science for Japanese Junior Scientists.

Received 11/17/87. Revised 3/21/88. Accepted 3/30/88.

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