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Somatostatin Regulation of Glycoprotein Hormone and Free Subunit Secretion in Clinically Nonfunctioning and Somatotroph Adenomas in Vitro^*

Neuroendocrine Unit, Departments of Medicine Massachusetts General Hospital Boston, Massachusetts 02114
Neurosurgery Massachusetts General Hospital Boston, Massachusetts 02114
Patholog Massachusetts General Hospital Boston, Massachusetts 02114

Address all correspondence and requests for reprints to: Anne Klibanski, M.D., Neuroendocrine Unit, Massachusetts General Hospital, Fruit Street, Boston, Massachusetts 02114.

There is increasing evidence that clinically nonfunctioning pituitary tumors produce and secrete glycoprotein hormone and/or free - and β-subunits. In addition, hypersecretion of free -subunit occurs in up to 37% of patients with somatotroph adenomas. An understanding of glycoprotein hormone regulation is important in developing effective therapeutic strategies for patients with tumors associated with intact glycoprotein hormone and free subunit hypersecretion. We investigated glycoprotein hormone and free subunit secretion by somatostatin in primary dispersed cultures of pituitary tumor cells from 23 patients with pituitary adenomas. Fifteen tumors from patients with clinically nonfunctioning adenomas (group 1) and 8 tumors from patients with somatotroph adenomas and cosecretion of -subunit (group 2) were studied. Cultures were incubated with control or somatostatin-supplemented media for 24 h. Media samples from group 1 tumors were assayed for intact glycoprotein hormones and free - and β-subunits secretion levels, while media samples from group 2 cultures were assayed for -subunit and GH secretion levels. Significant (P < 0.05- 0.001) inhibition of secretion of 1 or more intact hormones and/ or free subunits was found in 10 of the 15 group 1 tumors. SRIF[10^–7 M] suppressed intact gonadotropin secretion in 60% of FSH-producing tumors and 30% of LH-producing tumors. Media concentrations of FSHβ and LH/J were decreased in 31% and 50% of group 1 tumors, respectively, following somatostatin treatment in those tumors which secreted free β-subunits. - Subunit was secreted by 12 of the 15 tumors, but significant (P < 0.02-0.01) inhibition by somatostatin was observed in only 2 tumors. In contrast, significant (P < 0.05-0.001) inhibition of -subunit in the somatotroph adenomas was found in 6 of the 8 tumors. Significant decreases in -subunit were observed only in those tumors where GH was also significantly inhibited by somatostatin. We conclude that 1) somatostatin inhibits intact glycoprotein or free subunit secretion in the majority of clinically nonfunctioning pituitary tumors in vitro and 2) -subunit secretion is suppressed in 17% and 69% of clinically nonfunctioning and somatotroph adenomas, respectively, consistent with a differential regulation of -subunit by somatostatin in these two tumor types.

^* Supported in part by NIH Grants DK40947 and DK07028 and agrant from the American Cancer Society.

Received March 11, 1991.

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