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Section of Endocrinology (M.C.Z., D.P., A.M., E.C.d.U.), Department of Biomedical Sciences and Advanced Therapies, University of Ferrara, 44100 Ferrara, Italy; Department of Medical and Surgical Sciences (P.M., C.M., N.S.), Clinica Medica 3, and Department of Thoracic Surgery (F.R.), University of Padua, 35100 Padua, Italy; Nuclear Medicine Service (D.R.), Rovigo Hospital, 45100 Rovigo, Italy; and Biomeasure Incorporated/IPSEN (M.D.C.), Milford, Massachusetts 01757-3650
Address all correspondence and requests for reprints to: Ettore C. degli Uberti, Section of Endocrinology, Department of Biomedical Sciences and Advanced Therapies, University of Ferrara, Via Savonarola 9, 44100 Ferrara, Italy. E-mail: ti8{at}unife.it.
A 29-yr-old woman presented with acromegaly, pituitary gland enlargement, and an isolated pulmonary mass of 3.3 cm in diameter, which displayed a very high tracer uptake after OctreoScan. Plasma GHRH levels were markedly elevated. The patient underwent left lung upper lobectomy, and histopathology disclosed a bronchial atypical carcinoid. The tissue was examined for somatostatin (SRIH) receptor subtypes (SSTRs) 15 expression by RT-PCR. Cultured tumor cells were treated with SRIH, lanreotide (BIM-23014), or SRIH analogs selective for SSTR2 (BIM-23120), SSTR5 (BIM-23206), or SSTR1 (BIM-23926). GHRH was measured in the medium after 6 h, and cell viability was assessed after 48 h. RT-PCR analysis showed expression of SSTR1, -2, and -5. GHRH secretion was significantly reduced by SRIH (50%), Lan (35%), as well as by the SSTR2, SSTR5, and SSTR1 selective agonists (55, 75, and 20%, respectively), whereas cell viability was not affected.
Our data show SSTR expression in a GHRH-secreting bronchial carcinoid and provide evidence that, in vitro, selective SSTR activation differently inhibit ectopic GHRH secretion. These findings suggest that SSTR-specific SRIH analogs may be useful in the medical therapy of GHRH-secreting bronchial carcinoids.
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