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Submitted on November 2, 2004
Accepted on January 17, 2005
Section of Endocrinology, Department of Biomedical Sciences and Advanced Therapies, University of Ferrara, 44100 Ferrara, Italy; Department of Medical and Surgical Sciences, Clinica Medica 3, University of Padua, 35100 Padua, Italy; Department of Thoracic Surgery, University of Padua, 35100 Padua, Italy; Nuclear Medicine Service, Rovigo Hospital, 45100 Rovigo, Italy; Biomeasure Incorporated/ IPSEN, Milford, Massachusetts 01757-3650, USA
* To whom correspondence should be addressed. E-mail: ti8{at}unife.it.
A 29-year-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 up-take 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 1 to 5 (SSTR1 to 5) expression by RT-PCR. Cultured tumor cells were treated with either SRIH, Lanreotide (BIM-23014, Lan), 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, the SSTR5 and the SSTR1 selective agonists (-55%, -75%, and -20%, respectively), while cell viability was not affected.
Our data show SSTRs 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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