HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (3) Citing Articles via Google Scholar Google Scholar Articles by Zatelli, M. C. Articles by Uberti, E. C d. Search for Related Content PubMed PubMed Citation Articles by Zatelli, M. C. Articles by Uberti, E. C d.

Section of Endocrinology, Department of Biomedical Sciences and Advanced Therapies, University of Ferrara, Via Savonarola 9, 44100 Ferrara, Italy
¹ Institute of Endocrinology, Catholic University of Rome, 00168 Rome, Italy
² Novartis Institutes for Biomedical Research, Oncology, 4002 Basel, Switzerland
³ Division of Neurosurgery – Hospital of Padova, 35100 Padova, Italy
⁴ Department of Neurosurgery, Catholic University of Rome, 00168 Rome, Italy

(Requests for offprints should be addressed to E C degli Uberti; Email: dut{at}unife.it)

Somatostatin (SRIF) analogs have been employed in medical therapy of non-functioning pituitary adenomas (NFA), with contrasting results. Previous evidence showed that SRIF can exert its antiproliferative effects by reducing vascular endothelial growth factor (VEGF) secretion and action, and that VEGF expression may be related to pituitary tumor growth. The aim of our study was to clarify the possible effects of a multireceptor SRIF ligand on VEGF secretion and cell proliferation in human NFA primary cultures. We assessed the expression of SRIF receptors (SSTR1–5), the in vitro effects on VEGF secretion, and on cell viability of SRIF and of the stable SRIF analog pasireotide (SOM230), which activates SSTR1, 2, 3, and 5. Twenty-five NFA were examined by RT-PCR for expression of -subunit, SSTR, VEGF, and VEGF receptors 1 (VEGF-R1) and 2 (VEGF-R2). Primary cultures were tested with SRIF and with pasireotide. All NFA samples expressed -sub, VEGF and VEGFR-1 and 2, while SSTR expression pattern was highly variable. Two different groups were identified according to VEGF secretion inhibition by SRIF. VEGF secretion and cell viability were reduced by SRIF and pasireotide in the ‘responder’ group, but not in the ‘non-responder’ group, including NFA expressing SSTR5. SRIF and pasireotide completely blocked forskolin-induced VEGF secretion. In addition, SRIF and pasireotide completely abrogated the promoting effects of VEGF on NFA cell viability. Our data demonstrate that pasireotide can inhibit NFA cell viability by inhibiting VEGF secretion, and suggest that the multireceptor-SSTR agonist pasireotide might be useful in medical therapy of selected NFA.

This article has been cited by other articles:

				A. Colao, C. Di Somma, R. Pivonello, A. Faggiano, G. Lombardi, and S. Savastano Medical therapy for clinically non-functioning pituitary adenomas Endocr. Relat. Cancer, December 1, 2008; 15(4): 905 - 915. [Abstract] [Full Text] [PDF]

				S. Grozinsky-Glasberg, I. Shimon, M. Korbonits, and A. B Grossman Somatostatin analogues in the control of neuroendocrine tumours: efficacy and mechanisms Endocr. Relat. Cancer, September 1, 2008; 15(3): 701 - 720. [Abstract] [Full Text] [PDF]