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Submitted on June 12, 2006
Accepted on August 18, 2006
Neuroendocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA. 02114; Neuropathology Unit, Massachusetts General Hospital and Harvard Medical School, Boston MA. 02114; Division of Neurosurgery, Massachusetts General Hospital and Harvard Medical School Boston, MA, 02114.; Section on Endocrinology and Genetics, Developmental Endocrinology Branch, NICHD, National Institutes of Health, Bethesda, MD. 02892
* To whom correspondence should be addressed. E-mail: aklibanski{at}partners.org.
Context: There is no tumor-directed medical therapy available for Cushing's disease.
Objective: To determine the in vitro effect of the somatostatin analog SOM230 on cell proliferation in human corticotroph tumors.
Design/Methods: Expression of somatostatin receptors (SSTR 1-5) was determined by qRT-PCR in 13 human corticotroph tumors and by immunohistochemistry (IHC) in 12 of the 13 tumors. SOM230 effects on cell proliferation and ACTH release was evaluated in vitro using primary cultures of 6 of the 13 human corticotroph adenomas.
Results: In our series we found expression of SSTR subtypes 1, 2, 4, and 5 in human corticotroph tumors by qRT-PCR. All receptor subtypes were detected by IHC with SSTR subtype 5 having the highest IHC score in 83% (10/12) of the cases. Significant suppression of cell proliferation was observed in all tumors cultured (percent suppression range: 10% to 70%; p=0.045 to 0.001). SOM230 inhibited ACTH secretion in five out of the six tumors cultured (percent suppression range: 23% to 56%; P = 0.042 to 0.001).
Conclusion: Corticotroph tumors express multiple SSTR subtypes. SOM230 significantly suppressed cell proliferation and ACTH secretion in primary cultures of human corticotroph tumors. These in vitro results support the hypothesis that SOM230 may have a role in the medical therapy of corticotroph tumors.
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