title: Dopamine 2 receptor expression in various pathological types of clinically non-functioning pituitary adenomas.
abstract: Clinically non-functioning pituitary adenomas account for about one-third of pituitary tumors. The majority of them are pathologically classified as gonadotropinomas or null-cell adenomas without hormonal expression. The rest represent silent corticotroph adenomas and plurihormonal tumors. Conservative therapy with dopamine agonists is effective in some cases only depending on the expression of dopamine 2 receptors (D2R). The aim of this study was to quantitatively estimate D2R expression in clinically non-functioning pituitary adenomas and correlate the results with adenoma type according to pathological classification. Out of the 87 adenomas investigated, 63 expressed gonadotropins, 7 were silent corticotroph adenomas, 7 were plurihormonal tumors, and only 6 did not express any pituitary hormone on immunohistochemical investigation. With the use of the reverse transcriptase PCR technique, D2R mRNA was expressed in all adenomas with very heterogeneous quantity. The expression was very low in corticotroph adenomas (relative median quantity after normalization to housekeeping gene 0.01) and lower in plurihormonal tumors (median 0.4) than in gonadotroph (median 1.3) and null-cell adenomas (median 1.9). The difference between corticotroph adenomas and plurihormonal tumors in comparison with other pathological types was statistically significant. The expression of D2R did not depend on the presence or absence of gonadotropins. We conclude that D2R expression is very low in corticotroph adenomas and significantly lower in plurihormonal tumors. The positivity of gonadotropins does not predict the D2R quantity.
authors: Second Department of Internal Medicine, Charles University Faculty of Medicine and Teaching Hospital in Hradec Králové, Sokolská 581, 50005, Hradec Králové, Czech Republic. gabalec@fnhk.cz
authors: Filip
authors: F
authors: Gabalec
authors: Martin
authors: M
authors: Beranek
authors: David
authors: D
authors: Netuka
authors: Vaclav
authors: V
authors: Masopust
authors: Jiri
authors: J
authors: Nahlovsky
authors: Tomas
authors: T
authors: Cesak
authors: Josef
authors: J
authors: Marek
authors: Jan
authors: J
authors: Cap
references: Acta Neuropathol. 2006 Jan;111(1):1-7
references: 16328527
references: J Clin Neurosci. 2003 Jul;10(4):444-8
references: 12852883
references: Eur J Endocrinol. 2007 Feb;156(2):203-16
references: 17287410
references: Endocr J. 2009;56(4):579-84
references: 19318729
references: Physiol Rev. 1990 Apr;70(2):279-318
references: 2181497
references: Histochem Cell Biol. 2008 Sep;130(3):495-507
references: 18688636
references: Endocr Relat Cancer. 2008 Dec;15(4):905-15
references: 18780796
references: J Clin Endocrinol Metab. 1998 Jan;83(1):248-52
references: 9435450
references: Pituitary. 2006;9(4):317-21
references: 17082898
references: Eur J Endocrinol. 2010 Aug;163(2):193-200
references: 20460423
references: Clin Endocrinol (Oxf). 1986 Nov;25(5):561-72
references: 3621623
references: J Clin Endocrinol Metab. 1998 Apr;83(4):1368-75
references: 9543168
references: Best Pract Res Clin Endocrinol Metab. 2009 Oct;23(5):625-38
references: 19945027
references: Eur J Endocrinol. 2006 Dec;155(6):849-57
references: 17132755
references: J Clin Endocrinol Metab. 2004 Apr;89(4):1674-83
references: 15070930
references: J Clin Endocrinol Metab. 2009 Jun;94(6):1931-7
references: 19293270
references: Clin Endocrinol (Oxf). 2005 Jul;63(1):39-44
references: 15963059
references: Mol Cell Endocrinol. 2011 Jan 1;331(1):73-8
references: 20797424