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Pituitary Adenomas: Screening for Gq Mutations

Department of Neurosurgery and Laboratory of Molecular Neurosurgery and Biotechnology (N.M.O., C.-O.E., G.T.T.), Division of Pediatric Endocrinology and Department of Pediatrics (M.R.B., J.S.P.), Division of Endocrinology (L.S.B.), Department of Medicine, Emory University School of Medicine, Atlanta, Georgia 30322

Address all correspondence and requests for reprints to: Dr. Nelson M. Oyesiku, Section of Neurosurgery, The Emory Clinic, Inc., 1365 Clifton Road, N. E., Building B, Suite B2200, Atlanta, Georgia 30322. E-mail: noyesik{at}emory.edu

Mutant, guanosine triphosphatase-deficient, -subunits of the G protein, Gs, gsp ocogene have been discovered in 40% of GH-secreting pituitary adenomas. Therefore, we hypothesized that a novel G protein class, Gq, involved in pituitary signal transduction, might be involved in pituitary tumorigenesis. Recombinant mutations of Gq result in constitutive activation of phospholipase C and have transforming activity. Therefore, we screened tumor samples from 37 pituitary adenomas for the presence of activating mutations of the Gq gene. Importantly, our sample contains 8 FSH and LH adenomas. In the pituitary gland, FSH and LH are linked to the GnRH-Gq signaling cascade, making these tumors a logical choice for screening for Gq mutations. Complementary DNA (cDNA) was synthesized by RT-PCR with Gq specific primers to exclude pseudogene transcripts. Fragments of Gq cDNA-encompassing residues (Arg¹⁸³, Gln²⁰⁹) were screened by single-strand conformation polymorphism and then sequenced in both directions. No mutations were detected. We conclude that mutations in these regions of the Gq cDNA occur infrequently, if at all, in human pituitary adenomas. Alternative mechanisms underlying pituitary tumorigenesis should be explored.

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