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Proto-oncogenes GNAS (guanine nucleotide-binding protein, alpha stimulating), PTTG (pituitary tumor-transforming gene 1), and tumor suppressor gene AIP (aryl-hydrocarbon receptor-interacting protein) are the most prominent genetic factors involved in pituitary tumorigenesis and have been implicated in the development of somatotropinomas and non-functioning pituitary adenomas (NFPA) (2).
In this study, we assessed the presence of GNAS and AIP mutations as well as altered gene expressions of AIP and PTTG in sporadic somatotropinomas and NFPA patients admitted to a single endocrine tertiary-referral center.
Sixty-two patients with apparently sporadic pituitary adenomas (41 somatotropinomas and 21 NFPA) were evaluated.
They are classified by size (microadenoma, <10 mm or macroadenoma, >10 mm) and on the basis of their ability to produce hormones, as secreting or functioning tumors (about 50% of adenomas) or as clinically nonfunctioning pituitary adenomas (NFPA) that do not release hormones or, more often, secrete clinically nonrelevant (i.e., gonadotropins) or nonbioactive hormones ([alpha]-subunit of glycoproteic hormones) [14, 15].
Akt is overexpressed and hyperphosphorylated in NFPA [174], in a mouse model of TSH-oma [175], and in GH3 cells in which the inhibition of PI3K/Akt signaling by octreotide increases the expression of the tumor suppressor gene Zac1 [176,177].