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• W389924700 endingPage "110" @default.
• W389924700 startingPage "87" @default.
• W389924700 abstract "Though previously only 4–5% of pituitary adenomas were considered to occur in a family setting, either isolated or as part of an endocrine tumor syndrome, current data suggest a higher proportion of familial cases, especially for young patients. Multiple endocrine neoplasia type 1 (MEN1) syndrome and familial isolated pituitary adenoma (FIPA) are responsible for the majority of cases, while Carney complex (CNC) explains a few hundred of them worldwide, while multiple endocrine neoplasia type 4 (MEN4) and succinate-dehydrogenase (SDH)-related familial pituitary adenomas have only been described in a few patients. The gene(s) causing familial pituitary adenomas have not been identified in a large proportion of the cases. MEN1 is characterized by the association of pituitary tumors, hypercalcemia and pancreatic adenomas, as well as some nonendocrine tumors. In a few cases, an MEN1-like syndrome is caused by mutations in the gene coding for the cell cycle inhibitor p27Kip1. A small percentage (20–30%) of phenotypically well characterized FIPA cases are due to mutations in the aryl hydrocarbon receptor interacting protein gene (AIP). CNC is a rare syndrome, characterized by acromegaly due to pituitary hyperplasia, cardiac and dermal myxomatosis, primary pigmented nodular adrenocortical disease, lentiginoses, and a variety of benign and malignant tumors; in 70% of cases it is due to PRKAR1A mutations. Mutations in DICER1 are related to the development of pituitary blastomas in infants. The association of SDH mutations with a syndrome of pituitary adenomas and pheochromocytomas/paragangliomas has been recently described. Somatic mutations in these genes have been studied in sporadic pituitary adenomas: while mutations in the GNAS are common in somatotropinomas (30–40%), MEN1 mutations have very rarely been identified and no somatic mutations have been described in the other genes associated with familial pituitary adenomas. Genetic counseling is essential for these patients and their relatives. Follow-up of mutation carriers, by clinical, biochemical and imaging studies, should lead to earlier pituitary tumor detection, allowing for more efficient treatment." @default.
• W389924700 created "2016-06-24" @default.
• W389924700 creator A5017519053 @default.
• W389924700 creator A5035003046 @default.
• W389924700 date "2013-03-08" @default.
• W389924700 modified "2023-10-16" @default.
• W389924700 title "Familial Pituitary Adenomas" @default.
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