Abstract
Objective: The molecular pathogenesis of pituitary adenomas is still poorly understood so far. One of the rare mutations identified up to now are gsp-mutations causing the consecutive activation of cAMP pathway. However the role of the INK4 family of cyclin-dependent kinase (CDK) inhibitors is emerging. Deletion of p18 (INK4c) causes spontaneous pituitary tumors in mice. There is no data on mutational analysis of p18 in human pituitary adenomas in a larger series so far. Here we present a collaborative research initiative, which foster the establishment of a tumor bank for molecular-genetical studies on pituitary adenomas, also including p18.
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