A significant proportion of pituitary macroadenomas and by definition all microadenomas regain trophic stability after an initial period of deregulated growth. Classical proto-oncogene activation and tumor suppressor mutation are rarely responsible and no histological or molecular markers reliably predict behavior. GNAS1 activation and the mutations associated with MEN1 and Carney complex, aryl hydrocarbon receptor interacting protein gene mutations and a narrowing region of chromosome 11q13 in familial isolated acromegaly together account for such a small proportion of pituitary adenomas that the pituitary adenoma pathogenic epiphany has surely yet to come.
|Translated title of the contribution||Molecular and trophic mechanisms of tumorigenesis|
|Pages (from-to)||23 - 50|
|Number of pages||27|
|Journal||Endocrinology and Metabolism Clinics of North America|
|Publication status||Published - 2008|