Molecular and trophic mechanisms of tumorigenesis.
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 histologic or molecular markers reliably predict behavior. GNAS1 activation and the mutations associated with multiple endocrine neoplasia type 1 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 is surely yet to come.
Levy
Andy
A
Henry Wellcome Labs for Integrative Neuroscience & Endocrinology, University of Bristol, Dorothy Hodgkin Building, Whitson Street, Bristol BS1 3NY, UK. a.levy@bris.ac.uk
D000818:Animals; D002471:Cell Transformation, Neoplastic / Q000235:genetics / Q000473:pathology*; D002864:Chromogranins; D019205:GTP-Binding Protein alpha Subunits, Gs / Q000235:genetics / Q000502:physiology; D006801:Humans; D010641:Phenotype; D010911:Pituitary Neoplasms / Q000453:epidemiology / Q000235:genetics / Q000473:pathology*; D000090063:Proto-Oncogene Mas
D002864:Chromogranins; C000715470:MAS1 protein, human; D000090063:Proto-Oncogene Mas; C406732:GNAS protein, human; D019205:GTP-Binding Protein alpha Subunits, Gs