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Molecular and trophic mechanisms of tumorigenesis.

Levy 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

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.

Published 29 January 2008 in Endocrinol Metab Clin North Am, 37(1): 23-50, vii.
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