Journal
ENDOCRINOLOGY AND METABOLISM CLINICS OF NORTH AMERICA
Volume 37, Issue 1, Pages 23-+Publisher
W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1016/j.ecl.2007.10.009
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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 I 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.
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