Molecular and trophic mechanisms of tumorigenesis.

Abstract

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.

• Authors: Andy Levy
• Journal: Endocrinology and metabolism clinics of North America (Endocrinol Metab Clin North Am) Vol. 37 Issue 1 Pg. 23-50, vii (Mar 2008) ISSN: 0889-8529 [Print] United States
• PMID: 18226729 (Publication Type: Journal Article, Review)

Chemical References

• Chromogranins
• MAS1 protein, human
• Proto-Oncogene Mas
• GNAS protein, human
• GTP-Binding Protein alpha Subunits, Gs

Topics

• Animals
• Cell Transformation, Neoplastic (genetics, pathology)
• Chromogranins
• GTP-Binding Protein alpha Subunits, Gs (genetics, physiology)
• Humans
• Phenotype
• Pituitary Neoplasms (epidemiology, genetics, pathology)
• Proto-Oncogene Mas