Pituitary tumors

Abstract

Pituitary tumors are commonly encountered intracranial neoplasms that are invariably benign. Classic oncogene mutations are not encountered in these tumors, and disrupted cell cycle control and growth factor signaling likely contribute to pathogenesis and natural history. They have unique clinical features that are determined by the secreted hormone gene product.

Keywords: Hormone gene products; Neoplasm; Pituitary; Tumor.

Figure 1

Hormone secretion from pituitary tumors, although excessive and associated with unique phenotypic features, often retains intact trophic control. For example, dopaminergic agents appropriately suppress PRL secretion by prolactinomas, and dexamethasone may suppress ACTH secretion in patients with pituitary Cushing disease. From Melmed S 2003 Mechanisms for pituitary tumorigenesis: the plastic pituitary. J Clin Invest 112:1603-1618, with permission.

Figure 2

Pituitary adenoma signaling. Transcription of pituitary hormone genes and cell proliferation are induced by pituitary mitogenic factors including hypothalamic hormones and transcription factors, as well as peripheral hormones. Proliferative constraints include somastostatin and dopamine, as well as tumor suppressor genes. Cell cycle progression is mediated by CDK–cyclin complexes that phosphorylate Rb and cause it to release E2F, which drives cell proliferation. CDK inhibitors block kinase phosphorylation, thereby restraining cell cycle progression. Chromosomal instability, DNA damage and senescence may act to constrain malignant transformation of pituitary tumors. From Melmed S 2009 Acromegaly pathogenesis and treatment. J Clin Invest 119:3189-3202, with permission.