Pituitary function and neoplasia

Abstract

The molecular pathogenesis of pituitary adenomas appears multifactorial. Clearly early proximal DNA-altering events might occur that may involve transcription factor dysregulation or hereditary mutations. Multiple promoting influences might subsequently impinge on the previously initiated cell and determine clonal expansion. These factors include disordered hypothalamic hormone receptor signaling, overstimulation by ectopic hypothalamic hormones, disordered paracrine growth factor action, disordered signal transduction, loss of negative feedback inhibition leading to pituitary hyperplasia, estrogen-mediated or paracrine angiogenesis, and loss of tumor suppressor activity. Once the cell has been transformed, its ultimate growth characteristics and neo-plastic behavior appear to be determined by several genes acting relatively distally, including ras and nm23. © 2006 Humana Press Inc.