Pathology 4200A/B Lecture 4: Pathogenesis of Pituitary Tumors

• School: Western University
• Department: Pathology
• Course: Pathology 4200A/B
• Professor: Chandan Chakraborty

Document Summary

Ss: sphenoid sinus: pituitary cells are slow proliferating (~10 weeks) but have high plasticity. Pituitary: no prh (trh is what is stimulating prh production, focus on trh, prh, ghrh & ghih. Differentiation of anterior pituitary cells: e2f transcription-specific (ets) tfs are key regulators of gonadotroph & Lactotroph growth & differentiation: upregulation/downregulation of certain tfs will tell you where the problem is. I. e. upregulation in pit-1 can cause problems in lactotroph or thyrotroph: prop-1: precursor of pit-1. Without it, rathke"s pouch cells can"t give rise to pit-1 and can anticipate problem to arise in somato-, lacto-, or thyrotroph. Pit-1 is very important: securin: a pituitary endothelial growth factor (angiogenic abilities) Pituitary cell proliferation: mutation of pit-1, prop-1 or t-pit leads to hypoplasia, deficiency of cell cycle regulators leads to hypoplasia, pregnancy causes lactotroph hyperplasia e2, securin, fgf2, vegf, target organ failure causes respective pituitary cell hyperplasia.