title: Molecular mechanisms of pituitary adenoma senescence.
abstract: As commonly encountered pituitary adenomas are invariably benign, we examined protective pituitary proliferative mechanisms. Cellular senescence is characterized by a largely irreversible cell cycle arrest and constitutes a strong anti-proliferative response, which can be triggered by DNA damage, chromosomal instability and aneuploidy, loss of tumor suppressive signaling or oncogene activation. Cellular senescence may prevent cells from undergoing transformation in vitro. Recently, evidence has accumulated that in vivo senescence is an important protective mechanisms against cancer. In this review we highlight an intrinsic predisposition of pituitary tumors to exhibit senescence-associated molecular pathways and show prospective mechanisms underlying the benign nature of these commonly encountered tumors.
authors.forename: Vera
authors.initials: V
authors.lastname: Chesnokova
authors.forename: Svetlana
authors.initials: S
authors.lastname: Zonis
authors.forename: Anat
authors.initials: A
authors.lastname: Ben-Shlomo
authors.forename: Kolja
authors.initials: K
authors.lastname: Wawrowsky
authors.forename: Shlomo
authors.initials: S
authors.lastname: Melmed
mesh_terms: D000236:Adenoma / Q000473:pathology*; D000818:Animals; D016922:Cellular Senescence; D050759:Cyclin-Dependent Kinase Inhibitor p21 / Q000502:physiology; D006801:Humans; D009363:Neoplasm Proteins / Q000502:physiology; D010911:Pituitary Neoplasms / Q000473:pathology*; D064249:Securin
chemical_list: C493956:CDKN1A protein, human; D050759:Cyclin-Dependent Kinase Inhibitor p21; D009363:Neoplasm Proteins; D064249:Securin