title: Apoptosis: its role in pituitary development and neoplastic pituitary tissue.
abstract: Apoptosis, also known as programmed cell death, is a phenomenon in which different stimuli trigger cellular mechanisms that culminate in death, in the absence of inflammatory cell response. Two different activation pathways are known, the intrinsic pathway (or mitochondrial) and extrinsic (or death-receptor pathway), both pathways trigger enzymatic reactions that lead cells to break up and be phagocytized by neighboring cells. This process is a common occurrence in physiological and pathological states, participating in the control of cell proliferation, differentiation and remodeling of organs. In the early steps of pituitary gland formation, numerous apoptotic cells are detected in the separation of Rathke's pouch from the roof of oral ectoderm. In the distal part of the gland, which will form the adenohypophysis, the ratio of apoptosis was significantly lower. However, there is evidence that neoplastic pituitary cells undergo unbalance in genes that control apoptosis leading to uncontrolled cell growth. No direct evidence of apoptosis was found in the drugs used for tumors producing prolactin and growth hormone. In conclusion, an unbalancing in the apoptosis process is the boundary between development and tumor growth.
authors.affiliation: Neuroendocrine Unit, Division of Endocrinology and Metabolism, Hospital das Clínicas, University of Sao Paulo Medical School, São Paulo, Brazil.
authors.forename: M F
authors.initials: MF
authors.lastname: Guzzo
authors.forename: L R S
authors.initials: LR
authors.lastname: Carvalho
authors.forename: M D
authors.initials: MD
authors.lastname: Bronstein
mesh_terms: D017209:Apoptosis / Q000502:physiology*; D002454:Cell Differentiation / Q000502:physiology; D049109:Cell Proliferation; D002471:Cell Transformation, Neoplastic / Q000473:pathology; D006801:Humans; D010902:Pituitary Gland / Q000196:embryology* / Q000473:pathology / Q000502:physiology*; D010911:Pituitary Neoplasms / Q000473:pathology / Q000503:physiopathology*; D015398:Signal Transduction / Q000502:physiology