Mitosis and apoptosis in the pituitary gland: tumour formation or hyperplasia?
Direct analyses of trophic activity in the pituitary have been hampered by the lack of normal human tissue to study and by the short duration of the histologically overt phases of mitosis and apoptosis, which renders significant trophic events difficult to quantify. In rats and dogs, pituitary cell turnover is rapid in youth, declines markedly with age and virtually ceases by 'late middle age'. Specific stimuli superimpose brief but dramatic trophic events on this active background. There is little convincing evidence, as yet, for plasticity, i.e. the persistence of cell population changes after transient stimuli have passed. In contrast to spontaneous pituitary adenomas in rats, human pituitary tumours show relatively modest increases in mitotic activity. In the light of these observations, this chapter examines the accepted models of pituitary adenoma formation and propagation, with special reference to trophic activity, clonality and tumour behaviour.
Levy
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Division of Medicine Laboratories, Bristol Royal Infirmary, UK.
D000236:Adenoma / Q000473:pathology; D000818:Animals; D017209:Apoptosis; D002999:Clone Cells / Q000473:pathology; D006801:Humans; D006965:Hyperplasia; D008938:Mitosis; D010902:Pituitary Gland / Q000473:pathology*; D010911:Pituitary Neoplasms / Q000473:pathology*; D051381:Rats