Adult pituitary stem cells: from pituitary plasticity to adenoma development

Neuroendocrinology. 2011;94(4):265-77. doi: 10.1159/000330857. Epub 2011 Nov 22.


The pituitary needs high plasticity of the hormone-producing cell compartment to generate the continuously changing hormonal signals that govern the key physiological processes it is involved in, as well as homeostatic cell turnover. However, the underlying mechanisms are still poorly understood. It was proposed that adult stem cells direct the generation of newborn cells with a hormonal phenotype according to the physiological requirements. However, only in recent years adult pituitary stem cells have begun to be phenotypically characterized in several studies that identified multiple stem/progenitor cell candidates. Also considering the incompletely defined features of this cell subpopulation, some discrepancies among the different reports are clearly apparent and long-term self-renewal remains to be unequivocally demonstrated. Here, all the recently published evidence is analyzed, trying, when possible, to reconcile the results of the different studies. Finally, with the perspective of shedding light on pituitary tumorigenesis and the development of potentially new pharmacological approaches directed against these cells, very recent evidence on the presence of putative cancer stem cells in human pituitary adenomas is discussed.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adenoma / etiology
  • Adenoma / metabolism*
  • Adult
  • Adult Stem Cells / cytology
  • Adult Stem Cells / physiology*
  • Animals
  • Cell Differentiation / physiology
  • Cell Transformation, Neoplastic
  • Humans
  • Intermediate Filament Proteins / metabolism
  • Mice
  • Neoplastic Stem Cells / cytology
  • Neoplastic Stem Cells / metabolism*
  • Nerve Tissue Proteins / metabolism
  • Nestin
  • Phenotype
  • Pituitary Gland / cytology*
  • Pituitary Gland / growth & development
  • Pituitary Gland / physiology
  • Pituitary Neoplasms / etiology
  • Pituitary Neoplasms / metabolism*
  • SOXB1 Transcription Factors / genetics


  • Intermediate Filament Proteins
  • NES protein, human
  • Nerve Tissue Proteins
  • Nes protein, mouse
  • Nestin
  • SOXB1 Transcription Factors
  • Sox2 protein, mouse