Proopiomelanocortin heterozygous and homozygous null mutant mice develop pituitary adenomas

J. Karpac, D. Ostwald, G. Y. Li, S. Bui, P. Hunnewell, M. B. Brennan, U. Hochgeschwender

Research output: Contribution to journalArticlepeer-review

12 Scopus citations

Abstract

Mice lacking all pro-opiomelanocortin (POMC)-derived peptides have been created by gene targeting of the POMC locus in embryonic stem cells. Phenotypes of the POMC null homozygous mutants include obesity, pigmentation defects, and adrenal insufficiency. Here, we report that both POMC null homozygous and heterozygous mutants also develop pituitary gland tumors, which result in their premature death. The tumors occur with 100% penetrance in both POMC heterozygous and homozygous genotypes. Histological examinations reveal that tumors start from hyperplastic focal points of melanotrophic cells within the intermediate lobe. Based on the morphological and immunohistological features, we have classified the tumors as non-invasive, non-secreting, intermediate lobe adenomas. These findings uncover potential novel roles of melanocortins in the regulation of cell proliferation.

Original languageEnglish
Pages (from-to)47-52
Number of pages6
JournalCellular and Molecular Biology
Volume52
Issue number2
StatePublished - May 30 2006

Keywords

  • Melanocortin receptors
  • Melanotrophs
  • Pituitary adenoma
  • Proopiomelanocortin

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