The New Molecular Landscape of Cushing's Disease.

Abstract

Cushing's disease (CD) is caused by corticotropin-secreting pituitary adenomas and results in substantial morbidity and mortality. Its molecular basis has remained poorly understood until the past few years, when several proteins and genes [such as testicular orphan nuclear receptor 4 (TR4) and heat shock protein 90 (HSP90)] were found to play key roles in the disease. Most recently, mutations in the gene of ubiquitin-specific peptidase 8 (USP8) increasing its deubiquination activity were discovered in a high percentage of corticotroph adenomas. Here, we will discuss emerging insights in the molecular alterations that finally result in CD. The therapeutic potential of these findings needs to be carefully evaluated in the near future, hopefully resulting in new treatment options for this devastating disorder.

• Authors: Silviu Sbiera, Timo Deutschbein, Isabel Weigand, Martin Reincke, Martin Fassnacht, Bruno Allolio
• Journal: Trends in endocrinology and metabolism: TEM (Trends Endocrinol Metab) Vol. 26 Issue 10 Pg. 573-583 (Oct 2015) ISSN: 1879-3061 [Electronic] United States
• PMID: 26412158 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
• Copyright: Copyright © 2015 Elsevier Ltd. All rights reserved.

Chemical References

• 14-3-3 Proteins
• ErbB Receptors

Topics

• 14-3-3 Proteins (metabolism)
• Animals
• ErbB Receptors (metabolism)
• Humans
• Pituitary ACTH Hypersecretion (genetics, metabolism)