The New Molecular Landscape of Cushing's Disease

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• 作者：Silviu Sbiera¹ ; ^# ; Timo Deutschbein¹ ; ^# ; Isabel Weigand¹ ; Martin Reincke² ; Martin Fassnacht³ ; ^{fassnacht_m@ukw.de" class="auth_mail" title="E-mail the corresponding author} ; Bruno Allolio¹ ; ^&dagger ;
• 关键词：Cushing's disease ; pituitary ; gene expression ; epidermal growth factor receptor ; ubiquitin-specific peptidase 8 ; 14-3-3 proteins
• 刊名：Trends in Endocrinology & Metabolism
• 出版年：2015
• 出版时间：October 2015
• 年：2015
• 卷：26
• 期：10
• 页码：573-583
• 全文大小：2087 K

文摘

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.