›› 2010, Vol. 30 ›› Issue (5): 508-.

• Monographic report (Adrenal diseases) • Previous Articles     Next Articles

Research advance in molecular biochemistry of ACTH-independent Cushing syndrome

JIANG Yi-ran, reviewer;WANG Wei-qing, reviser   

  1. Department of Endocrine and Metabolic Diseases, Shanghai Institute of Endocrinology and Metabolism, Shanghai Clinical Center for Endocrine and Metabolic Diseases, Ruijin Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 200025, China
  • Online:2010-05-25 Published:2010-05-28
  • Supported by:

    National Natural Science Foundation of China, 30771018

Abstract:

Adrenocorticotropic hormone (ACTH)-independent Cushing syndrome includes adrenocortical adenoma, adrenocortical carcinoma and adrenocortical nodular hyperplasia, the  pathogenesis of which is related to genetic mutations (GNAS1, PRKAR1A and PDE11A), expression of aberrant hormone receptors, dysfunction of WNT pathway and loss of heterozygosity of tumor suppressor gene. The pathogenesis mentioned above is introduced in this article.

Key words: adrenocorticotropic hormone-independent Cushing syndrome, GNAS1gene, PRKAR1A gene;PDE11A gene, aberrant hormone receptors, WNT pathway