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Objective  Silent corticotroph tumors are a pituitary neuroendocrine tumor subtype of corticotroph lineage that do not clinically express Cushing’s disease. The silencing of this type of tumor is not fully understood. The aim of the present study was to delve into the lack of secretory activity, studying the post-transcriptional and post-translational regulation of POMC/ACTH in a series of molecularly identified functioning and silent corticotroph tumors.    Design  We analyzed 24 silent corticotroph, 23 functioning corticotroph and 25 silent gonadotroph tumors.    Methods  We used Sanger sequencing, quantitative real-time PCR and Western blot to analyze genetic alterations in  POMC , gene expression of  TBX19 ,  NEUROD1 ,  POMC ,  PCSK1 ,  PCSK2 ,  CPE  and  PAM  and protein expression of POMC, PC1/3, PC2, CPE and PAM.    Results  We found different polymorphisms in the  POMC  gene of corticotroph tumors, some of them related to deficiency of proopiomelanocortin. Silent corticotroph tumors showed lower PC1/3 gene and protein expression than functioning ones, especially compared to micro-functioning corticotroph tumors (all  P  &lt; 0.05). Moreover, we found a positive correlation between PC2 and CPE gene and protein expression (rho ≥ 0.670,  P  &lt; 0.009) in silent corticotroph tumors compared with functioning ones.    Conclusions  By studying the post-transcriptional and post-translational processing of  POMC  and ACTH, respectively, in a large series of silent and functioning corticotroph tumors, we found that the lack of secretory activity of these tumors is related to an impaired processing of  POMC  and a high degradation of ACTH, with the macro-functioning corticotroph tumor behaving as an intermediate state between micro-functioning and silent corticotroph tumors.

Why don’t corticotroph tumors always produce Cushing’s disease?