We have located links that may give you full text access.
Pathogenesis of benign unilateral adrenocortical tumours: focus on cAMP/PKA pathway.
Minerva Endocrinologica 2018 July 3
Somatic mutations affecting genes in the cAMP/PKA (Protein Kinase A) signaling pathway have been described as causative for the pathogenesis of benign unilateral adrenocortical adenomas associated with cortisol over secretion. These include predominantly somatic mutations in the PRKACA gene which encodes the catalytic subunit α of PKA. In addition, mutations in the GNAS gene, coding for the stimulatory G protein α, have been observed in approximately 10 % of cortisol producing adenomas (CPAs). The mutations render PKA signaling constitutively active and are therefore involved in cortisol over secretion of these tumours. Despite the prominent role of the cAMP/PKA pathway in the pathogenesis of unilateral CPAs, also mutations in the CTNNB1 gene, encoding β-catenin, were identified in CPAs. However, mutations in β-catenin are not limited to CPAs and are not associated with cortisol secretion since they were predominantly found in endocrine-inactive adenomas (EIAs) and might hence contribute to tumorigenesis in adrenocortical tissues. In this review, recent findings in the pathogenesis of benign adrenocortical tumours with a particular focus on the cAMP/PKA signaling pathway are summarised.
Full text links
Related Resources
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app