ReviewMolecular and cellular endocrinology2011
How does cAMP/protein kinase A signaling lead to tumors in the adrenal cortex and other tissues?
Review in Molecular and cellular endocrinology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
44 citing papers in PubMed, 80 citations in OpenAlex.
- cAMP/PKA signaling in endocrine hypertension: genetic mechanisms and pathophysiological insights.Frontiers in endocrinology · 2026Review
- Review
- Dracorhodin perchlorate alleviates sciatic nerve pain in CCI rats by modulating inflammation and promoting nerve repair.Scientific reports · 2025Article
- Review
- Local and distal changes in dynamics are caused by an L205R Cushing's syndrome mutant in PRKACA.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Oncogene addiction to GNAS in GNASOncogene · 2022Article
- Primary aldosteronism: Pathophysiological mechanisms of cell death and proliferation.Frontiers in endocrinology · 2022Review
- Juvenile Granulosa Cell Tumor as the Presenting Feature of McCune-Albright Syndrome.Journal of the Endocrine Society · 2021Article
- Review
- A novel role of ADGRF1 (GPR110) in promoting cellular quiescence and chemoresistance in human epidermal growth factor receptor 2-positive breast cancer.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- G Protein-Coupled receptors and heterotrimeric G proteins as cancer drivers.FEBS letters · 2020Review
- ARMC5 variants in PRKAR1A-mutated patients modify cortisol levels and Cushing's syndrome.Endocrine-related cancer · 2020Article
- 5-oxo-ETE activates migration of H295R adrenocortical cells via MAPK and PKC pathways.Prostaglandins & other lipid mediators · 2019Article
- SomaticJournal of the Endocrine Society · 2019Article
- Tumor mutation burden and recurrent tumors in hereditary lung cancer.Cancer medicine · 2019Article
- The curious case of Gαs gain-of-function in neoplasia.BMC cancer · 2018Article
- Age-dependent effects of Armc5 haploinsufficiency on adrenocortical function.Human molecular genetics · 2017Article
- The regulatory 1α subunit of protein kinase A modulates renal cystogenesis.American journal of physiology. Renal physiology · 2017Article
- A Role for Phosphodiesterase 11A (PDE11A) in the Formation of Social Memories and the Stabilization of Mood.Advances in neurobiology · 2017Review
- Loss of phosphodiesterase 4D mediates acquired triapine resistance via Epac-Rap1-Integrin signaling.Oncotarget · 2016Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The overwhelming majority of benign lesions of the adrenal cortex leading to Cushing syndrome are linked to one or another abnormality of the cAMP signaling pathway. A small number of both massive macronodular adrenocortical disease and cortisol-producing adenomas harbor somatic GNAS mutations. Micronodular adrenocortical hyperplasias are either pigmented (the classic form being that of primary pigmented nodular adrenocortical disease) or non-pigmented; micronodular adrenocortical hyperplasias can be seen in the context of other conditions or isolated; for example, primary pigmented nodular adrenocortical disease usually occurs in the context of Carney complex, but isolated primary pigmented nodular adrenocortical disease has also been described. Both Carney complex and isolated primary pigmented nodular adrenocortical disease are caused by germline PRKAR1A mutations; somatic mutations of this gene that regulates cAMP-dependent protein kinase are also found in cortisol-producing adenomas, and abnormalities of PKA are present in most cases of massive macronodular adrenocortical disease. Micronodular adrenocortical hyperplasias and some cortisol-producing adenomas are associated with phosphodiesterase 11A and 8B defects, coded, respectively, by the PDE11A and PDE8B genes. Mouse models of Prkar1a deficiency also show that increased cAMP signaling leads to tumors in adrenal cortex and other tissues. In this review, we summarize all recent data from ours and other laboratories, supporting the view that Wnt-signaling acts as an important mediator of tumorigenicity induced by abnormal PRKAR1A function and aberrant cAMP signaling.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.