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Updated: Jun 3, 2026

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The transcriptome that mediates increased cyclic adenosine monophosphate signaling in PRKAR1A defects and other

Monalisa F Azevedo1, Constantine A Stratakis

  • 1Section on Endocrinology and Genetics, Program on Developmental Endocrinology & Genetics, National Institutes of Health, 10 Center Drive, Bethesda, MD 20892, USA.

Endocrine Practice : Official Journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists
|April 2, 2011
PubMed
Abstract

Insights

Cyclic adenosine monophosphate (cAMP) and protein kinase A (PKA) signaling are key in developing adrenal hyperplasia and tumors. Abnormalities in cAMP/PKA and Wnt signaling pathways contribute to tumor formation in conditions like PPNAD.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Oncology

Background:

  • Primary pigmented nodular adrenocortical disease (PPNAD) and Carney complex are linked to bilateral adrenal hyperplasia (BAH).
  • Understanding the molecular mechanisms driving these conditions is crucial for effective treatment and prevention.

Purpose of the Study:

  • To review the role of cyclic adenosine monophosphate (cAMP) and associated signaling pathways in tumor formation.
  • To explore the involvement of these pathways in PPNAD, Carney complex, and other forms of BAH.

Main Methods:

  • Literature review of current knowledge on cAMP signaling and related pathways.
  • Discussion of genetic defects identified in endocrine and nonendocrine tumors.

Main Results:

  • PRKAR1A mutations, affecting cAMP/protein kinase A (PKA) signaling, are implicated in PPNAD and Carney complex.
  • Abnormalities in cAMP/PKA signaling and phosphodiesterase genes are found in various BAHs.
  • Aberrant cAMP/PKA signaling activates Wnt signaling, promoting tissue-specific cell proliferation and tumorigenesis.

Conclusions:

  • cAMP signaling plays a significant role in the pathogenesis of adrenocortical diseases.
  • The Wnt signaling pathway is a potential mediator of tumorigenesis driven by aberrant cAMP or PKA signaling.

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