ArticleScientific reports2016
Activating mutations in CTNNB1 in aldosterone producing adenomas.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.
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Who cites it
88 citing papers in PubMed, 167 citations in OpenAlex.
- Aldosterone-Producing Lesions HarboringHypertension (Dallas, Tex. : 1979) · 2026Article
- Inter- and intratumoral heterogeneity of aldosterone-producing adenomas: recent advances and clinical implications.Endocrine journal · 2026Review
- Primary aldosteronism.Nature reviews. Disease primers · 2026Review
- Rho/ROCK signaling and α-catenin mediate β-catenin-driven hyperplasia in the adrenal cortex via adherens junctions.The Journal of clinical investigation · 2026Article
- Emerging methods for subtype differentiation in primary aldosteronism.Journal of internal medicine · 2026Review
- Comparative Proteomic Profiling of Adrenocortical Neoplasia Using Mass Spectrometry.Journal of proteome research · 2025Article
- Molecular investigation of primary aldosteronism: exploring genetic heterogeneity in understudied populations.Archives of endocrinology and metabolism · 2025Article
- Somatic Mutations inHypertension (Dallas, Tex. : 1979) · 2025Article
- Review
- Intratumoural aldosterone and CYP11B2 expression levels among different genotypes of aldosterone producing tumours.Endocrine connections · 2025Article
- Sexual dimorphism in benign adrenocortical tumours.European journal of endocrinology · 2025Review
- Histopathological spectrum of common aldosterone-driver gene mutations in aldosterone-producing adenomas.Frontiers in medicine · 2025Article
- Germline targeted next-generation sequencing in patients with adrenal incidentalomas.Frontiers in endocrinology · 2025Article
- The adrenal gland and primary aldosteronism: anatomy, steroidogenesis, regulation, and genetic insights.Frontiers in endocrinology · 2025Review
- SomaticHypertension (Dallas, Tex. : 1979) · 2024Article
- Article
- Unilateral Primary Aldosteronism: Long-Term Disease Recurrence After Adrenalectomy.Hypertension (Dallas, Tex. : 1979) · 2024Article
- Molecular pathology of endocrine gland tumors: genetic alterations and clinicopathologic relevance.Virchows Archiv : an international journal of pathology · 2024Review
- Double somatic mutations inFrontiers in endocrinology · 2024Article
- Article
28 more citing papers are in PubMed but not listed here.
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Authors and funding
16 authors at 10 institutions in 4 countries.
Funding
Abstract
Primary aldosteronism (PA) is the most common cause of secondary hypertension with a prevalence of 5-10% in unreferred hypertensive patients. Aldosterone producing adenomas (APAs) constitute a large proportion of PA cases and represent a surgically correctable form of the disease. The WNT signaling pathway is activated in APAs. In other tumors, a frequent cause of aberrant WNT signaling is mutation in the CTNNB1 gene coding for β-catenin. Our objective was to screen for CTNNB1 mutations in a well-characterized cohort of 198 APAs. Somatic CTNNB1 mutations were detected in 5.1% of the tumors, occurring mutually exclusive from mutations in KCNJ5, ATP1A1, ATP2B3 and CACNA1D. All of the observed mutations altered serine/threonine residues in the GSK3β binding domain in exon 3. The mutations were associated with stabilized β-catenin and increased AXIN2 expression, suggesting activation of WNT signaling. By CYP11B2 mRNA expression, CYP11B2 protein expression, and direct measurement of aldosterone in tumor tissue, we confirmed the ability for aldosterone production. This report provides compelling evidence that aberrant WNT signaling caused by mutations in CTNNB1 occur in APAs. This also suggests that other mechanisms that constitutively activate the WNT pathway may be important in APA formation.
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