ArticleEndocrine-related cancer2019
Genetics of aldosterone-producing adenomas with pathogenic KCNJ5 variants.
Article in Endocrine-related cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Multiomics analysis unveils the cellular ecosystem with clinical relevance in aldosterone-producing adenomas withProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Primary Aldosteronism: Spatial Multiomics Mapping of Genotype-Dependent Heterogeneity and Tumor Expansion of Aldosterone-Producing Adenomas.Hypertension (Dallas, Tex. : 1979) · 2023Article
- Primary Aldosteronism: State-of-the-Art Review.American journal of hypertension · 2022Article
- Clinical Translationality ofInternational journal of molecular sciences · 2022Review
- Genetic, Cellular, and Molecular Heterogeneity in Adrenals With Aldosterone-Producing Adenoma.Hypertension (Dallas, Tex. : 1979) · 2020Article
- Genetic causes of primary aldosteronism.Experimental & molecular medicine · 2019Review
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Somatic variants in genes that regulate intracellular ion homeostasis have been identified in aldosterone-producing adenomas (APA). Although the mechanisms leading to an increased aldosterone production in APA cells has been well studied, the molecular events that cause cell proliferation and tumor formation are poorly understood. In the present study, we have performed whole exome sequencing (WES) to characterize the landscape of somatic alterations in a homogeneous series of APA with pathogenic KCNJ5 variants. In the WES analysis on eleven APA, 84 exonic somatic events were called by 3 different somatic callers. Besides the KCNJ5 gene, only two genes (MED13 and ZNF669) harbored somatic variants in more than one APA. Unlike adrenocortical carcinomas, no chromosomal instability was observed by the somatic copy-number alteration and loss of heterozygosity analyses. The estimated tumor purity ranged from 0.35 to 0.67, suggesting a significant proportion of normal cell infiltration. Based on the results of PureCN analysis, the KCNJ5 variants appear to be clonal. In conclusion, in addition to KCNJ5 somatic pathogenic variant, no significant somatic event that would obviously explain proliferation or tumor growth was observed in our homogeneous cohort of KCNJ5-mutated APA. The molecular mechanisms causing APA growth and tumorigenesis remain to be elucidated.
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