Evidence map›Paper›PMID 34852451›Full record

ArticleEndocrinology and metabolism (Seoul, Korea)2021

Clinical and Molecular Characteristics of PRKACA L206R Mutant Cortisol-Producing Adenomas in Korean Patients.

Insoon Jang, Su-Jin Kim, Ra-Young Song, Kwangsoo Kim, Seongmin Choi, Jang-Seok Lee, Min-Kyeong Gwon, Moon Woo Seong, Kyu Eun Lee, Jung Hee Kim

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Endocrinology and metabolism (Seoul, Korea), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact, top 76% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. Sexual dimorphism in benign adrenocortical tumours.European journal of endocrinology · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 1 country.

Insoon JangTranslational Research Institute, Biomedical Research Institute, Seoul National University Hospital, Seoul, Korea.
Su-Jin KimDepartment of Surgery, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Korea.
Ra-Young SongDepartment of Surgery, Chung-Ang University Hospital, Seoul, Korea.
Kwangsoo KimTranslational Research Institute, Biomedical Research Institute, Seoul National University Hospital, Seoul, Korea.
Seongmin ChoiTranslational Research Institute, Biomedical Research Institute, Seoul National University Hospital, Seoul, Korea.
Jang-Seok LeeTranslational Research Institute, Biomedical Research Institute, Seoul National University Hospital, Seoul, Korea.
Min-Kyeong GwonTranslational Research Institute, Biomedical Research Institute, Seoul National University Hospital, Seoul, Korea.
Moon Woo SeongDepartment of Laboratory Medicine, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Korea.
Kyu Eun LeeDepartment of Surgery, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Korea.
Jung Hee KimDepartment of Internal Medicine, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Korea.
Seoul National University Hospital · KRSeoul National University · KRChung-Ang University Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAn activating mutation (c.617A>C/p.Lys206Arg, L206R) in protein kinase cAMP-activated catalytic subunit alpha (PRKACA) has been reported in 35% to 65% of cases of cortisol-producing adenomas (CPAs). We aimed to compare the clinical characteristics and transcriptome analysis between PRKACA L206R mutants and wild-type CPAs in Korea.

methodsWe included 57 subjects with CPAs who underwent adrenalectomy at Seoul National University Hospital. Sanger sequencing for PRKACA was conducted in 57 CPA tumor tissues. RNA sequencing was performed in 13 fresh-frozen tumor tissues.

resultsThe prevalence of the PRKACA L206R mutation was 51% (29/57). The mean age of the study subjects was 42±12 years, and 87.7% (50/57) of the patients were female. Subjects with PRKACA L206R mutant CPAs showed smaller adenoma size (3.3±0.7 cm vs. 3.8±1.2 cm, P=0.059) and lower dehydroepiandrosterone sulfate levels (218±180 ng/mL vs. 1,511±3,307 ng/mL, P=0.001) than those with PRKACA wild-type CPAs. Transcriptome profiling identified 244 differentially expressed genes (DEGs) between PRKACA L206R mutant (n=8) and wild-type CPAs (n=5), including five upregulated and 239 downregulated genes in PRKACA L206R mutant CPAs (|fold change| ≥2, P<0.05). Among the upstream regulators of DEGs, CTNNB1 was the most significant transcription regulator. In several pathway analyses, the Wnt signaling pathway was downregulated and the steroid biosynthesis pathway was upregulated in PRKACA mutants. Protein-protein interaction analysis also showed that PRKACA downregulates Wnt signaling and upregulates steroid biosynthesis.

conclusionThe PRKACA L206R mutation in CPAs causes high hormonal activity with a limited proliferative capacity, as supported by transcriptome profiling.

Indexed as

AdenomaAdrenal Cortex NeoplasmsAdultCatalytic DomainCyclic AMP-Dependent Protein Kinase Catalytic SubunitsFemaleHumansHydrocortisoneMaleMiddle AgedProtein KinasesCyclic AMP-Dependent Protein Kinase Catalytic SubunitsHydrocortisonePRKACA protein, humanProtein KinasesAdrenocortical adenomasCushing syndromeGene expression profilingPRKACA mutationWnt signaling pathway

Identifiers

PMID34852451
PMCPMC8743585
OpenAlexW3216768856

What OpenQuestion holds

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Registered trials

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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.