ReviewPituitary2022
Genetics of Cushing's disease: from the lab to clinical practice.
Review in Pituitary, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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.
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.
Who cites it
9 citing papers in PubMed, 22 citations in OpenAlex.
- New Insights from the Expression of the Mismatch Repair System in Pituitary Neuroendocrine Tumors.Endocrine pathology · 2026Article
- Cushing syndrome.Nature reviews. Disease primers · 2025Review
- [Clinically active pituitary tumors].Innere Medizin (Heidelberg, Germany) · 2024Review
- A heterozygous germline deletion within USP8 causes severe neurodevelopmental delay with multiorgan abnormalities.Journal of human genetics · 2024Article
- Endocrine causes of hypertension: literature review and practical approach.Hypertension research : official journal of the Japanese Society of Hypertension · 2023Review
- [Molecular genetic abnormalities in ACTH-secreting pituitary tumors (corticotropinomas): fundamental research and prospects for use in clinical practice].Problemy endokrinologii · 2023Review
- Refractory corticotroph adenomas.Pituitary · 2023Review
- Special issue: Cushing's disease update.Pituitary · 2022Article
- Fusion of Platelet Derived Growth Factor Receptor Alpha (Cancer genomics & proteomicsArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Cushing's disease is a rare, but devastating condition, caused by corticotroph tumors. It rarely manifests as syndrome and very few isolated cases present with germline mutations. Instead, the vast majority of corticotroph tumors are sporadic monoclonal neoplasms. At present, the major recurrent somatic driver mutations are found in the USP8 gene, which encodes for a deubiquitinase that rescues proteins regulating ACTH synthesis. Almost half of functional corticotroph tumors carry somatic USP8 mutations that associate with a distinct transcriptomic and clinical profile. Other genes mutated in a small fraction of corticotroph tumors include the deubiquitinase encoding gene USP48 and the glucocorticoid receptor expressing NR3C1. Recent reports on somatic TP53 and ATRX mutations in corticotroph macroadenomas and carcinomas indicate that within specific patient subpopulations they are not as rare as assumed.
Indexed as
Identifiers
What OpenQuestion holds
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.