ArticleThe Journal of clinical investigation2001
Retinoic acid prevents experimental Cushing syndrome.
Article in The Journal of clinical investigation, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
What it found
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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
60 citing papers in PubMed, 188 citations in OpenAlex.
- Combination therapy for Cushing's disease: effectiveness of two schedules of treatment: should we start with cabergoline or ketoconazole?Pituitary · 2014Trial
- OCT4 modulates Pomc gene transcription by interfering with specific corticotroph transcription factors.Journal of endocrinological investigation · 2026Article
- Review
- Current understanding of the role of DNA methylation in pituitary neuroendocrine tumors.Neuro-oncology advances · 2025Article
- Current and Emerging Pharmacological Therapies for Cushing's Disease.Current pharmaceutical design · 2024Review
- Silibinin, an HSP90 Inhibitor, on Human ACTH-Secreting Adenomas.Neuroendocrinology · 2023Article
- Early transcriptomic response of mouse adrenal gland and Y-1 cells to dexamethasone.Endocrine connections · 2022Article
- Current and Emerging Medical Therapies in Pituitary Tumors.Journal of clinical medicine · 2022Review
- Dual effects of 9-cis retinoic acid on ACTH-dependent hyperplastic adrenal tissues.Scientific reports · 2021Article
- Multimodal Non-Surgical Treatments of Aggressive Pituitary Tumors.Frontiers in endocrinology · 2021Review
- Nuclear Receptors as Regulators of Pituitary Corticotroph Pro-Opiomelanocortin Transcription.Cells · 2020Review
- A common polymorphism in the retinoic acid pathway modifies adrenocortical carcinoma age-dependent incidence.British journal of cancer · 2020Article
- PROP1-Dependent Retinoic Acid Signaling Regulates Developmental Pituitary Morphogenesis and Hormone Expression.Endocrinology · 2020Article
- Cushing's Disease.Journal of clinical medicine · 2019Review
- Review
- The Pathophysiology and Treatment of Hypertension in Patients With Cushing's Syndrome.Frontiers in endocrinology · 2019Review
- The Treatment of Refractory Pituitary Adenomas.Frontiers in endocrinology · 2019Review
- Recent Updates on the Diagnosis and Management of Cushing's Syndrome.Endocrinology and metabolism (Seoul, Korea) · 2018Review
- A review of Cushing's disease treatment by the Department of Neuroendocrinology of the Brazilian Society of Endocrinology and Metabolism.Archives of endocrinology and metabolism · 2018Review
- AT-101 acts as anti-proliferative and hormone suppressive agent in mouse pituitary corticotroph tumor cells.Journal of endocrinological investigation · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cushing syndrome is caused by an excess of adrenocorticotropic hormone (ACTH) production by neuroendocrine tumors, which subsequently results in chronic glucocorticoid excess. We found that retinoic acid inhibits the transcriptional activity of AP-1 and the orphan receptors Nur77 and Nurr1 in ACTH-secreting tumor cells. Retinoic acid treatment resulted in reduced pro-opiomelanocortin transcription and ACTH production. ACTH inhibition was also observed in human pituitary ACTH-secreting tumor cells and a small-cell lung cancer cell line, but not in normal cells. This correlated with the expression of the orphan receptor COUP-TFI, which was found in normal corticotrophs but not in pituitary Cushing tumors. COUP-TFI expression in ACTH-secreting tumor cells blocked retinoic acid action. Retinoic acid also inhibited cell proliferation and, after prolonged treatment, increased caspase-3 activity and induced cell death in ACTH-secreting cells. In adrenal cortex cells, retinoic acid inhibited corticosterone production and cell proliferation. The antiproliferative action and the inhibition of ACTH and corticosterone produced by retinoic acid were confirmed in vivo in experimental ACTH-secreting tumors in nude mice. Thus, we conclude that the effects of retinoic acid combine in vivo to reverse the endocrine alterations and symptoms observed in experimental Cushing syndrome.
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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.