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1. Hosoyama T, Nishijo K, Garcia MM, Schaffer BS, Ohshima-Hosoyama S, Prajapati SI, Davis MD, Grant WF, Scheithauer BW, Marks DL, Rubin BP, Keller C: A Postnatal Pax7 Progenitor Gives Rise to Pituitary Adenomas. Genes Cancer; 2010 Apr 1;1(4):388-402
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  • [Title] A Postnatal Pax7 Progenitor Gives Rise to Pituitary Adenomas.
  • Pituitary adenomas are classified into functioning and nonfunctioning (silent) tumors on the basis of hormone secretion.
  • However, the mechanism of tumorigenesis and the cell of origin for pituitary adenoma subtypes remain to be elucidated.
  • Employing a tamoxifen-inducible mouse model, we demonstrate that a novel postnatal Pax7(+) progenitor cell population in the pituitary gland gives rise to silent corticotroph macro-adenomas when the retinoblastoma tumor suppressor is conditionally deleted.
  • While Pax transcriptional factors are critical for embryonic patterning as well as postnatal stem cell renewal for many organs, we have discovered that Pax7 marks a restricted cell population in the postnatal pituitary intermediate lobe.
  • This Pax7(+) early progenitor cell population is overlapping but ontologically downstream of the Nestin(+) pituitary stem cell population, yet upstream of another newly discovered Myf6(+) late progenitor cell population.
  • Interestingly, the Pax7(+) progenitor cell population is evolutionarily conserved in primates and humans, and Pax7 expression is maintained not only in murine tumors but also in human functioning and silent corticotropinomas.
  • Taken together, our results strongly suggest that human silent corticotroph adenomas may in fact arise from a Pax7 lineage of the intermediate lobe, a region of the human pituitary bearing closer scientific interest as a reservoir of pituitary progenitor cells.

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  • (PMID = 20811506.001).
  • [ISSN] 1947-6019
  • [Journal-full-title] Genes & cancer
  • [ISO-abbreviation] Genes Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA133229-03; United States / NCRR NIH HHS / RR / P41 RR012553; United States / NCI NIH HHS / CA / R01 CA133229
  • [Publication-type] JOURNAL ARTICLE
  • [Publication-country] United States
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2. Cooper O, Melmed S: Subclinical hyperfunctioning pituitary adenomas: the silent tumors. Best Pract Res Clin Endocrinol Metab; 2012 Aug;26(4):447-60
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  • [Title] Subclinical hyperfunctioning pituitary adenomas: the silent tumors.
  • Pituitary adenomas are classified by function as defined by clinical symptoms and signs of hormone hypersecretion with subsequent confirmation on immunohistochemical staining.
  • However, positive immunostaining for pituitary cell types has been shown for clinically nonfunctioning adenomas, and this entity is classified as silent functioning adenoma.
  • Most common in these subtypes include silent gonadotroph adenomas, silent corticotroph adenomas and silent somatotroph adenomas.
  • Appropriate classification of these adenomas may affect follow-up care after surgical resection.
  • Some silent adenomas such as silent corticotroph adenomas follow a more aggressive course, necessitating closer surveillance.
  • Furthermore, knowledge of the immunostaining characteristics of silent adenomas may determine postoperative medical therapy.
  • This article reviews the incidence, clinical behavior, and pathologic features of clinically silent pituitary adenomas.

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
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  • [Copyright] Copyright © 2012 Elsevier Ltd. All rights reserved.
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  • (PMID = 22863387.001).
  • [ISSN] 1878-1594
  • [Journal-full-title] Best practice & research. Clinical endocrinology & metabolism
  • [ISO-abbreviation] Best Pract. Res. Clin. Endocrinol. Metab.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / T32 DK007770; United States / NCI NIH HHS / CA / CA075979; United States / NIDDK NIH HHS / DK / K23DK085148; United States / Intramural NIH HHS / / ; United States / NCI NIH HHS / CA / R01 CA075979; United States / NCI NIH HHS / CA / R01 CA075979-13; United States / NIDDK NIH HHS / DK / K23 DK085148; United States / NIDDK NIH HHS / DK / T32 DK007770-10
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Review
  • [Publication-country] Netherlands
  • [Other-IDs] NLM/ NIHMS356291; NLM/ PMC3412996
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3. Yang Y, Sheng M, Huang F, Bu D, Liu X, Yao Y, Dai C, Sun B, Zhu J, Jiao Y, Wei Z, Zhu H, Lu L, Zhao Y, Jiang C, Wang R: Downregulation of Insulin-like growth factor binding protein 6 is associated with ACTH-secreting pituitary adenoma growth. Pituitary; 2014 Dec;17(6):505-13
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  • [Title] Downregulation of Insulin-like growth factor binding protein 6 is associated with ACTH-secreting pituitary adenoma growth.
  • BACKGROUND: Adrenocorticotrophic hormone (ACTH)-dependent Cushing's syndrome, called Cushing disease, is caused by a corticotroph tumor of the pituitary gland.
  • Insulin-like growth factor binding protein 6 (IGFBP6), which regulates insulin-like growth factor (IGF) activity and inhibits several IGF2-dependent cancer growths, plays a pivotal role in the tumorigenesis of malignancy, but its roles in ACTH-secreting pituitary adenomas remain unclear.
  • OBJECTIVE: To investigate IGFBP6 expression in ACTH-secreting pituitary adenomas, and its involvement in tumor growth.
  • METHODS: Sporadic ACTH-secreting pituitary adenomas specimens (n = 41) and adjacent non-tumorous pituitary tissues (n = 9) were collected by transphenoidal surgery.
  • Associations of IGFBP6 expression with maximum tumor diameter or Ki-67 labeling index were evaluated in ACTH-secreting pituitary adenomas.
  • RESULTS: IGFBP6 mRNA and protein expression were both decreased in ACTH-secreting pituitary adenomas, compared to adjacent non-tumorous pituitary tissues (P < 0.01).
  • IGFBP6 expression was correlated inversely with maximum tumor diameter (Rho = -0.53, P < 0.0001) and Ki-67 levels (Rho = -0.52, P < 0.05).
  • Moreover, IGFBP6 downregulation activated PI3 K-AKT-mTOR pathway in ACTH-secreting pituitary adenomas.
  • CONCLUSIONS: IGFBP6 attenuation in ACTH-secreting pituitary adenomas is associated with tumor growth, through activation of PI3K-AKT-mTOR pathway.
  • The finding underlies IGFBP6 roles in Cushing disease and would potentially provide a novel target of medical therapies.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / metabolism. Insulin-Like Growth Factor Binding Protein 6 / biosynthesis. Pituitary Neoplasms / metabolism
  • [MeSH-minor] Adult. Biomarkers, Tumor / metabolism. Down-Regulation. Female. Humans. In Vitro Techniques. Ki-67 Antigen. Male. Middle Aged. Oncogene Protein v-akt / metabolism. Phosphatidylinositol 3-Kinases / metabolism. Signal Transduction. TOR Serine-Threonine Kinases / metabolism. Young Adult

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  • (PMID = 24379119.001).
  • [ISSN] 1573-7403
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Insulin-Like Growth Factor Binding Protein 6; 0 / Ki-67 Antigen; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.11.1 / Oncogene Protein v-akt
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4. Brossaud J, Pallet V, Corcuff JB: Vitamin A, endocrine tissues and hormones: interplay and interactions. Endocr Connect; 2017 Jul 18;
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  • Vitamin A (retinol) is a micronutrient critical for cell proliferation and differentiation.
  • In adults, vitamin A and metabolites such as retinoic acid (RA) play major roles in vision, immune and brain functions, and tissue remodelling and metabolism.
  • In the pituitary, retinoids targets the corticotrophs with a possible therapeutic use in corticotropinomas.

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  • (PMID = 28720593.001).
  • [ISSN] 2049-3614
  • [Journal-full-title] Endocrine connections
  • [ISO-abbreviation] Endocr Connect
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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5. Vitale G, Tortora F, Baldelli R, Cocchiara F, Paragliola RM, Sbardella E, Simeoli C, Caranci F, Pivonello R, Colao A, A.B.C. Group: Pituitary magnetic resonance imaging in Cushing's disease. Endocrine; 2017 Mar;55(3):691-696
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pituitary magnetic resonance imaging in Cushing's disease.
  • Adrenocorticotropin-secreting pituitary tumor represents about 10 % of pituitary adenomas and at the time of diagnosis most of them are microadenomas.
  • Transsphenoidal surgery is the first-line treatment of Cushing's disease and accurate localization of the tumor within the gland is essential for selectively removing the lesion and preserving normal pituitary function.
  • Magnetic resonance imaging is the best imaging modality for the detection of pituitary tumors, but adrenocorticotropin-secreting pituitary microadenomas are not correctly identified in 30-50 % of cases, because of their size, location, and enhancing characteristics.
  • Several recent studies were performed with the purpose of better localizing the adrenocorticotropin-secreting microadenomas through the use in magnetic resonance imaging of specific sequences, reduced contrast medium dose and high-field technology.
  • Therefore, an improved imaging technique for pituitary disease is mandatory in the suspect of Cushing's disease.
  • The aims of this paper are to present an overview of pituitary magnetic resonance imaging in the diagnosis of Cushing's disease and to provide a magnetic resonance imaging protocol to be followed in case of suspicion adrenocorticotropin-secreting pituitary adenoma.
  • [MeSH-major] Adenoma / diagnostic imaging. Magnetic Resonance Imaging / methods. Pituitary ACTH Hypersecretion / diagnostic imaging. Pituitary Gland / diagnostic imaging. Pituitary Neoplasms / diagnostic imaging

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  • (PMID = 27435590.001).
  • [ISSN] 1559-0100
  • [Journal-full-title] Endocrine
  • [ISO-abbreviation] Endocrine
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Keywords] NOTNLM ; Cushing’s disease / Imaging / MRI / Pituitary microadenoma
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6. Sbiera S, Tryfonidou MA, Weigand I, Grinwis GC, Broeckx B, Herterich S, Allolio B, Deutschbein T, Fassnacht M, Meij BP: Lack of Ubiquitin Specific Protease 8 (USP8) Mutations in Canine Corticotroph Pituitary Adenomas. PLoS One; 2016;11(12):e0169009
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lack of Ubiquitin Specific Protease 8 (USP8) Mutations in Canine Corticotroph Pituitary Adenomas.
  • PURPOSE: Cushing's disease (CD), also known as pituitary-dependent hyperadrenocorticism, is caused by adrenocorticotropic hormone (ACTH)-secreting pituitary tumours.
  • Affected humans and dogs have similar clinical manifestations, however, the incidence of the canine disease is thousand-fold higher.
  • This makes the dog an obvious model for studying the pathogenesis of pituitary-dependent hyperadrenocorticism.
  • Recently, hotspot recurrent mutations in the gene encoding for ubiquitin specific protease 8 (USP8) have been identified as the main driver behind the formation of ACTH-secreting pituitary adenomas in humans.
  • METHODS: Presence of USP8 mutations was analysed by Sanger and PCR-cloning sequencing in 38 canine ACTH-secreting adenomas.
  • Furthermore, the role of USP8 and EGFR protein expression was assessed by immunohistochemistry in a subset of 25 adenomas.
  • RESULTS: None of the analysed canine ACTH-secreting adenomas presented mutations in the USP8 gene.
  • In a subset of these adenomas, however, we observed an increased nuclear expression of USP8, a phenotype characteristic for the USP8 mutated human tumours, that correlated with smaller tumour size but elevated ACTH production in those tumours.
  • CONCLUSIONS: Canine ACTH-secreting pituitary adenomas lack mutations in the USP8 gene suggesting a different genetic background of pituitary tumourigenesis in dogs.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / veterinary. Dog Diseases / genetics. Endopeptidases / genetics. Mutation. Ubiquitin Thiolesterase / genetics

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  • (PMID = 28005997.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.4.- / Endopeptidases; EC 3.4.19.12 / Ubiquitin Thiolesterase
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7. Fleseriu M, Petersenn S: New avenues in the medical treatment of Cushing's disease: corticotroph tumor targeted therapy. J Neurooncol; 2013 Aug;114(1):1-11
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  • [Title] New avenues in the medical treatment of Cushing's disease: corticotroph tumor targeted therapy.
  • Cushing's disease (CD) is a condition of chronic hypercortisolism caused by an adrenocorticotropic hormone-secreting pituitary adenoma.
  • First-line transsphenoidal surgery is not always curative and disease sometimes recurs.
  • Radiotherapy often requires months or years to be effective, and is also not curative in many cases.
  • Corticotroph adenomas frequently express both dopamine (D2) and somatostatin receptors (predominantly sstr5).
  • Pasireotide, a somatostatin analog with high sstr5 binding affinity, has shown urinary free cortisol (UFC) reductions in most patients with CD in a large phase 3 trial, with UFC normalization and tumor shrinkage in a subset of patients.
  • Glucocorticoid receptor blockade with mifepristone has recently demonstrated improvement in signs and symptoms of Cushing's and glycemic control; however, this modality does not address the etiology of the disease and has inherent adverse events related to its mechanism of action.
  • Pituitary-targeted medical therapies will soon play a more prominent role in treating CD, and may potentially become first-line medical therapy when surgery fails or is contraindicated.
  • [MeSH-major] Adrenocorticotropic Hormone / metabolism. Pituitary ACTH Hypersecretion / etiology. Pituitary ACTH Hypersecretion / therapy. Pituitary Neoplasms / complications
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Hormone Antagonists / therapeutic use. Humans. Mifepristone / therapeutic use. Pituitary Gland / drug effects. Pituitary Gland / metabolism. Pituitary Gland / pathology

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  • (PMID = 23673515.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Hormone Antagonists; 320T6RNW1F / Mifepristone; 9002-60-2 / Adrenocorticotropic Hormone
  • [Other-IDs] NLM/ PMC3724972
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8. Zhang N, Zhou P, Meng Y, Ye F, Jiang S: A retrospective review of 34 cases of pediatric pituitary adenoma. Childs Nerv Syst; 2017 Nov;33(11):1961-1967
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A retrospective review of 34 cases of pediatric pituitary adenoma.
  • PURPOSE: The purpose of this paper is to study invasiveness, tumor features and clinical symptoms of pediatric pituitary adenoma, and to discuss some inconclusive results in prior studies.
  • METHODS: We retrospectively reviewed 34 cases of children (<20 year-old) who were pathologically diagnosed with pituitary adenoma and surgically treated from 2010 to 2017.
  • Data of general information, clinical symptoms, invasive behaviors, surgery approaches, and tumor features were collected and analyzed.
  • Prolactinoma was most suffered, followed by GH-, none- and ACTH-secreting pituitary adenoma.
  • Macroadenoma account 70% of all cases.
  • Meanwhile, unlike prior studies, a significant raise of incidence on invasive tumor and pituitary adenoma apoplexy were observed.
  • Three cases of tumor recurrence received secondary surgery or radiotherapy.
  • Craniotomy is worth considering for total tumor removal.
  • Pituitary adenoma apoplexy needs further studies since its different features between children and adults in present study.

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  • (PMID = 28721598.001).
  • [ISSN] 1433-0350
  • [Journal-full-title] Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery
  • [ISO-abbreviation] Childs Nerv Syst
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Keywords] NOTNLM ; Invasion / Pediatric pituitary adenoma / Pituitary apoplexy / Transsphenoidal surgery
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9. Hernández-Ramírez LC, Gam R, Valdés N, Lodish MB, Pankratz N, Balsalobre A, Gauthier Y, Faucz FR, Trivellin G, Chittiboina P, Lane J, Kay DM, Dimopoulos A, Gaillard S, Neou M, Bertherat J, Assié G, Villa C, Mills JL, Drouin J, Stratakis CA: Loss-of-function mutations in the &lt;i&gt;CABLES1&lt;/i&gt; gene are a novel cause of Cushing's disease. Endocr Relat Cancer; 2017 Aug;24(8):379-392
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Loss-of-function mutations in the <i>CABLES1</i> gene are a novel cause of Cushing's disease.
  • The <i>CABLES1</i> cell cycle regulator participates in the adrenal-pituitary negative feedback, and its expression is reduced in corticotropinomas, pituitary tumors with a largely unexplained genetic basis.
  • We investigated the presence of <i>CABLES1</i> mutations/copy number variations (CNVs) and their associated clinical, histopathological and molecular features in patients with Cushing's disease (CD).
  • Samples from 146 pediatric (118 germline DNA only/28 germline and tumor DNA) and 35 adult (tumor DNA) CD patients were screened for <i>CABLES1</i> mutations.
  • CNVs were assessed in 116 pediatric CD patients (87 germline DNA only/29 germline and tumor DNA).
  • The four variants affected residues within or close to the predicted cyclin-dependent kinase-3 (CDK3)-binding region of the <i>CABLES1</i> protein and impaired its ability to block cell growth in a mouse corticotropinoma cell line (AtT20/D16v-F2).
  • We provide evidence for a role of <i>CABLES1</i> as a novel pituitary tumor-predisposing gene.
  • Its function might link two of the main molecular mechanisms altered in corticotropinomas: the cyclin-dependent kinase/cyclin group of cell cycle regulators and the epidermal growth factor receptor signaling pathway.
  • Further studies are needed to assess the prevalence of <i>CABLES1</i> mutations among patients with other types of pituitary adenomas and to elucidate the pituitary-specific functions of this gene.

  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
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  • [Copyright] © 2017 The authors.
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  • (PMID = 28533356.001).
  • [ISSN] 1479-6821
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Keywords] NOTNLM ; Cushing’s disease / corticotropinoma / germline mutation / whole-exome sequencing
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10. Cassarino MF, Sesta A, Pagliardini L, Losa M, Lasio G, Cavagnini F, Pecori Giraldi F: Proopiomelanocortin, glucocorticoid, and CRH receptor expression in human ACTH-secreting pituitary adenomas. Endocrine; 2017 Mar;55(3):853-860
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Proopiomelanocortin, glucocorticoid, and CRH receptor expression in human ACTH-secreting pituitary adenomas.
  • ACTH-secreting pituitary tumors are by definition partially autonomous, i.e., secrete ACTH independent of physiological control.
  • However, only few, small-sized studies on proopiomelanocortin (POMC) and its regulation by corticotropin-releasing hormone (CRH) or glucocorticoids are available.
  • Objective of the present study was to report on constitutive and CRH- and dexamethasone-regulated POMC, CRH (CRH-R1), and glucocorticoid receptor (NR3C1) gene expression in a large series of human corticotrope adenomas.
  • Fifty-three ACTH-secreting adenomas were incubated with 10 nM CRH or 10 nM dexamethasone for 24 h.
  • POMC, CRH-R1, NR3C1, and its alpha and beta isoforms were quantified and medium ACTH measured.
  • No correlation between POMC and ACTH was detected in any experimental condition.
  • CRH-R1 expression was not linked to the response to CRH while NR3C1 was expressed at greater levels in specimens who failed to inhibit during dexamethasone; glucocorticoid receptor α was the more abundant isoform and subject to down-regulation by dexamethasone.
  • Our results demonstrate a considerable variability in POMC expression among tumors and no correlation between POMC and ACTH, suggesting that POMC peptide processing/transport plays a major role in modulating ACTH secretion.
  • Further, CRH-R1 and NR3C1 expression were not linked to the expected ligand-induced outcome, indicating that receptor signaling rather than abundance determines corticotrope responses.
  • Our findings pave the way to new avenues of research into Cushing's disease pathophysiology.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / metabolism. Adenoma / metabolism. Pro-Opiomelanocortin / metabolism. Receptors, Corticotropin-Releasing Hormone / metabolism. Receptors, Glucocorticoid / metabolism
  • [MeSH-minor] Corticotropin-Releasing Hormone / pharmacology. Dexamethasone / pharmacology. Down-Regulation / drug effects. Female. Gene Expression / drug effects. Glucocorticoids / pharmacology. Humans. Male

  • Hazardous Substances Data Bank. DEXAMETHASONE .
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  • (PMID = 27220856.001).
  • [ISSN] 1559-0100
  • [Journal-full-title] Endocrine
  • [ISO-abbreviation] Endocrine
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CRF receptor type 1; 0 / Glucocorticoids; 0 / Receptors, Corticotropin-Releasing Hormone; 0 / Receptors, Glucocorticoid; 66796-54-1 / Pro-Opiomelanocortin; 7S5I7G3JQL / Dexamethasone; 9015-71-8 / Corticotropin-Releasing Hormone
  • [Keywords] NOTNLM ; ACTH / CRH / Cushing’s disease / Dexamethasone / POMC
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