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1. Giacomini D, Páez-Pereda M, Theodoropoulou M, Gerez J, Nagashima AC, Chervin A, Berner S, Labeur M, Refojo D, Renner U, Stalla GK, Arzt E: Bone morphogenetic protein-4 control of pituitary pathophysiology. Front Horm Res; 2006;35:22-31
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  • [Title] Bone morphogenetic protein-4 control of pituitary pathophysiology.
  • Bone morphogenetic protein-4 (BMP-4), a member of the transforming growth factor-Beta(TGF-Beta) family, is overexpressed in different prolactinoma models and induces the development of these lineage adenomas.
  • SMAD proteins activated by growth factors of the TGF-Beta and BMP family interact with estrogen receptors to stimulate the proliferation of prolactin and growth hormone-secreting cells.
  • Furthermore, BMP-4 presents differential expression in normal and adenomatous corticotropes and inhibitory action on corticotropinoma cell proliferation.
  • The present review highlights not only the crucial and opposite role of BMP-4 in the progression of pituitary adenomas but also that BMP-4 and retinoic acid interaction might serve as a potential new mechanism target for therapeutic approaches for Cushing disease.
  • [MeSH-major] Bone Morphogenetic Proteins / physiology. Pituitary Diseases / etiology
  • [MeSH-minor] Adrenocorticotropic Hormone / secretion. Animals. Bone Morphogenetic Protein 4. Gene Expression. Humans. Models, Biological. Neurons / secretion. Pituitary Gland / cytology. Pituitary Gland / growth & development. Pituitary Gland / metabolism. Pituitary Gland / secretion. Receptors, Transforming Growth Factor beta / metabolism. Transforming Growth Factor beta / physiology. Tretinoin / pharmacology

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  • (PMID = 16809920.001).
  • [ISSN] 0301-3073
  • [Journal-full-title] Frontiers of hormone research
  • [ISO-abbreviation] Front Horm Res
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / BMP4 protein, human; 0 / Bone Morphogenetic Protein 4; 0 / Bone Morphogenetic Proteins; 0 / Receptors, Transforming Growth Factor beta; 0 / Transforming Growth Factor beta; 5688UTC01R / Tretinoin; 9002-60-2 / Adrenocorticotropic Hormone
  • [Number-of-references] 42
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2. Gallelli MF, Cabrera Blatter MF, Castillo V: A comparative study by age and gender of the pituitary adenoma and ACTH and alpha-MSH secretion in dogs with pituitary-dependent hyperadrenocorticism. Res Vet Sci; 2010 Feb;88(1):33-40
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  • [Title] A comparative study by age and gender of the pituitary adenoma and ACTH and alpha-MSH secretion in dogs with pituitary-dependent hyperadrenocorticism.
  • Pituitary-dependent hyperadrenocorticism (PDH) is frequent in dogs.
  • Using magnetic resonance, pituitary tumours were intra-sellar (IS) in 30.8% and extra-sellar (ES) in 62.6% and the pars intermedia (PI) was affected in 6.5%.
  • ACTH concentration was greater in the ES vs. IS (p<0.05).
  • alpha-MSH did not present significant differences according to tumour size, showing a negative correlation (r=-0.47; p<0.01) vs. ACTH.
  • Differences in adenoma size according to gender and their age-related frequency of apparition could be because of different origins of the corticotrophinoma.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / veterinary. Adrenocortical Hyperfunction / veterinary. Adrenocorticotropic Hormone / secretion. Dog Diseases / pathology. Pituitary Neoplasms / veterinary. alpha-MSH / secretion
  • [MeSH-minor] Age Factors. Animals. Dogs. Female. Magnetic Resonance Imaging. Male. Pituitary Gland / pathology. Pituitary Gland / physiopathology. Pituitary Gland / secretion. Retrospective Studies. Sex Factors

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  • [Copyright] Copyright 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19683322.001).
  • [ISSN] 1532-2661
  • [Journal-full-title] Research in veterinary science
  • [ISO-abbreviation] Res. Vet. Sci.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 581-05-5 / alpha-MSH; 9002-60-2 / Adrenocorticotropic Hormone
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3. Barber TM, Adams E, Ansorge O, Byrne JV, Karavitaki N, Wass JA: Nelson's syndrome. Eur J Endocrinol; 2010 Oct;163(4):495-507
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  • Nelson's syndrome is a potentially life-threatening condition that does not infrequently develop following total bilateral adrenalectomy (TBA) for the treatment of Cushing's disease.
  • In this review article, we discuss some controversial aspects of Nelson's syndrome including diagnosis, predictive factors, aetiology, pathology and management based on data from the existing literature and the experience of our own tertiary centre.
  • We propose that Nelson's syndrome should be diagnosed in any patient with prior TBA for the treatment of Cushing's disease and with at least one of the following criteria: i) an expanding pituitary mass lesion compared with pre-TBA images;.
  • ii) an elevated 0800 h plasma level of ACTH (>500 ng/l) in addition to progressive elevations of ACTH (a rise of >30%) on at least three consecutive occasions.
  • Regarding predictive factors for the development of Nelson's syndrome post TBA, current evidence favours the presence of residual pituitary tumour on magnetic resonance imaging (MRI) post transsphenoidal surgery (TSS); an aggressive subtype of corticotrophinoma (based on MRI growth rapidity and histology of TSS samples); lack of prophylactic neoadjuvant pituitary radiotherapy at the time of TBA and a rapid rise of ACTH levels in year 1 post TBA.
  • Finally, more studies are needed to assess the efficacy of therapeutic strategies in Nelson's syndrome, including the alkylating agent, temozolomide, which holds promise as a novel and effective therapeutic agent in the treatment of associated aggressive corticotroph tumours.

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  • (PMID = 20668020.001).
  • [ISSN] 1479-683X
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Alkylating Agents; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; 9002-60-2 / Adrenocorticotropic Hormone
  • [Number-of-references] 101
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4. Kawashima ST, Usui T, Sano T, Iogawa H, Hagiwara H, Tamanaha T, Tagami T, Naruse M, Hojo M, Takahashi JA, Shimatsu A: P53 gene mutation in an atypical corticotroph adenoma with Cushing's disease. Clin Endocrinol (Oxf); 2009 Apr;70(4):656-7
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  • [Title] P53 gene mutation in an atypical corticotroph adenoma with Cushing's disease.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / complications. ACTH-Secreting Pituitary Adenoma / genetics. Adenoma / genetics. Mutation / genetics. Pituitary ACTH Hypersecretion / etiology. Pituitary Neoplasms / genetics. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 18771563.001).
  • [ISSN] 1365-2265
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53
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5. Guignat L, Assie G, Bertagna X, Bertherat J: [Corticotroph adenoma]. Presse Med; 2009 Jan;38(1):125-32
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  • [Title] [Corticotroph adenoma].
  • [Transliterated title] Adénome corticotrope.
  • Corticotroph adenomas cause ACTH oversecretion responsible for Cushing's disease.
  • This represents the most frequent cause of Cushing's syndrome, or chronic excess of endogenous glucocorticoids.
  • Ninety percent of corticotroph adenomas are microadenomas, sometime not visible on MRI.
  • Corticotroph macroadenomas are rare, but can be responsible for an aggressive tumor.
  • Cushing's disease diagnosis requires careful hormonal and imaging investigations, aiming first at the diagnosis of Cushing's syndrome and in a second step at the diagnosis of its pituitary origin.
  • The treatment of corticotroph adenoma is mainly based on pituitary surgery.
  • In case of failure of pituitary surgery, or in patients in whom surgery is not appropriate as a first line treatment, medical therapy (mainly anticortisolic drugs), pituitary radiotherapy or surgical bilateral adrenalectomy can be discussed.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / complications. Pituitary ACTH Hypersecretion / etiology. Pituitary Neoplasms / complications
  • [MeSH-minor] Adrenalectomy. Adrenocorticotropic Hormone / analysis. Chemotherapy, Adjuvant. Corticotropin-Releasing Hormone / analysis. Cushing Syndrome / diagnosis. Cushing Syndrome / etiology. Cushing Syndrome / therapy. Diagnosis, Differential. Humans. Hydrocortisone / analysis. Hydrocortisone / antagonists & inhibitors. Magnetic Resonance Imaging. Neoadjuvant Therapy. Radiotherapy, Adjuvant

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  • (PMID = 19041214.001).
  • [ISSN] 2213-0276
  • [Journal-full-title] Presse medicale (Paris, France : 1983)
  • [ISO-abbreviation] Presse Med
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone; 9015-71-8 / Corticotropin-Releasing Hormone; WI4X0X7BPJ / Hydrocortisone
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6. Saveanu A, Gunz G, Guillen S, Dufour H, Culler MD, Jaquet P: Somatostatin and dopamine-somatostatin multiple ligands directed towards somatostatin and dopamine receptors in pituitary adenomas. Neuroendocrinology; 2006;83(3-4):258-63
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  • [Title] Somatostatin and dopamine-somatostatin multiple ligands directed towards somatostatin and dopamine receptors in pituitary adenomas.
  • AIM: We report the comparative efficacy of octreotide, cabergoline and multiple ligands directed towards the different somatostatin subtypes (ssts), such as BIM-23A779 and SOM-230, and of chimeric analogs which bind both somatostatin and the dopamine D2 receptors (D2R), such as BIM-23A760 and BIM-23A781, in cell cultures from human growth hormone (GH)-secreting pituitary adenomas.
  • PROCEDURES: RT-PCR analysis of the quantitative expression of the different ssts and D2R mRNAs was performed on tumor fragments of 22 GH-secreting adenomas collected after surgery.
  • Pharmacological studies, using the different ligands, were performed on cell cultures of such tumors.
  • In each tumor tested, 3 patterns of response, in terms of GH suppression, were observed.
  • Among the compounds tested, the most potent inhibitors of GH secretion were the sst2, sst5, D2R chimeric compound BIM-23A760, followed by the sst universal ligand SOM-230.
  • The effect of multiple receptor activation on the functions of other pituitary tumor types, such as prolactinomas and corticotropinomas, is not presently analyzed, and the efficacy of multireceptor ligands remains to be elucidated.
  • [MeSH-major] Adenoma / drug therapy. Antineoplastic Agents, Hormonal / therapeutic use. Dopamine / analogs & derivatives. Pituitary Neoplasms / drug therapy. Somatostatin / analogs & derivatives
  • [MeSH-minor] Adult. Drug Screening Assays, Antitumor. Ergolines / therapeutic use. Female. Human Growth Hormone / drug effects. Human Growth Hormone / metabolism. Humans. Ligands. Male. Octreotide / therapeutic use. RNA, Messenger / analysis. Receptors, Dopamine D2 / drug effects. Receptors, Dopamine D2 / genetics. Receptors, Dopamine D2 / metabolism. Receptors, Somatostatin / classification. Receptors, Somatostatin / drug effects. Receptors, Somatostatin / genetics. Receptors, Somatostatin / metabolism. Recombinant Fusion Proteins / therapeutic use. Tumor Cells, Cultured

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  • (PMID = 17047391.001).
  • [ISSN] 0028-3835
  • [Journal-full-title] Neuroendocrinology
  • [ISO-abbreviation] Neuroendocrinology
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / BIM 23268; 0 / Ergolines; 0 / Ligands; 0 / RNA, Messenger; 0 / Receptors, Dopamine D2; 0 / Receptors, Somatostatin; 0 / Recombinant Fusion Proteins; 12629-01-5 / Human Growth Hormone; 51110-01-1 / Somatostatin; LL60K9J05T / cabergoline; RWM8CCW8GP / Octreotide; VTD58H1Z2X / Dopamine
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7. Roelfsema F, Kok S, Kok P, Pereira AM, Biermasz NR, Smit JW, Frolich M, Keenan DM, Veldhuis JD, Romijn JA: Pituitary-hormone secretion by thyrotropinomas. Pituitary; 2009;12(3):200-10
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  • [Title] Pituitary-hormone secretion by thyrotropinomas.
  • Hormone secretion by somatotropinomas, corticotropinomas and prolactinomas exhibits increased pulse frequency, basal and pulsatile secretion, accompanied by greater disorderliness.
  • Regulation of non-TSH pituitary hormones in this context is not well understood.
  • Cross-ApEn synchrony between TSH and GH did not differ between patients and controls, but TSH and PRL synchrony was reduced in patients.
  • We conclude that TSH secretion by thyrotropinomas shares many characteristics of other pituitary hormone-secreting adenomas.
  • In addition, abnormalities in GH and PRL secretion exist ranging from decreased (joint) regularity to overt hypersecretion, although not always clinically obvious, suggesting tumoral transformation of thyrotrope lineage cells.
  • [MeSH-major] Adenoma / physiopathology. Pituitary Hormones / blood. Pituitary Hormones / secretion. Pituitary Neoplasms / blood

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  • (PMID = 19051037.001).
  • [ISSN] 1573-7403
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / M01 RR000585
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Pituitary Hormones; 67763-96-6 / Insulin-Like Growth Factor I; 9002-62-4 / Prolactin; 9002-71-5 / Thyrotropin; 9002-72-6 / Growth Hormone
  • [Other-IDs] NLM/ PMC2712623
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8. Castillo VA, Gómez NV, Lalia JC, Cabrera Blatter MF, García JD: Cushing's disease in dogs: cabergoline treatment. Res Vet Sci; 2008 Aug;85(1):26-34
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  • [Title] Cushing's disease in dogs: cabergoline treatment.
  • The treatment of pituitary-dependent hyperadrenocorticism (PDH) in dogs has for a long time been focused on inhibiting the adrenal gland using drugs such as o-p'-DDD, Ketoconazole and Trilostane, without attacking the primary cause: the corticotrophinoma.
  • Corticotroph cells can express the D2 dopaminergic receptor; therefore cabergoline (Cbg) could be effective as a treatment.
  • A year after the treatment, there was a significant decrease in ACTH (p<0.0001), alpha-MSH (p<0.01), urinary cortisol/creatinine ratio (p<0.001), and of the tumor size (p<0.0001) evaluated by nuclear magnetic resonance.
  • [MeSH-major] Dog Diseases / drug therapy. Dopamine Agonists / therapeutic use. Ergolines / therapeutic use. Pituitary ACTH Hypersecretion / veterinary

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  • (PMID = 17910968.001).
  • [ISSN] 0034-5288
  • [Journal-full-title] Research in veterinary science
  • [ISO-abbreviation] Res. Vet. Sci.
  • [Language] eng
  • [Publication-type] Controlled Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Dopamine Agonists; 0 / Ergolines; 581-05-5 / alpha-MSH; 9002-60-2 / Adrenocorticotropic Hormone; LL60K9J05T / cabergoline; R9400W927I / Ketoconazole
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9. Dam-Hieu P, Irthum B, Seizeur R, Roudaut N, Besson G: Management of ACTH-secreting supradiaphragmatic adenomas. Clin Neurol Neurosurg; 2007 Oct;109(8):698-704
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Management of ACTH-secreting supradiaphragmatic adenomas.
  • Supradiaphragmatic adrenocorticotropic hormone (ACTH) secreting pituitary adenomas are exceptionally encountered (14 cases previously described) and raise issues concerning their nosology and management.
  • To illustrate this issue, we presented two cases of supradiaphragmatic ACTH secreting pituitary adenomas successfully excised via a subfrontal approach.
  • Both patients were female (20 and 41 years) and had a typical Cushing's syndrome.
  • MRI revealed, in both cases, a suprasellar mass in contact with the pars tuberalis of the pituitary.
  • One year later, the patient was operated on again via a subfrontal approach, allowing excision of a supradiaphragmatic adenoma and a complete cure of Cushing's disease.
  • In both cases, the diaphragma sellae was found to be intact and the pituitary stalk could be preserved.
  • Postoperative MRI demonstrated a clearly visible intact pituitary stalk in conjunction with normal aspect of the pituitary.
  • Supradiaphragmatic pituitary adenomas are most likely adenomas of the pituitary stalk with extra-axial development.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / pathology. ACTH-Secreting Pituitary Adenoma / surgery. Adenoma / pathology. Adenoma / surgery

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  • (PMID = 17532556.001).
  • [ISSN] 0303-8467
  • [Journal-full-title] Clinical neurology and neurosurgery
  • [ISO-abbreviation] Clin Neurol Neurosurg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
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10. Brito LP, Lerário AM, Bronstein MD, Soares IC, Mendonca BB, Fragoso MC: Influence of the fibroblast growth factor receptor 4 expression and the G388R functional polymorphism on Cushing's disease outcome. J Clin Endocrinol Metab; 2010 Oct;95(10):E271-9
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  • [Title] Influence of the fibroblast growth factor receptor 4 expression and the G388R functional polymorphism on Cushing's disease outcome.
  • CONTEXT: Abnormal FGFR4 expression has been detected in pituitary tumors, especially in larger and invasive adenomas.
  • Then, we hypothesized that FGFR4 expression and genotype could be markers of adverse outcome of Cushing's disease after transsphenoidal surgery.
  • OBJECTIVES: The objective was to investigate whether there is an association between the postoperative outcome of Cushing's disease (remission/recurrence) and the FGFR4 G388R genotype or the FGFR4 expression in corticotrophinomas.
  • FGFR4 expression was assessed by real-time PCR in 18 corticotrophinomas.
  • MAIN OUTCOME MEASURES: The outcome measures included the FGFR4 G388R genotype and FGFR4 expression in postoperative remission and recurrence of Cushing's disease.
  • RESULTS: Homozygosis for FGFR4 glycine (Gly(388)) allele was associated with reduced disease-free survival, in the univariate analysis (hazard ratio of 6.91; 95% confidence interval of 1.14-11.26; P = 0.028).
  • Male gender (P = 0.036), lack of pathology confirmation (P = 0.009), and cortisol levels more than 2 μg/dl in the early postoperative period (P < 0.001) were also significant predictors of Cushing's disease recurrence in the univariate analysis.
  • FGFR4 overexpression was found in 44% of the corticotrophinomas, and it was associated with lower postoperative remission rate (P = 0.009).
  • CONCLUSIONS: Our data suggest that homozygosis for FGFR4 Gly(388) allele and FGFR4 overexpression are associated with higher frequency of postoperative recurrence and persistence of Cushing's disease, respectively.
  • [MeSH-major] Pituitary ACTH Hypersecretion / genetics. Polymorphism, Single Nucleotide. Receptor, Fibroblast Growth Factor, Type 4 / genetics
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / diagnosis. ACTH-Secreting Pituitary Adenoma / genetics. ACTH-Secreting Pituitary Adenoma / surgery. Adolescent. Adult. Amino Acid Substitution / genetics. Arginine / genetics. Child. Female. Gene Expression / physiology. Glycine / genetics. Humans. Hypophysectomy. Male. Middle Aged. Pituitary Neoplasms / diagnosis. Pituitary Neoplasms / genetics. Pituitary Neoplasms / surgery. Prognosis. Recurrence. Retrospective Studies. Treatment Outcome. Young Adult

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  • (PMID = 20660043.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 94ZLA3W45F / Arginine; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 4; TE7660XO1C / Glycine
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11. Castillo VA, Gallelli MF: Corticotroph adenoma in the dog: pathogenesis and new therapeutic possibilities. Res Vet Sci; 2010 Feb;88(1):26-32
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  • [Title] Corticotroph adenoma in the dog: pathogenesis and new therapeutic possibilities.
  • The corticotrophinoma, causing pituitary dependent hypercortisolism, represents the highest percentage of pituitary tumours in the dog.
  • It is not clear either what factors are involved in the tumour genesis; nevertheless, firm candidates are the Rb1 gene, proteins p27, p21 and p16, as are also defects in the glucocorticoid receptor and Nur77/Nurr1.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / veterinary. Adenoma / veterinary. Dog Diseases / etiology

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  • [Copyright] Copyright 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19733374.001).
  • [ISSN] 1532-2661
  • [Journal-full-title] Research in veterinary science
  • [ISO-abbreviation] Res. Vet. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 95
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12. Gao C, Fu X, Pan Y, Li Q: Surgical treatment of pancreatic neuroendocrine tumors: report of 112 cases. Dig Surg; 2010 Aug;27(3):197-204
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  • OBJECTIVES: To review the clinical data of a group of patients with pancreatic neuroendocrine tumors (pNETs) and to investigate the role of surgery in the treatment for pNETs by analyzing clinical manifestations and postoperative course of this rare disease.
  • Patients' data related to demographics and characteristics, diagnostic studies, surgical and tumor characteristics and survival were retrospectively reviewed.
  • RESULTS: Forty-six patients (41.1%) had a well-differentiated neuroendocrine tumor (WDT), 44 (48.2%) a well-differentiated neuroendocrine carcinoma (WD-Ca) and 12 (10.7%) a poorly differentiated neuroendocrine carcinoma (PD-Ca).
  • Nonfunctional tumors were seen in 65 (58.0%) patients, whereas functional tumors were found in 47 (42.0%) patients, including 26 insulinomas, 17 gastrinomas, 2 VIPomas, 1 glucagonoma, and 1 ACTHoma.
  • Survival was significantly related to the type of neuroendocrine tumor (p = 0.001).
  • The 5-year survival rate differed significantly between patients with tumor node metastasis (TNM) stage I and II disease and those with stage III and IV tumors (p = 0.011).
  • Malignant cases should be treated with aggressive radical surgery to achieve complete tumor resection and potential for long-term survival.

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  • (PMID = 20571266.001).
  • [ISSN] 1421-9883
  • [Journal-full-title] Digestive surgery
  • [ISO-abbreviation] Dig Surg
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
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13. Chowdhury IN, Sinaii N, Oldfield EH, Patronas N, Nieman LK: A change in pituitary magnetic resonance imaging protocol detects ACTH-secreting tumours in patients with previously negative results. Clin Endocrinol (Oxf); 2010 Apr;72(4):502-6
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  • [Title] A change in pituitary magnetic resonance imaging protocol detects ACTH-secreting tumours in patients with previously negative results.
  • OBJECTIVE: While detection of pituitary tumours with magnetic resonance imaging (MRI) may reduce diagnostic costs and improve surgical outcomes for patients with Cushing's disease, the optimal T1-weighted spin-echo (SE) MRI protocol remains unknown.
  • We hypothesized that specific MR scanning parameters influence detection of corticotropinomas.
  • DESIGN AND PATIENTS: Between December 1997 and November 2004, 21 of 84 consecutive patients with Cushing's disease had a falsely negative initial pituitary MRI study and a lesion identified subsequently at the National Institutes of Health Clinical Center.
  • This study retrospectively reviewed and compared technical parameters used for the two pituitary T1-weighted SE MRIs in 18 patients with available scans.
  • Immunohistochemistry of tumours resected at transsphenoidal surgery confirmed all to be corticotropinomas.
  • CONCLUSIONS: Not all 'T1-weighted SE' scans are equally accurate.
  • We recommend that endocrinologists consider pituitary MRI parameters when interpreting the results.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / diagnosis. Magnetic Resonance Imaging / methods. Pituitary Neoplasms / diagnosis
  • [MeSH-minor] Adult. False Negative Reactions. Female. Humans. Male. Middle Aged. Pituitary ACTH Hypersecretion / pathology. Pituitary Gland / pathology. Retrospective Studies

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  • (PMID = 19500112.001).
  • [ISSN] 1365-2265
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 HD008833-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] England
  • [Other-IDs] NLM/ NIHMS139974; NLM/ PMC2866063
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14. Keil MF, Stratakis CA: Facial metrics in children with corticotrophin-producing pituitary adenomas suggest abnormalities in midface development. J Pediatr Endocrinol Metab; 2009 Jan;22(1):47-53
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  • [Title] Facial metrics in children with corticotrophin-producing pituitary adenomas suggest abnormalities in midface development.
  • BACKGROUND: Tumors of the hypothalamic-pituitary unit have been linked to genetic syndromes that are associated with midfacial abnormalities.
  • AIM: We hypothesized that mutations of genes that affect the development of the face (and consequently of the anterior pituitary) may be present in children with ACTH-producing pituitary adenomas, and if this is true then facial measurements would be different from those predicted by parental features.
  • METHODS: We studied 20 children with corticotropinomas and a control group and their parents.
  • RESULTS: Significant differences were seen between the children with pituitary adenomas and their parents for vertical facial height measures: nasal length (p < 0.001), lower facial height (p < 0.03) and overall facial height (p < 0.01).
  • CONCLUSION: We conclude that some of the indices of midline craniofacial development, in particular those affecting the vertical axis, are different in children with corticotroph adenomas producing ACTH.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / pathology. Adenoma / pathology. Face / pathology. Maxillofacial Abnormalities / etiology. Maxillofacial Development / physiology

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  • (PMID = 19344074.001).
  • [ISSN] 0334-018X
  • [Journal-full-title] Journal of pediatric endocrinology & metabolism : JPEM
  • [ISO-abbreviation] J. Pediatr. Endocrinol. Metab.
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00001595
  • [Grant] United States / NICHD NIH HHS / HD / Z01 HD000642; United States / Intramural NIH HHS / / ZIA HD000642-13; United States / NICHD NIH HHS / HD / Z01-HD-000642-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] Germany
  • [Other-IDs] NLM/ NIHMS310299; NLM/ PMC3143028
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15. Suzuki M, Egashira N, Kajiya H, Minematsu T, Takekoshi S, Tahara S, Sanno N, Teramoto A, Osamura RY: ACTH and alpha-subunit are co-expressed in rare human pituitary corticotroph cell adenomas proposed to originate from ACTH-committed early pituitary progenitor cells. Endocr Pathol; 2008;19(1):17-26
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  • [Title] ACTH and alpha-subunit are co-expressed in rare human pituitary corticotroph cell adenomas proposed to originate from ACTH-committed early pituitary progenitor cells.
  • The functional differentiation of pituitary cells and adenomas follows the combination of transcription factors and co-factors in three cell lineages [growth hormone-prolactin-thyroid-stimulating hormone lineage, adrenocorticotrophic hormone (ACTH)/pro-opiomelanocortin (POMC) lineage, and follicular stimulating hormone (FSH)/luteinizing hormone (LH) lineage], which include Pit-1, GATA-2, SF-1, NeuroD1/beta2, Tpit, ERalpha, and others.
  • Only rarely are hormones from different lineages co-expressed in the same adenoma cells.
  • Most corticotroph cell adenomas belonging to the ACTH/POMC lineage are mono-hormonal.
  • In our study of 89 corticotroph cell adenomas, 5 cases expressed both ACTH and alpha-subunit; these adenomas did not express any other anterior pituitary hormones or subunits.
  • To clarify the mechanism involved, we studied the transcription factors that regulate pituitary cell differentiation.
  • NeuroD1 and T-pit, markers of the ACTH/POMC lineage, and SF-1 and DAX-1, related to the LH/FSH cell lineage were expressed in all cases.
  • GATA2, a synergistic factor in the gonadotroph cell lineage with SF-1, was also expressed in three of five cases.
  • As ACTH and alpha-subunit are the earliest hormones to appear during development, we speculate that these particular adenomas are derived from committed ACTH progenitor cells.
  • The molecular process governing functional differentiation of these adenomas requires further investigation.
  • [MeSH-major] Adenoma / genetics. Adrenocorticotropic Hormone / genetics. Gene Expression Regulation, Neoplastic. Glycoprotein Hormones, alpha Subunit / genetics. Pituitary Neoplasms / genetics. Pituitary Neoplasms / pathology

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  • (PMID = 18228160.001).
  • [ISSN] 1559-0097
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Glycoprotein Hormones, alpha Subunit; 0 / NEUROD1 protein, human; 0 / Transcription Factor Pit-1; 0 / Transcription Factors; 66796-54-1 / Pro-Opiomelanocortin; 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
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16. Xing B, Deng K, Ren ZY, Su CB, Wang RZ, Yang Y, Ma WB, Li YN: Magnetic resonance imaging characteristics and surgical results of adrenocorticotropin-secreting pituitary adenomas. Chin Med Sci J; 2008 Mar;23(1):44-8
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  • [Title] Magnetic resonance imaging characteristics and surgical results of adrenocorticotropin-secreting pituitary adenomas.
  • OBJECTIVE: To evaluate magnetic resonance imaging (MRI) characteristics and surgical results of adrenocorticotropin (ACTH)-secreting pituitary adenomas.
  • METHODS: MRI characteristics and relationship between MRI positive rate and surgical results of 266 patients with pathologically confirmed Cushing's disease were analyzed retrospectively.
  • All patients underwent thin-section sagittal and coronal scans of the pituitary gland before and after administration of gadolinium-diethylene triamine pentaacetic acid (Gd-DTPA) on a 1.5 Tesla MRI scanner, and dynamic enhanced MRI was performed in 39 patients.
  • RESULTS: Preoperative MRI revealed normal results in 41 (15.4%) cases, microadenoma in 179 (67.3%), macroadenoma in 42 (15.8%), and huge adenoma in 4 (1.5%).
  • Pituitary apoplexy was found in 13 (4.9%) cases.
  • Positive rate of ACTH-secreting adenomas was 84.6% (225/266) on MRI scans, and that of small microadenomas was 87.2% (34/39) on dynamic enhanced MRI scans.
  • Preoperative endocrinological tests of 199 cases supported the diagnosis of typical Cushing's disease, while the other 67 cases had atypical endocrinological results.
  • CONCLUSIONS: Enhanced coronal pituitary MRI is helpful for preoperative localization of ACTH-secreting pituitary microadenoma.

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  • (PMID = 18437910.001).
  • [ISSN] 1001-9294
  • [Journal-full-title] Chinese medical sciences journal = Chung-kuo i hsueh k'o hsueh tsa chih
  • [ISO-abbreviation] Chin. Med. Sci. J.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone
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17. Karavitaki N, Scheithauer BW, Watt J, Ansorge O, Moschopoulos M, Llaguno AV, Wass JA: Collision lesions of the sella: co-existence of craniopharyngioma with gonadotroph adenoma and of Rathke's cleft cyst with corticotroph adenoma. Pituitary; 2008;11(3):317-23
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  • [Title] Collision lesions of the sella: co-existence of craniopharyngioma with gonadotroph adenoma and of Rathke's cleft cyst with corticotroph adenoma.
  • Most contributions include a pituitary adenoma or a cyst/cystic tumor, particularly a Rathke cleft cyst.
  • The association of craniopharyngioma with an adenoma is particularly rare.
  • Among reported cases, some have included secondary prolactin cell hyperplasia due to pituitary stalk section effect.
  • Herein, we report two collision lesions, including a gonadotroph adenoma with adamantinomatous craniopharyngioma and a corticotroph adenoma with Rathke's cleft cyst.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / complications. Adenoma / complications. Central Nervous System Cysts / complications. Corticotrophs / pathology. Craniopharyngioma / complications. Gonadotrophs / pathology. Pituitary Neoplasms / complications. Sella Turcica / pathology

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  • (PMID = 17917812.001).
  • [ISSN] 1386-341X
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 65
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18. Takeshita A, Inoshita N, Taguchi M, Okuda C, Fukuhara N, Oyama K, Ohashi K, Sano T, Takeuchi Y, Yamada S: High incidence of low O(6)-methylguanine DNA methyltransferase expression in invasive macroadenomas of Cushing's disease. Eur J Endocrinol; 2009 Oct;161(4):553-9
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  • [Title] High incidence of low O(6)-methylguanine DNA methyltransferase expression in invasive macroadenomas of Cushing's disease.
  • CONTEXT: Crooke's cell adenoma (CCA), characterized by massive Crooke's hyaline change in corticotroph adenoma, causes a rare subtype of Cushing's disease.
  • In contrast to ordinary corticotroph adenomas, CCAs are generally aggressive and present as invasive macroadenomas, which are refractory to both surgery and radiotherapy and have a high-recurrence rate.
  • OBJECTIVE: We report a patient with Crooke's cell carcinoma who presented with local invasion and liver metastases, which was refractory to conventional therapeutic modalities including transsphenoidal surgery, radiosurgery, medications, and hepatic transcatheter arterial embolization.
  • After all these treatments failed, the patient had monthly temozolomide administrations, resulting in gradual clinical improvement and biochemical data that were consistent with tumor shrinkage.
  • METHODS: We thus investigated MGMT expression, immunohistochemically, in seven CCAs (five invasive macroadenomas and two invasive microadenomas) and 17 ordinary-type adenomas (OTAs; three noninvasive macroadenomas, 12 noninvasive microadenomas, and two invasive microadenomas) from patients with Cushing's disease.
  • In 17 OTAs, only one adenoma showed low MGMT expression.
  • CONCLUSION: In Cushing's disease, invasive macroadenomas including CCA usually have low-MGMT expression.

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  • (PMID = 19589911.001).
  • [ISSN] 1479-683X
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; 9002-60-2 / Adrenocorticotropic Hormone; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase; WI4X0X7BPJ / Hydrocortisone
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19. van der Hoek J, Waaijers M, van Koetsveld PM, Sprij-Mooij D, Feelders RA, Schmid HA, Schoeffter P, Hoyer D, Cervia D, Taylor JE, Culler MD, Lamberts SW, Hofland LJ: Distinct functional properties of native somatostatin receptor subtype 5 compared with subtype 2 in the regulation of ACTH release by corticotroph tumor cells. Am J Physiol Endocrinol Metab; 2005 Aug;289(2):E278-87
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  • [Title] Distinct functional properties of native somatostatin receptor subtype 5 compared with subtype 2 in the regulation of ACTH release by corticotroph tumor cells.
  • In a series of human corticotroph adenomas, we recently found predominant mRNA expression of somatostatin (SS) receptor subtype 5 (sst5).
  • After 72 h, the multiligand SS analog SOM230, which has a very high sst5 binding affinity, but not Octreotide (OCT), significantly inhibited basal ACTH release.
  • To further explore the role of sst5 in the regulation of ACTH release, we conducted additional studies with mouse AtT-20 cells.
  • SOM230 showed a 7-fold higher ligand binding affinity and a 19-fold higher potency in stimulating guanosine 5'-O-(3-thiotriphosphate) binding in AtT-20 cell membranes compared with OCT.
  • SOM230 potently suppressed CRH-induced ACTH release, which was not affected by 48-h dexamethasone (DEX) pretreatment.
  • However, DEX attenuated the inhibitory effects of OCT on ACTH release, whereas it increased the inhibitory potency of BIM-23268, an sst5-specific analog, on ACTH release.
  • Quantitative PCR analysis showed that DEX lowered sst(2A+2B) mRNA expression significantly after 24 and 48 h, whereas sst5 mRNA levels were not significantly affected by DEX treatment.
  • Finally, after SS analog preincubation, compared with OCT both SOM230 and BIM-23268 showed a significantly higher inhibitory effect on CRH-induced ACTH release.
  • In conclusion, our data support the concept that the sst5 receptor might be a target for new therapeutic agents to treat Cushing's disease.
  • [MeSH-major] Adrenocorticotropic Hormone / secretion. Corticotropin-Releasing Hormone / physiology. Pituitary Gland / secretion. Receptors, Somatostatin / physiology
  • [MeSH-minor] Animals. Dose-Response Relationship, Drug. Down-Regulation. Glucocorticoids / physiology. Mice. Octreotide / pharmacology. Pituitary Neoplasms. RNA, Messenger / analysis. Somatostatin / analogs & derivatives. Somatostatin / pharmacology. Stimulation, Chemical. Tumor Cells, Cultured

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  • (PMID = 15769796.001).
  • [ISSN] 0193-1849
  • [Journal-full-title] American journal of physiology. Endocrinology and metabolism
  • [ISO-abbreviation] Am. J. Physiol. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BIM 23268; 0 / Glucocorticoids; 0 / RNA, Messenger; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 0 / somatostatin receptor 5; 51110-01-1 / Somatostatin; 9002-60-2 / Adrenocorticotropic Hormone; 9015-71-8 / Corticotropin-Releasing Hormone; 98H1T17066 / pasireotide; RWM8CCW8GP / Octreotide
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20. Gruszka A, Kunert-Radek J, Pawlikowski M, Stepien H: Serum endostatin levels are elevated and correlate with serum vascular endothelial growth factor levels in patients with pituitary adenomas. Pituitary; 2005;8(2):163-8
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  • [Title] Serum endostatin levels are elevated and correlate with serum vascular endothelial growth factor levels in patients with pituitary adenomas.
  • The purpose of our study was to evaluate serum concentrations of endostatin in patients harbouring various pituitary adenoma types and to examine the relationship of serum endostatin levels to circulating vascular endothelial growth factor (VEGF) levels.
  • Preoperative serum endostatin and VEGF concentrations were measured using competitive enzyme immunoassays in 71 patients with pituitary adenomas (20 somatotropinomas, 3 corticotropinomas, 6 prolactinomas and 42 clinically nonfunctioning pituitary adenomas - CNFPAs) and compared with levels from age-matched controls.
  • Serum endostatin concentrations were significantly higher in all pituitary adenoma types, except for prolactinomas (somatotropinomas: 124 +/- 16; p < 0.02, corticotropinomas: 157 +/- 42; p < 0.02, prolactinomas: 141 +/- 37; p > 0.05, CNFPAs: 169 +/- 11 ng/ml; p < 0.000005 vs 73 +/- 10 ng/ml in controls).
  • There was a significant positive correlation between endostatin and VEGF serum levels in patients with pituitary adenomas (r = +0.322; p = 0.006).
  • The simultaneous elevation of endostatin and VEGF may attenuate the pro-angiogenic action of VEGF and be responsible for rather weak neovascularization of pituitary adenomas.
  • Prospective studies are required to assess the usefulness of circulating endostatin and VEGF as markers of progression or recurrence of pituitary tumors.
  • [MeSH-major] Adenoma / blood. Endostatins / blood. Pituitary Neoplasms / blood. Vascular Endothelial Growth Factor A / blood

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  • (PMID = 16379029.001).
  • [ISSN] 1386-341X
  • [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 / Endostatins; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A
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21. Walsh MT, Couldwell WT: Symptomatic cystic degeneration of a clinically silent corticotroph tumor of the pituitary gland. Skull Base; 2010 Sep;20(5):367-70
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  • [Title] Symptomatic cystic degeneration of a clinically silent corticotroph tumor of the pituitary gland.
  • Clinically silent corticotroph tumors of the pituitary gland are those tumors that stain for adrenocorticotropic hormone (ACTH) but do not manifest with clinical or laboratory features of Cushing disease.
  • These tumors have been described as exhibiting more aggressive behavior than other nonfunctional pituitary tumors.
  • We present an unusual case of a clinically silent corticotropic adenoma of the pituitary gland that underwent cystic degeneration following recurrence after transsphenoidal surgery and radiation therapy.
  • Patients with clinically silent ACTH-secreting tumors should be monitored for aggressive tumor behavior and may require closer follow-up than those patients harboring other nonfunctional tumors.

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  • [Cites] Nucleic Acids Res. 1983 Oct 25;11(20):7191-203 [6634412.001]
  • (PMID = 21359002.001).
  • [ISSN] 1532-0065
  • [Journal-full-title] Skull base : official journal of North American Skull Base Society ... [et al.]
  • [ISO-abbreviation] Skull Base
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC3023327
  • [Keywords] NOTNLM ; Cortisol / Cushing disease / adrenocorticotropic hormone / corticotroph cells / cystic degeneration / nonfunctional pituitary adenoma
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22. Rosales C, Fierrard H, Bertagna X, Raffin-Sanson ML: [Management of hypercortisolism]. Rev Med Interne; 2008 Apr;29(4):337-46
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  • PURPOSE: Cushing's syndrome is a rare but frequently considered disease.
  • Its diagnosis can lead to some difficulties, including confirming the effective endogenous hypercortisolism and determining its cause.
  • The severity of this disease, the diversity of its complications and the multiple therapeutic options make its management challenging.
  • The aim of this review is to present the most recent data about management of Cushing's syndrome, especially diagnostic approaches and therapeutic options.
  • MAIN POINTS: We retained the following points: midnight salivary cortisol is a useful tool in the diagnosis of Cushing's syndrome; the desmopressin test can help to distinguish between Cushing's syndrome and "pseudoCushing's" due to alcohol consumption or psychiatric disorders; cavernous sinus and inferior petrosal sinus sampling is indicated in the evaluation of ACTH-dependent Cushing's syndromes when pituitary imaging is normal or equivocal or when dynamic tests are contradictory; multislice computed-tomography of the chest and the abdomen and somatostatin analogue scintigraphy, eventually combined, are the best imaging procedures in occult ectopic ACTH syndromes; patients with Cushing's disease should be referred to a neurosurgeon experienced in corticotroph adenomas surgery; metabolic consequences of Cushing's syndrome, such as cardiovascular risk factors and osteoporosis need an aggressive treatment.
  • PERSPECTIVES: The incidence of Cushing's syndrome is only 1/100000 per year.
  • Endocrinological management of the disease improves metabolic disorders in these patients.
  • If these results are confirmed, screening for Cushing's syndrome should be systematically performed in these populations.

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  • (PMID = 18226430.001).
  • [ISSN] 0248-8663
  • [Journal-full-title] La Revue de medecine interne
  • [ISO-abbreviation] Rev Med Interne
  • [Language] FRE
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Enzyme Inhibitors; 78E4J5IB5J / Mitotane; R9400W927I / Ketoconazole
  • [Number-of-references] 42
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23. Hashiba T, Saitoh Y, Asanuma N, Kouhara H, Maruo T, Fujinaka T, Kasayama S, Yoshimine T: Reduction of a pancreatic tumor after total removal of an ACTH secreting pituitary tumor: differential diagnosis of Cushing's syndrome. Endocr J; 2006 Apr;53(2):203-8
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  • [Title] Reduction of a pancreatic tumor after total removal of an ACTH secreting pituitary tumor: differential diagnosis of Cushing's syndrome.
  • Endocrinologic tests sometimes fail to distinguish adrenocorticotropic hormone (ACTH)-secreting pituitary adenoma from ectopic ACTH-secreting tumor.
  • The authors experienced a case of Cushing's disease associated with a pancreatic tumor.
  • Venous sampling contributed to the final diagnosis of Cushing's disease in this complex case, while endocrinologic tests showed paradoxical results.
  • A 54-year-old woman presented with Cushing's syndrome and pancreatic tumor.
  • Magnetic resonance imaging (MRI) failed to reveal a pituitary tumor, but a gadolinium-enhanced tumor with cystic components was seen in the pancreatic tail.
  • Results of conventional endocrinologic tests suggested ectopic ACTH syndrome, but venous sampling including cavernous sinus sampling indicated an ACTH-secreting pituitary adenoma.
  • Transsphenoidal surgery revealed a pituitary microadenoma, and total removal of the tumor was achieved.
  • Postoperative abdominal MRI revealed that the pancreatic tumor diminished gradually without treatment.
  • Selective cavernous sinus sampling was useful for distinguishing ACTH-secreting pituitary adenoma from ectopic ACTH syndrome in this complex case.
  • This was a rare case in which the pancreatic tumor diminished after total removal of the ACTH-secreting pituitary adenoma.
  • [MeSH-major] Adrenocorticotropic Hormone / secretion. Cushing Syndrome / diagnosis. Pancreatic Neoplasms / complications. Pituitary Neoplasms / secretion
  • [MeSH-minor] ACTH Syndrome, Ectopic / diagnosis. Adenoma / secretion. Adenoma / surgery. Diagnosis, Differential. Female. Follow-Up Studies. Humans. Magnetic Resonance Imaging. Middle Aged. Pituitary ACTH Hypersecretion / diagnosis. Positron-Emission Tomography


24. Hofland LJ, van der Hoek J, Feelders R, van Aken MO, van Koetsveld PM, Waaijers M, Sprij-Mooij D, Bruns C, Weckbecker G, de Herder WW, Beckers A, Lamberts SW: The multi-ligand somatostatin analogue SOM230 inhibits ACTH secretion by cultured human corticotroph adenomas via somatostatin receptor type 5. Eur J Endocrinol; 2005 Apr;152(4):645-54
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  • [Title] The multi-ligand somatostatin analogue SOM230 inhibits ACTH secretion by cultured human corticotroph adenomas via somatostatin receptor type 5.
  • OBJECTIVE: Currently, there is no effective medical treatment for patients with pituitary-dependent Cushing's disease.
  • We compared the in vitro effects of the sst(2)-preferring SS analogue octreotide (OCT) and the multi-ligand SOM230 on ACTH release by human and mouse corticotroph tumour cells.
  • METHODS: By quantitative RT-PCR the sst subtype expression level was determined in human corticotroph adenomas.
  • In vitro, the inhibitory effect of OCT and SOM230 on ACTH release by dispersed human corticotroph adenoma cells and mouse AtT20 corticotroph adenoma cells was determined.
  • RESULTS: Corticotroph adenomas expressed predominantly sst(5) mRNA (six out of six adenomas), whereas sst(2) mRNA expression was detected at significantly lower levels.
  • In a 72 h incubation with 10 nmol/l SOM230, ACTH release was inhibited in three out of five cultures (range -30 to -40%).
  • Ten nmol/l OCT slightly inhibited ACTH release in only one of five cultures (- 28%).
  • In AtT20 cells, expressing sst(2), sst(3) and sst(5), SOM230 inhibited ACTH secretion with high potency (IC(50) 0.2 nmol/l).
  • Dexamethasone (10 nmol/l) pre-treatment did not influence the sensitivity of the cells to the inhibitory effect of SOM230, suggesting that sst(5) is relatively resistant to negative control by glucocorticoids.
  • CONCLUSIONS: The selective expression of sst(5) receptors in corticotroph adenomas and the preferential inhibition of ACTH release by human corticotroph adenoma cells by SOM230 in vitro, suggest that SOM230 may have potential in the treatment of patients with pituitary-dependent Cushing's disease.


25. Castillo V, Giacomini D, Páez-Pereda M, Stalla J, Labeur M, Theodoropoulou M, Holsboer F, Grossman AB, Stalla GK, Arzt E: Retinoic acid as a novel medical therapy for Cushing's disease in dogs. Endocrinology; 2006 Sep;147(9):4438-44
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  • [Title] Retinoic acid as a novel medical therapy for Cushing's disease in dogs.
  • Cushing's disease is almost always caused by an ACTH-secreting pituitary tumor, but effective medical therapy is currently limited.
  • Because retinoic acid has been shown to be potentially useful in decreasing corticotroph secretion and proliferation in rodent models, we have studied its action in dogs with Cushing's disease.
  • A randomized treatment with retinoic acid (n = 22) vs. ketoconazole (n = 20) in dogs with Cushing's disease was assigned for a period of 180 d.
  • Clinical signs, plasma ACTH and alpha-MSH, the cortisol/creatinine urine ratio, and pituitary magnetic resonance imaging were assessed and compared at different time points.
  • We recorded a significant reduction in plasma ACTH and alpha-MSH, and also in the cortisol/creatinine urine ratio, of the dogs treated with retinoic acid.
  • Pituitary adenoma size was also significantly reduced at the end of retinoic acid treatment.
  • No adverse events or signs of hepatotoxicity were observed, suggesting that the drug is not only effective but also safe.
  • Retinoic acid treatment controls ACTH and cortisol hyperactivity and tumor size in dogs with ACTH-secreting tumors, leading to resolution of the clinical phenotype.
  • This study highlights the possibility of using retinoic acid as a novel therapy in the treatment of ACTH-secreting tumors in humans with Cushing's disease.
  • [MeSH-major] Dog Diseases / drug therapy. Pituitary ACTH Hypersecretion / veterinary. Tretinoin / therapeutic use
  • [MeSH-minor] Adenoma / pathology. Adrenocorticotropic Hormone / blood. Animals. Body Weight. Creatinine / urine. Dogs. Female. Hydrocortisone / urine. Ketoconazole / therapeutic use. Magnetic Resonance Imaging / veterinary. Male. Pituitary Gland / pathology. Pituitary Neoplasms / pathology. Survival Rate. alpha-MSH / blood

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  • (PMID = 16740975.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 5688UTC01R / Tretinoin; 581-05-5 / alpha-MSH; 9002-60-2 / Adrenocorticotropic Hormone; AYI8EX34EU / Creatinine; R9400W927I / Ketoconazole; WI4X0X7BPJ / Hydrocortisone
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26. Cavagnini F, Scacchi M, Pecori Giraldi F: Hypopituitarism in Cushing's disease. J Endocrinol Invest; 2008 Sep;31(9 Suppl):44-7
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  • [Title] Hypopituitarism in Cushing's disease.
  • Impaired GH secretion usually accompanies Cushing's syndrome and a variable proportion of patients reportedly fail to recover normal GH secretion after successful treatment.
  • We prospectively studied 34 patients (27 females and 7 males, age range 21- 68 yr) formerly affected by Cushing's disease.
  • All patients had undergone transsphenoidal surgery with the removal of an ACTH-secreting adenoma.
  • Our experience has demonstrated a GHD in a high percentage of patients with Cushing's disease even after long-term remission of hypercortisolism obtained by surgery alone.
  • This finding is significant as it highlights that even the most favorable therapeutical course, i.e. remission achieved by surgery, is often accompanied by impaired GH release.
  • Assessment of GH secretion is therefore recommended in all patients cured from Cushing's disease, even if not submitted to radiotherapy.
  • [MeSH-major] Hypopituitarism / complications. Pituitary ACTH Hypersecretion / complications
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / complications. ACTH-Secreting Pituitary Adenoma / surgery. Adenoma / complications. Adenoma / surgery. Adult. Aged. Female. Follow-Up Studies. Growth Disorders / epidemiology. Growth Disorders / etiology. Human Growth Hormone / blood. Human Growth Hormone / secretion. Humans. Male. Middle Aged. Prevalence. Young Adult

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  • (PMID = 19020385.001).
  • [ISSN] 0391-4097
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 12629-01-5 / Human Growth Hormone
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27. Rudnik A, Zawadzki T, Gałuszka-Ignasiak B, Bazowski P, Duda I, Wojtacha M, Rudnik AI, Krawczyk I: Endoscopic transsphenoidal treatment in recurrent and residual pituitary adenomas--first experience. Minim Invasive Neurosurg; 2006 Feb;49(1):10-4
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  • [Title] Endoscopic transsphenoidal treatment in recurrent and residual pituitary adenomas--first experience.
  • AIM OF THE STUDY: The aim of the study has been the assessment of the endoscopic method in the surgical management of recurrent and residual pituitary adenomas, as concerns treatment efficiency, substantial complications, and its possible advantages for the operating surgeon and patient.
  • MATERIAL AND METHODS: In Department of Neurosurgery, Silesian University School of Medicine in Katowice, between October 2001 and June 2004, 125 patients underwent endoscopic surgery due to pituitary adenoma.
  • The analysis comprised 20 patients, who were operated on due to recurrent adenomas or residual tumour not completely removed during the first surgical procedure.
  • The analysed group had 14 non-functioning adenomas, 4 GH-secreting adenomas, 1 PRL-secreting adenoma and 1 ACTH-secreting adenoma.
  • 11 of the 20 adenomas infiltrated the cavernous sinuses.
  • In the group of 11 patients with adenomas not infiltrating the cavernous sinuses, recovery was reported for 8 of them, that is 73%.
  • CONCLUSIONS: The endoscopic method is a safe, hardly invasive and efficient surgical technique in the treatment of recurrent and residual pituitary adenomas.
  • [MeSH-major] Adenoma / surgery. Neoplasm Recurrence, Local / surgery. Neuroendoscopy. Pituitary Neoplasms / surgery. Sphenoid Sinus / surgery
  • [MeSH-minor] Adult. Aged. Female. Follow-Up Studies. Humans. Male. Middle Aged. Neoplasm, Residual. Reoperation. Treatment Outcome

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  • (PMID = 16547875.001).
  • [ISSN] 0946-7211
  • [Journal-full-title] Minimally invasive neurosurgery : MIN
  • [ISO-abbreviation] Minim Invasive Neurosurg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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28. Andrioli M, Pecori Giraldi F, Losa M, Terreni M, Invitti C, Cavagnini F: Cushing's disease due to double pituitary ACTH-secreting adenomas: the first case report. Endocr J; 2010;57(9):833-7
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  • [Title] Cushing's disease due to double pituitary ACTH-secreting adenomas: the first case report.
  • Double pituitary adenomas are rare occurrences in autoptical, surgical and neuroradiological series and are mostly due to non-functioning pituitary adenomas, GH-secreting and prolactin-secreting adenomas.
  • ACTH secreting tumours are more rare and, to our knowledge, two distinct ACTH-producing adenomas within the same pituitary have never been reported.
  • We herewith describe a 56 year old woman with Cushing' s disease due to two clearly distinct ACTH-secreting pituitary adenomas.
  • She presented with signs and symptoms of hypercortisolism and hormonal testing was indicative for pituitary-dependent Cushing' s syndrome.
  • Sellar MRI visualized an asymmetric pituitary gland with suspect lesions in both the right and the left pituitary lobes.
  • Pathology confirmed the existence of two distinct adenomas located in different sites in the gland.
  • Both presented ACTH immunoreactivity but displayed distinct morphological features.
  • Our case indicates that double ACTH-secreting pituitary adenomas may occur in patients with Cushing' s disease.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / pathology. Adenoma / pathology. Neoplasms, Multiple Primary / pathology. Pituitary ACTH Hypersecretion / etiology
  • [MeSH-minor] Cushing Syndrome / etiology. Female. Humans. Middle Aged. Pituitary Neoplasms / pathology

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  • (PMID = 20595779.001).
  • [ISSN] 1348-4540
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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29. Minniti G, Traish D, Ashley S, Gonsalves A, Brada M: Fractionated stereotactic conformal radiotherapy for secreting and nonsecreting pituitary adenomas. Clin Endocrinol (Oxf); 2006 May;64(5):542-8
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  • [Title] Fractionated stereotactic conformal radiotherapy for secreting and nonsecreting pituitary adenomas.
  • OBJECTIVE: To assess the medium-term outcome in a cohort of patients with residual or recurrent pituitary adenoma treated with fractionated stereotactic conformal radiotherapy (SCRT).
  • PATIENTS AND METHODS: Ninety-two patients (median age 50 years) with a residual or recurrent nonfunctioning (67) or a secreting (25) pituitary adenoma were treated between 1995 and 2003.
  • Eighteen patients had a GH-secreting, five PRL-secreting and two an ACTH-secreting pituitary adenoma.
  • In secreting adenomas, hormone levels declined progressively, becoming normal in more than a third of patients with GH-secreting and PRL-secreting pituitary tumours.
  • Hypopituitarism was the most common long-term effect; 22% of patients had worsening of pituitary function.
  • CONCLUSION: SCRT as a high-precision technique of localized irradiation achieves tumour and hormone control of pituitary adenomas comparable with previously published data on the efficacy of conventional radiotherapy.
  • Despite the potential advantage of reducing the volume of normal brain irradiated, the theoretical benefit over conventional radiotherapy in terms of the reduction in long-term morbidity has not yet been demonstrated and requires longer follow-up.
  • Potential effect on long-term cognitive function has not been tested.
  • [MeSH-major] Adenoma / radiotherapy. Pituitary Neoplasms / radiotherapy. Radiotherapy, Conformal / methods
  • [MeSH-minor] Adrenocorticotropic Hormone / secretion. Adult. Aged. Cohort Studies. Female. Growth Hormone / secretion. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Neoplasm Recurrence, Local / pathology. Neoplasm Recurrence, Local / radiotherapy. Neoplasm, Residual / pathology. Neoplasm, Residual / radiotherapy. Prolactinoma / radiotherapy. Prolactinoma / secretion. Radiotherapy Dosage. Statistics, Nonparametric. Treatment Outcome

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  • (PMID = 16649974.001).
  • [ISSN] 0300-0664
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone; 9002-72-6 / Growth Hormone
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30. Raverot G, Wierinckx A, Jouanneau E, Auger C, Borson-Chazot F, Lachuer J, Pugeat M, Trouillas J: Clinical, hormonal and molecular characterization of pituitary ACTH adenomas without (silent corticotroph adenomas) and with Cushing's disease. Eur J Endocrinol; 2010 Jul;163(1):35-43
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  • [Title] Clinical, hormonal and molecular characterization of pituitary ACTH adenomas without (silent corticotroph adenomas) and with Cushing's disease.
  • OBJECTIVE: Silent corticotroph adenomas (SCAs) are rare pituitary tumours immunoreactive for ACTH, but without clinical evidence of Cushing's disease.
  • We characterized SCAs based on clinical, hormonal and molecular data, and compared the characteristics of these tumours with those of macro (MCA)- and micro (mCA)-ACTH adenomas with Cushing's disease.
  • METHODS: Fifty ACTH adenomas (14 SCAs, 15 MCAs and 21 mCAs) with complete corresponding clinical, radiological and biochemical data were selected.
  • Histological corticotroph differentiation; immunostaining for ACTH, beta-endorphin and beta-LPH; and mRNA expression levels of TPIT, POMC, GRalpha, prohormone convertase 1/3 (PC1/3) and galectin-3 were compared in 21 representative tumours.
  • RESULTS: Despite the absence of clinical hypercortisolism in patients with SCA, elevated plasma ACTH levels that were similar to those associated with mCA were observed.
  • The cortisol/ACTH ratio was similar between SCA and MCA groups and lower than that found with mCA (P<0.05).
  • After an i.v. dexamethasone suppression test, ACTH levels were significantly higher in patients with MCA than in those with mCA (P<0.05).
  • Cytological and immunocytochemical analyses as well as mRNA expression levels of TPIT, POMC and GRalpha confirmed corticotroph differentiation in both mCAs and MCAs and in half of the SCAs, with a strong correlation between TPIT and POMC mRNA expression levels in SCAs (R(2)=0.72; P<0.01) and in MCAs (R(2)=0.65; P<0.05).
  • CONCLUSIONS: Despite the absence of hypercortisolism, SCAs exhibit histological, biochemical and molecular corticotroph differentiation.

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  • (PMID = 20385723.001).
  • [ISSN] 1479-683X
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Galectin 3; 0 / Homeodomain Proteins; 0 / Receptors, Glucocorticoid; 0 / T-Box Domain Proteins; 0 / TBX19 protein, human; 0 / glucocorticoid receptor alpha; 66796-54-1 / Pro-Opiomelanocortin; 9002-60-2 / Adrenocorticotropic Hormone; EC 3.4.21.93 / Proprotein Convertase 1; WI4X0X7BPJ / Hydrocortisone
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31. Niveiro M, Aranda FI, Peiró G, Alenda C, Picó A: Immunohistochemical analysis of tumor angiogenic factors in human pituitary adenomas. Hum Pathol; 2005 Oct;36(10):1090-5
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  • [Title] Immunohistochemical analysis of tumor angiogenic factors in human pituitary adenomas.
  • Microvessel density (MVD) has been studied in a number of neoplasias, and apparently, there is a relationship between angiogenesis and tumor progression, response to treatment, and outcome.
  • In pituitary adenoma, the association between MVD and vascular endothelial growth factor (VEGF) with tumor behavior has been described, but correlation with other angiogenic factors such as fetal liver kinase 1 (Flk-1) or proliferative markers is unknown.
  • We investigated MVD, VEGF, and its receptor Flk-1 expression in 60 human pituitary adenomas: 13 growth hormone cell adenomas, 7 prolactin cell adenomas, 5 corticotroph cell adenomas, 2 thyrotroph cell adenomas, and 33 nonfunctioning adenomas (30 gonadotroph cell adenomas and 3 null cell adenomas).
  • Adenomas with higher MVD were thyrotroph cell adenomas (299.9 +/- 87.5), and those with lower MVD were prolactin cell adenomas (168.6 +/- 63.3; P = .45, analysis of variance).
  • We found a trend toward higher MVD in the adenomas of older patients (P = .142), but no difference was found regarding sex, extrasellar extension, or Ki-67 (P > .05).
  • Low expression of VEGF was seen predominantly in prolactin cell adenomas, and high in nonfunctioning adenomas, or in cases of older patients (P < or = .032).
  • High expression was observed in nonfunctioning adenomas, cases presenting at older ages, and with extrasellar extension (P < or = .022).
  • Our study shows that VEGF and Flk-1 are widely expressed in pituitary adenomas, predominantly in nonfunctioning adenomas and those presenting at older ages.
  • [MeSH-major] Adenoma / metabolism. Immunohistochemistry / methods. Pituitary Neoplasms / metabolism. Vascular Endothelial Growth Factor A / analysis. Vascular Endothelial Growth Factor Receptor-2 / analysis

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  • (PMID = 16226108.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD34; 0 / Ki-67 Antigen; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
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32. Bucciarelli LG, Pecori Giraldi F, Cavagnini F: No mutations in TPIT, a corticotroph-specific gene, in human tumoral pituitary ACTH-secreting cells. J Endocrinol Invest; 2005 Dec;28(11):1015-8
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  • [Title] No mutations in TPIT, a corticotroph-specific gene, in human tumoral pituitary ACTH-secreting cells.
  • BACKGROUND: TPIT is a recently identified transcription factor specific to proopiomelanocortin (POMC)-expressing cells within the pituitary and plays a pivotal role in the embryonal development of POMC lineage.
  • As with other transcription factors, TPIT could theoretically also be involved in corticotroph adenomatous transformation and ACTH hypersecretion and published data indicate that TPIT is present in normal and adenomatous human corticotrophs.
  • OBJECTIVE: The aim of the present study was to corroborate this finding and to seek evidence for mutations in the TPIT coding sequence in human tumoral corticotrophs.
  • DESIGN AND METHODS: Eight human ACTH-secreting pituitary adenomas were collected during surgery, mRNA extracted from primary cultures and reverse transcribed.
  • RESULTS: TPIT mRNA was detected in all 8 ACTH-secreting pituitary adenomas without apparent mRNA variants.
  • Lastly, sequencing did not reveal differences in the nucleotide arrangement compared with the published sequence.
  • CONCLUSIONS: Aberrant TPIT is unlikely to play a role in corticotroph tumoral trasformation, ie, Cushing's disease, as the entire coding sequence is expressed without any mutation by human pituitary ACTH-secreting adenomas.
  • Conversely, the significance of this transcription factor in tumoral ACTH hypersecretion remains to be clarified.
  • [MeSH-major] Adrenocorticotropic Hormone / secretion. Homeodomain Proteins / genetics. Mutation / genetics. Pituitary Neoplasms / genetics. Transcription Factors / genetics
  • [MeSH-minor] Humans. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism. Reverse Transcriptase Polymerase Chain Reaction. T-Box Domain Proteins. Tumor Cells, Cultured

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  • (PMID = 16483181.001).
  • [ISSN] 0391-4097
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
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33. Daems T, Verhelst J, Michotte A, Abrams P, De Ridder D, Abs R: Modification of hormonal secretion in clinically silent pituitary adenomas. Pituitary; 2009;12(1):80-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Modification of hormonal secretion in clinically silent pituitary adenomas.
  • BACKGROUND: Silent pituitary adenomas are a subtype of adenomas characterized by positive immunoreactivity for one or more hormones classically secreted by normal pituitary cells but without clinical expression, although in some occasions enhanced or changed secretory activity can develop over time.
  • Silent corticotroph adenomas are the classical example of this phenomenon.
  • PATIENTS AND METHODS: A series of about 500 pituitary adenomas seen over a period of 20 years were screened for modification in hormonal secretion.
  • RESULTS: Two cases were retrieved, one silent somatotroph adenoma and one thyrotroph adenoma, both without specific clinical features or biochemical abnormalities, which presented 20 years after initial surgery with evidence of acromegaly and hyperthyroidism, respectively.
  • While the acromegaly was controlled by a combination of somatostatin analogs and growth hormone (GH) receptor antagonist therapy, neurosurgery was necessary to manage the thyrotroph adenoma.
  • Apparently, the mechanisms responsible for the secretory modifications are different, being a change in secretory capacity in the silent somatotroph adenoma and a quantitative change in the silent thyrotroph adenoma.
  • CONCLUSIONS: These two cases, one somatotroph and one thyrotroph adenoma, are an illustration that clinically silent pituitary adenomas may in rare circumstances evolve over time and become active, as previously demonstrated in silent corticotroph adenomas.
  • [MeSH-major] Pituitary Neoplasms / metabolism

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  • (PMID = 18350381.001).
  • [ISSN] 1573-7403
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I; 9002-71-5 / Thyrotropin
  • [Number-of-references] 30
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34. Nolan LA, Schmid HA, Levy A: Octreotide and the novel multireceptor ligand somatostatin receptor agonist pasireotide (SOM230) block the adrenalectomy-induced increase in mitotic activity in male rat anterior pituitary. Endocrinology; 2007 Jun;148(6):2821-7
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  • [Title] Octreotide and the novel multireceptor ligand somatostatin receptor agonist pasireotide (SOM230) block the adrenalectomy-induced increase in mitotic activity in male rat anterior pituitary.
  • Acting principally through the latter, it inhibits basal and CRH-stimulated ACTH secretion from the AtT20 corticotroph cell line and ACTH release from a proportion of human corticotroph adenomas both in vitro and in vivo.
  • Data supporting an additional antiproliferative effect has led to pasireotide being explored as a potential therapy for patients with Cushing's disease.
  • We have compared the effects of pasireotide and octreotide on adrenalectomy-induced mitotic and apoptotic activity in the male rat anterior pituitary.
  • Pasireotide and octreotide had no effect on baseline pituitary cell turnover and no measurable effects on apoptosis.
  • However, the wave of increased mitotic activity normally seen in the pituitary after adrenalectomy was completely abolished.
  • Nevertheless, pasireotide and octreotide did not diminish the increase in ACTH-immunopositive cell index after adrenalectomy, indicating that cell division and differentiation of hormonally null cells in the pituitary are under independent control.
  • In conclusion, basal cell turnover in the pituitary is not inhibited by pasireotide or octreotide.
  • Bilateral adrenalectomy stimulates differentiation of preexisting null cells into ACTH-positive cells.
  • Cell division after bilateral adrenalectomy occurs in a specific subpopulation of hormonally null cells that are equally sensitive to the antiproliferative effects of pasireotide and octreotide, implicating SSTR2 receptors in this antimitotic response.
  • [MeSH-major] Adrenalectomy. Mitosis / drug effects. Octreotide / pharmacology. Pituitary Gland, Anterior / drug effects. Receptors, Somatostatin / agonists. Somatostatin / analogs & derivatives

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  • (PMID = 17347306.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Somatostatin; 0 / Sstr2 protein, rat; 51110-01-1 / Somatostatin; 9002-60-2 / Adrenocorticotropic Hormone; 98H1T17066 / pasireotide; RWM8CCW8GP / Octreotide
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35. Rotondo F, Scheithauer BW, Kovacs K, Bell DC: Rab3B immunoexpression in human pituitary adenomas. Appl Immunohistochem Mol Morphol; 2009 May;17(3):185-8
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  • [Title] Rab3B immunoexpression in human pituitary adenomas.
  • To shed light on its presence in the normal human pituitary and in adenomas, a detailed immunohistochemical study of 130 surgically removed human pituitary adenomas was undertaken, including 23 somatotroph, 32 lactotroph, 19 functional corticotroph, 10 silent subtype 1 and 8 silent subtype 2 corticotroph adenomas, 12 gonadotroph hormone producing, 10 thyrotroph, 7 silent subtype 3 adenomas, and 9 null cell adenomas, 5 of the latter being of oncocytic type.
  • Among the 32 prolactin lactotroph adenomas, 10 had been treated preoperatively with bromocriptine, a dopamine agonist.
  • Among the 23 somatotroph adenomas, 10 were pretreated with octreotide, a long acting somatostatin analog.
  • The results showed Rab3B immunopositivity to be strongest in corticotroph adenomas followed by thyrotroph, lactotroph, gonadotroph, null cell, and somatotroph adenomas.
  • No difference was noted between endocrinologically active and silent corticotroph adenomas.
  • Our results add new information to the view that Rab3B is involved in the regulation of pituitary hormone secretion.

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  • (PMID = 19384079.001).
  • [ISSN] 1533-4058
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 3A64E3G5ZO / Bromocriptine; EC 3.6.1.- / RAB3B protein, human; EC 3.6.5.2 / rab3 GTP-Binding Proteins; RWM8CCW8GP / Octreotide
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36. Candrina R, Sleiman I, Zorzi F: ACTH-secreting pituitary adenoma within an ovarian teratoma. Eur J Intern Med; 2005 Sep;16(5):359-60
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  • [Title] ACTH-secreting pituitary adenoma within an ovarian teratoma.
  • The differential diagnosis of Cushing's syndrome is one of the most difficult tasks in medicine, and it is especially problematic in cases with "occult" ectopic ACTH syndrome.
  • We describe the case of a 26-year-old woman who was found to suffer from ectopic ACTH syndrome due to pituitary microadenoma, localized within a mature ovarian teratoma.
  • Cushing's syndrome caused by ovarian neoplasia is unusual, but when it occurs, it is most often due to excessive cortisol production by the ovary.
  • Only rarely has ectopic ACTH syndrome in association with an ovarian tumor been described.

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  • (PMID = 16137552.001).
  • [ISSN] 0953-6205
  • [Journal-full-title] European journal of internal medicine
  • [ISO-abbreviation] Eur. J. Intern. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
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37. Amaral FC, Torres N, Saggioro F, Neder L, Machado HR, Silva WA Jr, Moreira AC, Castro M: MicroRNAs differentially expressed in ACTH-secreting pituitary tumors. J Clin Endocrinol Metab; 2009 Jan;94(1):320-3
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  • [Title] MicroRNAs differentially expressed in ACTH-secreting pituitary tumors.
  • OBJECTIVE: The aim of the study was to analyze the differential expression of let-7a, miR-15a, miR-16, miR-21, miR-141, miR-143, miR-145, and miR-150 in corticotropinomas and normal pituitary tissue and verify whether their profile of expression correlates with tumor size or remission after treatment.
  • MATERIAL AND METHODS: ACTH-secreting pituitary tumor samples were obtained during transphenoidal surgery from patients with Cushing disease and normal pituitary tissues from autopsies.
  • RESULTS: We found underexpression of miR-145 (2.0-fold; P = 0.04), miR-21 (2.4-fold; P = 0.004), miR-141 (2.6-fold; P = 0.02), let-7a (3.3-fold; P = 0.003), miR-150 (3.8-fold; P = 0.04), miR-15a (4.5-fold; P = 0.03), miR-16 (5.0-fold; P = 0.004), and miR-143 (6.4-fold; P = 0.004) in ACTH-secreting pituitary tumors when compared to normal pituitary tissues.
  • There were no differences between miRNA expression and tumor size as well as miRNA expression and ratio of remission after surgery, except in patients presenting lower miR-141 expression who showed a better chance of remission.
  • However, the lack of knowledge about miRNA target genes postpones full understanding of the biological functions of down-regulated or up-regulated miRNAs in corticotropinomas.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / genetics. Adenoma / genetics. MicroRNAs / analysis
  • [MeSH-minor] Adolescent. Adult. Female. Humans. Male. Middle Aged. Pituitary ACTH Hypersecretion / genetics. Young Adult

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  • (PMID = 18840638.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MicroRNAs
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38. Labeur M, Paez-Pereda M, Arzt E, Stalla GK: Potential of retinoic acid derivatives for the treatment of corticotroph pituitary adenomas. Rev Endocr Metab Disord; 2009 Jun;10(2):103-9
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  • [Title] Potential of retinoic acid derivatives for the treatment of corticotroph pituitary adenomas.
  • Cushing's disease is a severe clinical condition caused by hypersecretion of corticosteroids due to excessive ACTH secretion from a pituitary adenoma.
  • This complex endocrine disorder still represents a major challenge for the physician in terms of efficient treatment.
  • In the last years there was only little progress in elucidating the molecular mechanisms responsible for the constitutive and autonomous ACTH secretion of pituitary corticotrophinomas.
  • As a consequence, no effective drug therapy is currently available, particularly if surgical excision is not successful.
  • In the present article we examine recent studies that have investigated the therapeutic potential of retinoic acid receptors as nuclear receptor targets for the treatment of Cushing's disease.
  • Retinoic acid is an efficient drug used for the treatment of different types of cancers and it proved to act in animal models of Cushing's disease.
  • The efficiency of this treatment in patients with this disorder still needs to be tested in clinical trials.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / drug therapy. Antineoplastic Agents / therapeutic use. Pituitary Neoplasms / drug therapy. Tretinoin / therapeutic use
  • [MeSH-minor] Animals. Humans. Pituitary ACTH Hypersecretion / drug therapy. Pituitary ACTH Hypersecretion / metabolism

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  • (PMID = 18604646.001).
  • [ISSN] 1573-2606
  • [Journal-full-title] Reviews in endocrine & metabolic disorders
  • [ISO-abbreviation] Rev Endocr Metab Disord
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 5688UTC01R / Tretinoin
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39. van der Klaauw AA, Kienitz T, Strasburger CJ, Smit JW, Romijn JA: Malignant pituitary corticotroph adenomas: report of two cases and a comprehensive review of the literature. Pituitary; 2009;12(1):57-69
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  • [Title] Malignant pituitary corticotroph adenomas: report of two cases and a comprehensive review of the literature.
  • Corticotroph pituitary carcinomas are tumors, defined by the presence of distant metastases that determine their poor prognosis.
  • The diagnosis and therapy of malignant corticotroph adenomas remains a clinical challenge.
  • The molecular mechanisms of malignant transformation of pituitary adenomas are unclear, although they are believed to arise in an adenoma-to-carcinoma sequence.
  • We describe two cases of malignant Cushing's disease with metastases in liver and bone, respectively.
  • The primary pituitary tumors were treated by a combination of radiotherapy and transsphenoidal surgery, but recurred several times in both patients.
  • The time interval between the diagnosis of Cushing's disease and the discovery of metastases was 32 and 17 years, respectively.
  • In the first case the patient died within 6 months after diagnosis of metastasis, whereas the second patient is alive at a follow-up of 2 years after the discovery of the metastasis.
  • Furthermore, we reviewed all available cases of corticotroph pituitary carcinomas reported in the literature and analyzed their clinical features and therapeutical management.
  • In conclusion, frequent relapses of Cushing's disease, aggressive growth of macroadenoma, Nelson's syndrome after adrenalectomy or persistently high ACTH levels should prompt the clinician to consider the possibility of pituitary corticotroph carcinomas.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / diagnosis. ACTH-Secreting Pituitary Adenoma / pathology. Pituitary ACTH Hypersecretion / complications

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  • (PMID = 18176844.001).
  • [ISSN] 1573-7403
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 62
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40. Labeur M, Refojo D, Wölfel B, Stalla J, Vargas V, Theodoropoulou M, Buchfelder M, Paez-Pereda M, Arzt E, Stalla GK: Interferon-gamma inhibits cellular proliferation and ACTH production in corticotroph tumor cells through a novel janus kinases-signal transducer and activator of transcription 1/nuclear factor-kappa B inhibitory signaling pathway. J Endocrinol; 2008 Nov;199(2):177-89
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  • [Title] Interferon-gamma inhibits cellular proliferation and ACTH production in corticotroph tumor cells through a novel janus kinases-signal transducer and activator of transcription 1/nuclear factor-kappa B inhibitory signaling pathway.
  • Moreover, IFNG modulates normal pituitary hormone secretion, and was shown to inhibit the expression of the ACTH precursor POMC in murine ACTH-secreting AtT-2010/21/2008 tumor cells.
  • We have studied the functional role of IFNG on pituitary tumor cells, focusing on the involvement of IFNG in the molecular events leading to the control of POMC transcriptional repression.
  • Herein, it is shown that IFNG inhibits AtT-20 tumor cell proliferation without inducing apoptosis.
  • In addition, 1 and 2 IFNG receptor immunoreactivity was detected in human corticotropinoma cells.
  • Interestingly, IFNG inhibits ACTH production from these cells in primary cell culture, without affecting basal ACTH biosynthesis in normal non-tumoral pituitary cells.
  • [MeSH-major] Adrenocorticotropic Hormone / biosynthesis. Cell Proliferation / drug effects. Interferon-gamma / pharmacology. Janus Kinases / metabolism. NF-kappa B / metabolism. Pituitary Neoplasms / metabolism. STAT1 Transcription Factor / metabolism

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  • (PMID = 18715881.001).
  • [ISSN] 1479-6805
  • [Journal-full-title] The Journal of endocrinology
  • [ISO-abbreviation] J. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / NF-kappa B; 0 / STAT1 Transcription Factor; 66796-54-1 / Pro-Opiomelanocortin; 82115-62-6 / Interferon-gamma; 9002-60-2 / Adrenocorticotropic Hormone; EC 2.7.10.2 / Janus Kinases
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41. Johnson MD, Fan X, Bourne P, Walters D: Neuronal differentiation and expression of neural epitopes in pituitary adenomas. J Histochem Cytochem; 2007 Dec;55(12):1265-71
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  • [Title] Neuronal differentiation and expression of neural epitopes in pituitary adenomas.
  • Neural transdifferentiation is increasingly recognized in neural crest and neural stem cell tumors.
  • Neuronal differentiation has been anecdotally described primarily in somatotroph cell adenomas associated with acromegaly, but its prevalence in adenomas and relationship to adenoma type has not been completely established.
  • In this study we performed a retrospective morphological and immunohistochemical analysis of neurofilament, phosphoneurofilament, Neu-N, class III tubulin, and Hu in WHO grade I pituitary adenomas.
  • Limited numbers of cells with neuronal features and neuron-associated epitopes may be more common in pituitary adenomas than previously recognized.
  • These may occur in many forms of adenomas including somatotroph, lactotroph, mixed somatotroph and lactotroph, null cell/gonadotroph cell and, rarely, corticotroph cell adenomas.
  • [MeSH-major] Adenoma / metabolism. Biomarkers, Tumor / biosynthesis. Epitopes. Neurons / metabolism. Pituitary Neoplasms / metabolism
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / metabolism. ACTH-Secreting Pituitary Adenoma / pathology. Adult. Aged. Aged, 80 and over. Antibodies. Cell Differentiation. Female. Gonadotrophs / metabolism. Gonadotrophs / pathology. Human Growth Hormone / metabolism. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Staging. Prolactin / metabolism. Prolactinoma / metabolism. Prolactinoma / pathology. Retrospective Studies

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  • (PMID = 17875653.001).
  • [ISSN] 0022-1554
  • [Journal-full-title] The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society
  • [ISO-abbreviation] J. Histochem. Cytochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Biomarkers, Tumor; 0 / Epitopes; 12629-01-5 / Human Growth Hormone; 9002-62-4 / Prolactin
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42. Roelfsema F, Pereira AM, Keenan DM, Veldhuis JD, Romijn JA: Thyrotropin secretion by thyrotropinomas is characterized by increased pulse frequency, delayed diurnal rhythm, enhanced basal secretion, spikiness, and disorderliness. J Clin Endocrinol Metab; 2008 Oct;93(10):4052-7
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  • CONTEXT: Hormone secretion by somatotropinomas, corticotropinomas, and prolactinomas exhibits increased pulsatility and basal secretion, accompanied by greater disorderliness.
  • CONCLUSION: TSH secretion by thyrotropinomas shares many characteristics with other pituitary hormone-secreting adenomas.
  • [MeSH-major] Adenoma / physiopathology. Adenoma / secretion. Circadian Rhythm / physiology. Pituitary Neoplasms / physiopathology. Pituitary Neoplasms / secretion. Pulsatile Flow / physiology. Thyrotropin / secretion

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  • (PMID = 18682501.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 9002-71-5 / Thyrotropin
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43. Jankowska A, Wasko R, Waligorska-Stachura J, Andrusiewicz M, Jaskula M, Liebert W, Sowinski J: Survivin products in pituitary tumors. Neuro Endocrinol Lett; 2008 Dec;29(6):1033-7
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  • [Title] Survivin products in pituitary tumors.
  • Still very little is known about survivin expression in pituitary tumors.
  • In spite of the fact that pituitary tumors in histological examination are usually benign, in the clinical process a certain number of pituitary adenomas is capable of aggressive growth, recurrence and invasion of the surrounding structures.
  • The aim of the present study was to assess the presence of survivin transcripts and protein in different types of pituitary tumors and to evaluate survivin expression levels in invasive and non-invasive pituitary tumors.
  • DESIGN AND METHODS: The analyzed material consisted of tumor tissue samples obtained during standard neurosurgical removal of the tumor from 23 patients in whom acromegaly (n=14), non-functioning pituitary tumor (n=6), prolactinoma (n=2) and corticotropinoma (n=1) were diagnosed.
  • As a control of the study normal pituitary tissue obtained at autopsy was used.
  • RESULTS: Our study demonstrated the presence of survivin mRNA in all 23 analyzed pituitary tumors.
  • Survivin expression was also observed in normal pituitary, but the level of its expression was 6-fold lower than in tumors tissue when studied by real time RT-PCR.
  • The difference between the levels of survivin expression in invasive and non-invasive tumors was not statistically significant.
  • Immunohistochemical analyses revealed the presence of the protein in both normal and tumor tissue of pituitary.
  • Immunostaining of tumor tissue was not uniform.
  • The presence of the protein in normal pituitary was restricted to small population of cells.
  • CONCLUSIONS: The present study showed that overexpression of survivin is characteristic for pituitary tumors.
  • Further analysis of this protein expression profile should demonstrate whether survivin might be use as a prognostic marker in diagnosis and therapy of pituitary adenomas.
  • [MeSH-major] Adenoma / metabolism. Apoptosis Regulatory Proteins / metabolism. Microtubule-Associated Proteins / metabolism. Neoplasm Proteins / metabolism. Pituitary Gland / metabolism. Pituitary Neoplasms / metabolism
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / metabolism. Adult. Female. Growth Hormone-Secreting Pituitary Adenoma / metabolism. Humans. Inhibitor of Apoptosis Proteins. Male. Middle Aged. Prolactinoma / metabolism. RNA, Messenger / analysis

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  • (PMID = 19112393.001).
  • [ISSN] 0172-780X
  • [Journal-full-title] Neuro endocrinology letters
  • [ISO-abbreviation] Neuro Endocrinol. Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Sweden
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / RNA, Messenger
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44. Tauchmanovà L, Pivonello R, De Martino MC, Rusciano A, De Leo M, Ruosi C, Mainolfi C, Lombardi G, Salvatore M, Colao A: Effects of sex steroids on bone in women with subclinical or overt endogenous hypercortisolism. Eur J Endocrinol; 2007 Sep;157(3):359-66
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  • PATIENTS: Seventy-one consecutive women were enrolled: 36 with overt hypercortisolism (26 with ACTH-secreting pituitary adenoma and 10 with cortisol-secreting adrenal tumor) and 35 with subclinical hypercortisolism due to adrenal incidentalomas.
  • METHODS: At diagnosis, we measured serum cortisol, FSH, LH, estradiol, testosterone, androstenedione and DHEAS, and urinary cortisol excretion.
  • RESULTS: Between women with overt and subclinical hypercortisolism BMD values and prevalence of any vertebral (69 vs 57%, P = 0.56), clinical (28 vs 11.4%, P = 0.22), and multiple vertebral fractures (36 vs 31%, P = 0.92) did not differ.
  • The deleterious effects of hypercortisolism on the spine may be partly counterbalanced by DHEAS increase at any degree of cortisol excess, and by preserved menstrual cycles in women with subclinical but not in those with overt hypercortisolism.

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  • (PMID = 17766720.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Gonadal Steroid Hormones; 3XMK78S47O / Testosterone; 409J2J96VR / Androstenedione; 4TI98Z838E / Estradiol; 57B09Q7FJR / Dehydroepiandrosterone Sulfate; 9002-68-0 / Follicle Stimulating Hormone; WI4X0X7BPJ / Hydrocortisone
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45. Alexandraki KI, Grossman AB: Medical therapy of Cushing's disease: where are we now? Front Horm Res; 2010;38:165-73
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  • [Title] Medical therapy of Cushing's disease: where are we now?
  • The goals of ideal medical therapy for Cushing's disease should be to target the aetiology of the disorder, and thus surgery is the current 'gold standard' treatment.
  • However, no effective drug that directly and effectively targets the adrenocorticotropin-secreting pituitary adenoma has been found to date, and treatments to control the hypercortisolaemic state by adrenal-based therapy are frequently used.
  • Inhibitors of adrenal steroidogenesis, adrenolytic agents, compounds with neuromodulatory properties, and ligands of different nuclear hormone receptors involved in hypothalamo-pituitary regulation currently used have been reviewed.
  • The somatostatin analogue pasireotide and the dopamine agonist cabergoline, as well as their combination, show some therapeutic promise, while retinoic acid analogues should be further investigated in the pituitary-targeted medical therapy of Cushing's disease.
  • Since a percentage of patients treated with surgery are not cured, or improve and subsequently relapse, there is an urgent need for effective medical therapies for this disorder.
  • [MeSH-major] Pituitary ACTH Hypersecretion / drug therapy

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  • [Copyright] Copyright (c) 2010 S. Karger AG, Basel.
  • (PMID = 20616508.001).
  • [ISSN] 0301-3073
  • [Journal-full-title] Frontiers of hormone research
  • [ISO-abbreviation] Front Horm Res
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Dopamine Agonists; 320T6RNW1F / Mifepristone; 51110-01-1 / Somatostatin; 78E4J5IB5J / Mitotane; R9400W927I / Ketoconazole; WI4X0X7BPJ / Hydrocortisone; ZS9KD92H6V / Metyrapone
  • [Number-of-references] 50
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46. Arnaldi G, Polenta B, Cardinaletti M, Boscaro M: Potential indications for somatostatin analogs in Cushing's syndrome. J Endocrinol Invest; 2005;28(11 Suppl International):106-10
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  • [Title] Potential indications for somatostatin analogs in Cushing's syndrome.
  • In recent years, somatostatin analogs have been proposed and used in the diagnosis and therapy in Cushing's syndrome (CS).
  • The strong expression of somatostatin receptors (SSTR) type 5 in human corticotroph cells and the demonstrated efficacy of SOM230, a novel multi-ligand somatostatin analog, in inhibiting ACTH release in vitro suggest that this new drug may be effective in the treatment of ACTH hypersecretion.
  • Very preliminary in vivo results suggest that SOM230 could be a promising drug in medical therapy for patients with Cushing's disease (CD).
  • [MeSH-major] Cushing Syndrome / diagnosis. Cushing Syndrome / drug therapy. Somatostatin / analogs & derivatives
  • [MeSH-minor] Adenoma / chemistry. Adenoma / secretion. Adrenal Gland Neoplasms / chemistry. Adrenal Gland Neoplasms / secretion. Adrenocorticotropic Hormone / secretion. Animals. Humans. Hydrocortisone / blood. Octreotide / therapeutic use. Pituitary Neoplasms / chemistry. Pituitary Neoplasms / secretion. Receptors, Somatostatin / analysis. Receptors, Somatostatin / physiology

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  • (PMID = 16625858.001).
  • [ISSN] 0391-4097
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Receptors, Somatostatin; 51110-01-1 / Somatostatin; 9002-60-2 / Adrenocorticotropic Hormone; 98H1T17066 / pasireotide; RWM8CCW8GP / Octreotide; WI4X0X7BPJ / Hydrocortisone
  • [Number-of-references] 53
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47. Yamada S, Ohyama K, Taguchi M, Takeshita A, Morita K, Takano K, Sano T: A study of the correlation between morphological findings and biological activities in clinically nonfunctioning pituitary adenomas. Neurosurgery; 2007 Sep;61(3):580-4; discussion 584-5
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  • [Title] A study of the correlation between morphological findings and biological activities in clinically nonfunctioning pituitary adenomas.
  • OBJECTIVE: The aims of this study are to review the histology of the clinically nonfunctioning pituitary adenomas (CNFPAs) we have observed and to determine whether or not the frequency of cavernous sinus invasion is different among each type of morphology.
  • METHODS: In addition, several proliferative markers, including Ki67, p53, E-cadherin, matrix metallo-proteinase 9 and pituitary tumor derived fibroblast growth factor receptor 4 (ptd-FGFR4), were also investigated in invasive and non-invasive tumors.
  • RESULTS: Our consequent 213 CNFPAs were diagnosed as follows: 64% were silent gonadotroph adenomas, 18% were null cell adenomas, 12% were silent corticotroph adenomas, 4% were silent Subtype 3 adenomas, and 1% were other types of adenomas.
  • Female patients or younger patients showed a significant preponderance in silent corticotroph adenomas and in silent Subtype 3 adenomas, respectively.
  • Cavernous sinus invasion occurs most frequently in silent corticotroph adenomas (85%) followed by Subtype 3 adenomas (67%), null cell adenomas (38%), and silent gonadotroph adenomas (11%).
  • CONCLUSION: From a clinical standpoint, it is quite important to differentiate morphological type in CNFPAs to aid the clinician in assessing the clinical behavior and prognosis of the tumor.
  • Therefore, we suggest that all CNFPAs be examined not only by conventional light microscopy but also by immunohistochemistry, preferably by electron microscopy, to achieve a correct morphological diagnosis.
  • [MeSH-major] Adenoma / classification. Adenoma / pathology. Pituitary Neoplasms / classification. Pituitary Neoplasms / pathology


48. Bangaru ML, Woodliff J, Raff H, Kansra S: Growth suppression of mouse pituitary corticotroph tumor AtT20 cells by curcumin: a model for treating Cushing's disease. PLoS One; 2010;5(4):e9893
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  • [Title] Growth suppression of mouse pituitary corticotroph tumor AtT20 cells by curcumin: a model for treating Cushing's disease.
  • BACKGROUND: Pituitary corticotroph tumors secrete excess adrenocorticotrophic hormone (ACTH) resulting in Cushing's disease (CD).
  • Standard treatment includes surgery and, if not successful, radiotherapy, both of which have undesirable side effects and frequent recurrence of the tumor.
  • Curcumin, a commonly used food additive in South Asian cooking, has potent growth inhibitory effects on cell proliferation.
  • Our laboratory recently demonstrated that curcumin inhibited growth and induced apoptosis in prolactin- and growth hormone-producing tumor cells.
  • Subsequently, Schaaf et.al. confirmed our findings and also showed the in vivo effectiveness of curcumin to suppress pituitary tumorigenesis.
  • PRINCIPAL FINDINGS: Using the mouse corticotroph tumor cells, AtT20 cells, we report that curcumin had a robust, irreversible inhibitory effect on cell proliferation and clonogenic property.
  • Further, curcumin down-regulated the pro-survival protein Bcl-xL, depolarized the mitochondrial membrane, increased PARP cleavage, which led to apoptotic cell death.
  • Finally, curcumin had a concentration-dependent suppressive effect on ACTH secretion from AtT20 cells.
  • CONCLUSION: The ability of curcumin to inhibit NFkappaB and induce apoptosis in pituitary corticotroph tumor cells leads us to propose developing it as a novel therapeutic agent for the treatment of CD.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / drug therapy. Cell Proliferation / drug effects. Curcumin / pharmacology. Pituitary ACTH Hypersecretion / drug therapy
  • [MeSH-minor] Adrenocorticotropic Hormone / secretion. Animals. Antineoplastic Agents. Apoptosis / drug effects. Cell Line, Tumor. Dose-Response Relationship, Drug. Mice. NF-kappa B / antagonists & inhibitors

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  • (PMID = 20405005.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / NF-kappa B; 9002-60-2 / Adrenocorticotropic Hormone; IT942ZTH98 / Curcumin
  • [Other-IDs] NLM/ PMC2854133
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49. Pawlikowski M, Kunert-Radek J, Radek M: "Silent"corticotropinoma. Neuro Endocrinol Lett; 2008 Jun;29(3):347-50
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  • [Title] "Silent"corticotropinoma.
  • OBJECTIVES: The aim of the study was to evaluate the ACTH-immunopositive pituitary adenomas, especially those without manifestation of Cushing's disease MATERIAL AND METHODS: 148 pituitary adenomas removed surgically in years 1994--2007 were studied.
  • The paraffin sections were immunostained with antibodies against the pituitary hormones.
  • In 79 adenomas the immunostaining with anti-ACTH antibody was performed Additionally, 23 tumors were also immunostained with anti-Ki-67 (MIB-1) antibody.
  • RESULTS: ACTH immunopositivity was found in 34 cases (23%).
  • Fourteen ACTH-immunopositive tumors manifested themselves as Cushing's disease (including 1 case of Nelson's syndrome).
  • In the remaining 20 cases in spite of the positive immunostaining for ACTH of the tumor cells, no features of hypercortisolism were observed (in several cases even hypocortisolism was found).
  • Thus, those tumors represented so-called "silent" corticotropinomas.
  • Over one third (37%) of "clinically" nonfunctioning pituitary adenomas, when immunostained with anti-ACTH antibody, showed ACTH immunopositivity.
  • Three adenomas in patients with Cushing's disease (21.4%) and 7 "silent" corticotropinomas (35%) were recurrent tumors.
  • In contrast, the recurrence rate in the group of ACTH-immunonegative clinically nonfunctioning pituitary adenomas was 14.7%.
  • The "silent" corticotropinomas exhibited a tendency towards the higher expression of a proliferation marker, Ki-67 antigen as compared to the "active" corticotropinomas.
  • CONCLUSIONS: (i) "Silent" corticotropinomas are rather frequent. (ii) This adenoma type should be considered as aggressive. (iii) It is hypothetized that--like in Nelson's syndrome--the lack of hypercortisolism or even presence of hypocortisolism favorizes the exaggerated growth of tumoral corticotrophs.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / metabolism. Adenoma / metabolism. Adrenocorticotropic Hormone / metabolism
  • [MeSH-minor] Adult. Cushing Syndrome / blood. Cushing Syndrome / pathology. Female. Humans. Immunohistochemistry. Ki-67 Antigen / blood. Male. Nelson Syndrome / blood. Paraffin Embedding. Pituitary Hormones / metabolism

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  • (PMID = 18580839.001).
  • [ISSN] 0172-780X
  • [Journal-full-title] Neuro endocrinology letters
  • [ISO-abbreviation] Neuro Endocrinol. Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Sweden
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Pituitary Hormones; 9002-60-2 / Adrenocorticotropic Hormone
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50. Giorgi RR, Correa-Giannella ML, Casarini AP, Machado MC, Bronstein MD, Cescato VA, Giannella-Neto D: Metallothionein isoform 3 gene is differentially expressed in corticotropin-producing pituitary adenomas. Neuroendocrinology; 2005;82(3-4):208-14
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  • [Title] Metallothionein isoform 3 gene is differentially expressed in corticotropin-producing pituitary adenomas.
  • In order to search for candidate genes related to pituitary adenoma aggressiveness, the present investigation was intended to compare the mRNA expression profile from a pool of four nonfunctional pituitary adenomas (NFPA) with a spinal cord metastasis of a nonfunctional pituitary carcinoma (MNFPC).
  • The metallothionein isoform 3 (MT3) gene was differentially expressed in nonfunctional adenomas in comparison to the metastasis of nonfunctional carcinoma.
  • A microarray dataset comprising 19,881 probes was employed for comparing expression profiles of a spinal cord metastasis of a nonfunctional pituitary carcinoma with a pool of four nonfunctional pituitary adenomas.
  • RT-qPCR confirmed the microarray findings and was used to investigate MT3 mRNA gene expression in tumor samples of a series of 52 different pituitary adenoma subtypes comprising 10 corticotropin (ACTH)-producing, 18 growth hormone (GH)-producing, 8 prolactin (PRL)-producing, and 16 nonfunctional adenomas.
  • MT3 mRNA expression was statistically significantly higher in ACTH-producing pituitary adenomas and in nonfunctional pituitary adenomas in comparison to the other pituitary adenoma subtypes.
  • The more abundant expression of this gene in ACTH-producing pituitary adenomas suggests that MT3 could be related to distinct pituitary cell lineage regulating the activity of some transcription factor of importance in hormone production and/or secretion.
  • [MeSH-major] Adenoma / metabolism. Adrenocorticotropic Hormone / metabolism. Nerve Tissue Proteins / biosynthesis. Pituitary Neoplasms / metabolism

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  • (PMID = 16601360.001).
  • [ISSN] 0028-3835
  • [Journal-full-title] Neuroendocrinology
  • [ISO-abbreviation] Neuroendocrinology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Nerve Tissue Proteins; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / growth inhibitory factor; 12629-01-5 / Human Growth Hormone; 9002-60-2 / Adrenocorticotropic Hormone; 9002-62-4 / Prolactin
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51. Nandagopal R, Vortmeyer A, Oldfield EH, Keil MF, Stratakis CA: Cushing's syndrome due to a pituitary corticotropinoma in a child with tuberous sclerosis: an association or a coincidence? Clin Endocrinol (Oxf); 2007 Oct;67(4):639-41
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  • [Title] Cushing's syndrome due to a pituitary corticotropinoma in a child with tuberous sclerosis: an association or a coincidence?
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / complications. Cushing Syndrome / etiology. Pituitary Neoplasms / complications. Tuberous Sclerosis / complications


52. Fernando MA, Heaney AP: Alpha1-adrenergic receptor antagonists: novel therapy for pituitary adenomas. Mol Endocrinol; 2005 Dec;19(12):3085-96
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  • [Title] Alpha1-adrenergic receptor antagonists: novel therapy for pituitary adenomas.
  • Pituitary tumors are common and cause considerable morbidity due to local invasion and altered hormone secretion.
  • Doxazosin (dox), a selective alpha(1)-adrenergic receptor antagonist, used to treat hypertension, also inhibits prostate cancer cell proliferation.
  • We examined the effects of dox on murine and human pituitary tumor cell proliferation in vitro and in vivo. dox treatment inhibited proliferation of murine pituitary tumor cells, induced G(0)-G(1) cell cycle arrest, and reduced phosphorylated retinoblastoma levels.
  • In addition, increased annexin-fluorescein isothiocyanate immunoreactivity and cleaved caspase-3 levels, in keeping with dox-mediated apoptosis, were observed in the human and murine pituitary tumor cells, and dox administration to mice, harboring corticotroph tumors, decreased tumor growth and reduced plasma ACTH levels. dox-mediated antiproliferative and proapoptotic actions were not confined to alpha-adrenergic receptor-expressing pituitary tumor cells and were unaffected by cotreatment with the alpha-adrenergic receptor blocker, phenoxybenzamine. dox treatment led to reduced phosphorylated inhibitory kappaB (IkappaB)-alpha expression, and nuclear factor-kappaB transcription and decreased basal and TNFalpha-induced proopiomelanocortin transcriptional activation.
  • These results demonstrate that the selective alpha(1)-adrenergic receptor antagonist dox inhibits pituitary tumor cell growth in vitro and in vivo by mechanisms that are in part independent of its alpha-adrenergic receptor-blocking actions and involve down-regulation of nuclear factor-kappaB signaling. dox is proposed as a possible novel medical therapy for pituitary tumors.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / drug therapy. Adenoma / drug therapy. Adrenergic alpha-1 Receptor Antagonists. Adrenergic alpha-Antagonists / therapeutic use. Antineoplastic Agents / therapeutic use. Doxazosin / therapeutic use
  • [MeSH-minor] Adrenocorticotropic Hormone / blood. Animals. Apoptosis. Caspase 3. Caspases / metabolism. Cell Cycle / drug effects. Cell Proliferation / drug effects. Humans. I-kappa B Proteins / metabolism. Mice. Mice, Nude. NF-kappa B / metabolism. Neoplasm Transplantation. Pro-Opiomelanocortin / genetics. Receptors, Adrenergic, alpha-1 / genetics. Receptors, Adrenergic, alpha-1 / metabolism. Transcriptional Activation. Tumor Cells, Cultured. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 16020484.001).
  • [ISSN] 0888-8809
  • [Journal-full-title] Molecular endocrinology (Baltimore, Md.)
  • [ISO-abbreviation] Mol. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenergic alpha-1 Receptor Antagonists; 0 / Adrenergic alpha-Antagonists; 0 / Antineoplastic Agents; 0 / I-kappa B Proteins; 0 / NF-kappa B; 0 / Receptors, Adrenergic, alpha-1; 0 / Tumor Necrosis Factor-alpha; 139874-52-5 / NF-kappaB inhibitor alpha; 66796-54-1 / Pro-Opiomelanocortin; 9002-60-2 / Adrenocorticotropic Hormone; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases; NW1291F1W8 / Doxazosin
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53. Hara Y, Teshima T, Taoda T, Ishino H, Nezu Y, Harada Y, Yogo T, Masuda H, Teramoto A, Tagawa M: Efficacy of transsphenoidal surgery on endocrinological status and serum chemistry parameters in dogs with Cushing's disease. J Vet Med Sci; 2010 Apr;72(4):397-404
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  • [Title] Efficacy of transsphenoidal surgery on endocrinological status and serum chemistry parameters in dogs with Cushing's disease.
  • Postoperative changes in endocrinological status and serum chemistry during the 4 years after transsphenoidal surgery (TSS) in 25 dogs with Cushing's disease were investigated in a prospective study.
  • In all 25 dogs, Cushing's disease was diagnosed from resected pituitary tissues as a corticotroph adenoma in the anterior lobe of the pituitary.
  • After TSS, the ACTH stimulation test showed continued low serum cortisol concentrations in 21 dogs (84%).
  • In regard to serum chemistry, alkaline phosphatase (ALP), alanine aminotransferase (ALT) and total cholesterol are commonly increased in canine Cushing's disease.
  • These results show that TSS is an effective treatment for canine Cushing's disease and for long-term improvement of hypercortisolemia.

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  • (PMID = 19996557.001).
  • [ISSN] 0916-7250
  • [Journal-full-title] The Journal of veterinary medical science
  • [ISO-abbreviation] J. Vet. Med. Sci.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 97C5T2UQ7J / Cholesterol; EC 2.6.1.1 / Aspartate Aminotransferases; EC 2.6.1.2 / Alanine Transaminase; WI4X0X7BPJ / Hydrocortisone
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54. Jiang ZQ, Gui SB, Zhang YZ: Differential gene expression by fiber-optic beadarray and pathway in adrenocorticotrophin-secreting pituitary adenomas. Chin Med J (Engl); 2010 Dec;123(23):3455-61
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  • [Title] Differential gene expression by fiber-optic beadarray and pathway in adrenocorticotrophin-secreting pituitary adenomas.
  • BACKGROUND: Adrenocorticotrophin (ACTH)-secreting pituitary adenomas account for approximately 7% - 14% of all pituitary adenomas, but its pathogenesis is still enigmatic.
  • This study aimed to explore mechanisms underlying the pathogenesis of ACTH-secreting pituitary adenomas.
  • METHODS: We used fiber-optic beadarray to examine gene expression in three ACTH-secreting adenomas compared with three normal pituitaries.
  • Four differentially expressed genes from the three ACTH-secreting adenomas and three normal pituitaries were chosen randomly for validation by reverse transcriptase-real time quantitative polymerase chain reaction (RT-qPCR).
  • Bioinformatic and pathway analysis showed that the genes HIGD1B, EPS8, HPGD, DAPK2, and IGFBP3 and the transforming growth factor (TGF)-β signaling pathway and extracellular matrix (ECM)-receptor interaction pathway may play important roles in tumorigenesis and progression of ACTH-secreting pituitary adenomas.
  • CONCLUSIONS: Our data suggest that numerous aberrantly expressed genes and several pathways are involved in the pathogenesis of ACTH-secreting pituitary adenomas.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / etiology. Adenoma / etiology. Gene Expression Profiling. Oligonucleotide Array Sequence Analysis / methods. Signal Transduction / physiology
  • [MeSH-minor] Adult. Disease Progression. Expressed Sequence Tags. Extracellular Matrix Proteins / physiology. Female. Fiber Optic Technology. Humans. Male. Middle Aged. Real-Time Polymerase Chain Reaction. Reverse Transcriptase Polymerase Chain Reaction. Transforming Growth Factor alpha / physiology

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  • (PMID = 22166531.001).
  • [ISSN] 0366-6999
  • [Journal-full-title] Chinese medical journal
  • [ISO-abbreviation] Chin. Med. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Extracellular Matrix Proteins; 0 / Transforming Growth Factor alpha
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55. Bezerra MG, Latronico AC, Fragoso MC: [Endocrine tumors associated to protein Gsalpha/Gi2alpha mutations]. Arq Bras Endocrinol Metabol; 2005 Oct;49(5):784-90
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  • Many oncogenic mutations promote tumor growth by inducing autonomous activity of proteins that normally transmit proliferative signal initiated by extracellular factors.
  • The G proteins couple an array of seven transmembrane receptors at the cell surface with a variety of intracellular effectors, which produce second messenger molecules.
  • A subset of endocrine tumors, such as GH- or ACTH-secreting pituitary adenomas, functioning thyroid adenomas, adrenocortical and gonadal tumors were associated with somatic activating mutations in the highly conserved codons of the Gs (Arg201 and Gln227) and Gi (Arg179 and Gln205) proteins.
  • [MeSH-major] Endocrine Gland Neoplasms / genetics. GTP-Binding Protein alpha Subunits, Gi-Go / genetics. GTP-Binding Protein alpha Subunits, Gs / genetics. Mutation / genetics. Oncogenes / genetics

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  • (PMID = 16444361.001).
  • [ISSN] 0004-2730
  • [Journal-full-title] Arquivos brasileiros de endocrinologia e metabologia
  • [ISO-abbreviation] Arq Bras Endocrinol Metabol
  • [Language] por
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Brazil
  • [Chemical-registry-number] EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gi-Go; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs
  • [Number-of-references] 64
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56. Durán-Prado M, Gahete MD, Martínez-Fuentes AJ, Luque RM, Quintero A, Webb SM, Benito-López P, Leal A, Schulz S, Gracia-Navarro F, Malagón MM, Castaño JP: Identification and characterization of two novel truncated but functional isoforms of the somatostatin receptor subtype 5 differentially present in pituitary tumors. J Clin Endocrinol Metab; 2009 Jul;94(7):2634-43
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  • [Title] Identification and characterization of two novel truncated but functional isoforms of the somatostatin receptor subtype 5 differentially present in pituitary tumors.
  • DESIGN AND RESULTS: A rapid amplification of cDNA ends PCR approach on samples from a human pituitary tumor and a cell line enabled identification of two novel alternatively spliced sst5 receptor variants.
  • Both novel receptors show a differential expression pattern in normal tissues and are also present in pituitary tumors of diverse etiology including nonfunctioning adenomas, corticotropinomas, somatotropinomas, and a prolactinoma.
  • Specifically, whereas sst5TMD5 is selectivity activated by somatostatin compared with cortistatin, cells transfected with sst5TMD4 almost exclusively respond to cortistatin and not to somatostatin.
  • CONCLUSIONS: Our results demonstrate the existence of two previously unidentified sst5 spliced variants with distinct distribution in normal tissues and pituitary tumors, unique ligand-selective signaling properties, and subcellular distribution, which could contribute to somatostatin and cortistatin signaling in normal and tumoral cells.
  • [MeSH-major] Adenoma / genetics. Pituitary Neoplasms / genetics. Receptors, Somatostatin / genetics

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  • (PMID = 19401364.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Isoforms; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 5
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57. Fratticci A, Grieco FA, Spilioti C, Giangaspero F, Ventura L, Esposito V, Piccirilli M, Santoro A, Gulino A, Cantore G, Alesse E, Jaffrain-Rea ML: Differential expression of neurogenins and NeuroD1 in human pituitary tumours. J Endocrinol; 2007 Sep;194(3):475-84
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  • [Title] Differential expression of neurogenins and NeuroD1 in human pituitary tumours.
  • Basic helix-loop-helix (bHLH) transcription factors are involved in neuroendocrine cell growth and differentiation.
  • Though NeuroD1 is viewed as corticotroph specific, its overexpression in non-corticotroph pituitary adenomas (PAs) may reflect the activation of molecular pathways involving other bHLH factors, like neurogenins.
  • To search for neurogenin-NeuroD1 molecular pathways in the human normal and tumoural pituitary.
  • Fifty-one PAs--22 clinically non-secreting (CNS) and 29 secreting respectively--and normal human pituitaries (NP) were studied for NeuroD1 and neurogenins (Ngn1, Ngn2 and Ngn3) gene expression by RT-PCR and quantitative real-time RT-PCR (qRT-PCR).
  • Whereas NeuroD1 expression was higher in corticotroph and CNS adenomas (P=0.0001 versus Pit-1-dependent PA), Ngn2 expression was higher in secreting PA, especially in Pit-1-dependent PA (P=0.007 and P=0.0006 versus CNS respectively).
  • Nuclear Ngn2 was observed in NP and in most PA, especially ACTH- and GH-secreting adenomas.
  • Nuclear Ngn3 was observed in a minority of secreting PA.
  • Ngn2 is normally expressed in the anterior pituitary and frequently expressed in PA, but does not account for NeuroD1 overexpression where present.
  • Owing to their low and inconstant expression, the biological significance of Ngn1/3 in the adult pituitary is uncertain.
  • [MeSH-major] Adenoma / metabolism. Basic Helix-Loop-Helix Transcription Factors / genetics. Gene Expression Regulation, Neoplastic. Pituitary Neoplasms / metabolism

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  • (PMID = 17761887.001).
  • [ISSN] 0022-0795
  • [Journal-full-title] The Journal of endocrinology
  • [ISO-abbreviation] J. Endocrinol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / NEUROD1 protein, human; 0 / NEUROG1 protein, human; 0 / NEUROG2 protein, human; 0 / NEUROG3 protein, human; 0 / Nerve Tissue Proteins; 0 / RNA, Messenger; 9002-60-2 / Adrenocorticotropic Hormone; 9002-72-6 / Growth Hormone
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58. Fernandez A, Karavitaki N, Wass JA: Prevalence of pituitary adenomas: a community-based, cross-sectional study in Banbury (Oxfordshire, UK). Clin Endocrinol (Oxf); 2010 Mar;72(3):377-82
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  • [Title] Prevalence of pituitary adenomas: a community-based, cross-sectional study in Banbury (Oxfordshire, UK).
  • BACKGROUND: Pituitary adenomas (PAs) are associated with increased morbidity and mortality.
  • All cases of PAs were found following an exhaustive computer database search of agreed terms by the staff of each Practice and data on age, gender, presenting manifestations and their duration, imaging features at diagnosis, history of multiple endocrine neoplasia type 1 and family history of PA were collected.
  • RESULTS: A total of 63 patients with PA were identified amongst the study population of 81,149, with a prevalence of 77.6 PA cases/100,000 inhabitants (prolactinomas; PRLoma: 44.4, nonfunctioning PAs: 22.2, acromegaly; ACRO: 8.6, corticotroph adenoma: 1.2 and unknown functional status; UFS: 1.2/100,000 inhabitants).
  • The distribution of each PA subtype was for PRLoma 57%, nonfunctioning PAs 28%, ACRO 11%, corticotroph adenoma 2% and UFS 2%.
  • The median age at diagnosis and the duration of symptoms until diagnosis (in years) were for PRLoma 32.0 and 1.5, nonfunctioning PAs 51.5 and 0.8, ACRO 47 and 4.5 and corticotroph adenoma 57 and 7, respectively.
  • Five patients (7.9%) presented with classical pituitary apoplexy, with a prevalence of 6.2 cases/100,000 inhabitants.
  • [MeSH-major] Adenoma / epidemiology. Pituitary Neoplasms / epidemiology
  • [MeSH-minor] Adolescent. Adult. Aged. Cross-Sectional Studies. Delayed Diagnosis. England / epidemiology. Female. Humans. Male. Middle Aged. Prevalence. Young Adult

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  • [CommentIn] Clin Endocrinol (Oxf). 2010 Mar;72(3):290-1 [19832856.001]
  • (PMID = 19650784.001).
  • [ISSN] 1365-2265
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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59. Leontiou CA, Gueorguiev M, van der Spuy J, Quinton R, Lolli F, Hassan S, Chahal HS, Igreja SC, Jordan S, Rowe J, Stolbrink M, Christian HC, Wray J, Bishop-Bailey D, Berney DM, Wass JA, Popovic V, Ribeiro-Oliveira A Jr, Gadelha MR, Monson JP, Akker SA, Davis JR, Clayton RN, Yoshimoto K, Iwata T, Matsuno A, Eguchi K, Musat M, Flanagan D, Peters G, Bolger GB, Chapple JP, Frohman LA, Grossman AB, Korbonits M: The role of the aryl hydrocarbon receptor-interacting protein gene in familial and sporadic pituitary adenomas. J Clin Endocrinol Metab; 2008 Jun;93(6):2390-401
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  • [Title] The role of the aryl hydrocarbon receptor-interacting protein gene in familial and sporadic pituitary adenomas.
  • CONTEXT: Mutations have been identified in the aryl hydrocarbon receptor-interacting protein (AIP) gene in familial isolated pituitary adenomas (FIPA).
  • It is not clear, however, how this molecular chaperone is involved in tumorigenesis.
  • OBJECTIVE: AIP sequence changes and expression were studied in FIPA and sporadic adenomas.
  • The function of normal and mutated AIP molecules was studied on cell proliferation and protein-protein interaction.
  • Cellular and ultrastructural AIP localization was determined in pituitary cells.
  • PATIENTS: Twenty-six FIPA kindreds and 85 sporadic pituitary adenoma patients were included in the study.
  • Overexpression of wild-type AIP in TIG3 and HEK293 human fibroblast and GH3 pituitary cell lines dramatically reduced cell proliferation, whereas mutant AIP lost this ability.
  • In normal pituitary, AIP colocalizes exclusively with GH and prolactin, and it is found in association with the secretory vesicle, as shown by double-immunofluorescence and electron microscopy staining.
  • In sporadic pituitary adenomas, however, AIP is expressed in all tumor types.
  • In addition, whereas AIP is expressed in the secretory vesicle in GH-secreting tumors, similar to normal GH-secreting cells, in lactotroph, corticotroph, and nonfunctioning adenomas, it is localized to the cytoplasm and not in the secretory vesicles.
  • CONCLUSIONS: Our functional evaluation of AIP mutations is consistent with a tumor-suppressor role for AIP and its involvement in familial acromegaly.
  • The abnormal expression and subcellular localization of AIP in sporadic pituitary adenomas indicate deranged regulation of this protein during tumorigenesis.
  • [MeSH-major] Adenoma / genetics. Pituitary Neoplasms / genetics. Proteins / physiology
  • [MeSH-minor] Acromegaly / genetics. Acromegaly / metabolism. Adolescent. Adult. Aged. Cell Proliferation. Child. Cyclic Nucleotide Phosphodiesterases, Type 4 / metabolism. Female. Gene Expression Regulation, Neoplastic. Genetic Testing. Human Growth Hormone / secretion. Humans. Intracellular Signaling Peptides and Proteins. Male. Middle Aged. Protein Binding. Transfection. Tumor Cells, Cultured


60. Minniti G, Osti M, Jaffrain-Rea ML, Esposito V, Cantore G, Maurizi Enrici R: Long-term follow-up results of postoperative radiation therapy for Cushing's disease. J Neurooncol; 2007 Aug;84(1):79-84
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  • [Title] Long-term follow-up results of postoperative radiation therapy for Cushing's disease.
  • OBJECTIVES: Radiotherapy is currently used in patients with residual or recurrent pituitary adenomas after surgery.
  • However, there is little information of long-term outcome of patients with Cushing's disease following radiotherapy.
  • We assessed the long-term efficacy and toxicity of conventional radiotherapy in the control of Cushing's disease after unsuccessful transsphenoidal surgery.
  • PATIENTS AND METHODS: Forty patients with Cushing's disease were treated with conventional external beam radiotherapy at our Institution between 1988 and 2002.
  • The persistence of active disease after surgery was diagnosed by the increased high plasma cortisol levels, high 24 h urinary cortisol levels and absence of cortisol suppression after administration of dexamethasone.
  • CONCLUSION: Radiotherapy is effective in the long-term tumour- and hormone hypersecretion control of ACTH-secreting pituitary adenomas, however with a high prevalence of hypopituitarism.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / radiotherapy. Adenoma / radiotherapy. Neoplasm Recurrence, Local / radiotherapy. Neoplasm, Residual / radiotherapy. Pituitary ACTH Hypersecretion / radiotherapy
  • [MeSH-minor] Adult. Disease-Free Survival. Female. Follow-Up Studies. Humans. Hydrocortisone / blood. Male. Middle Aged

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  • (PMID = 17356896.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] WI4X0X7BPJ / Hydrocortisone
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61. Mohammed S, Kovacs K, Mason W, Smyth H, Cusimano MD: Use of temozolomide in aggressive pituitary tumors: case report. Neurosurgery; 2009 Apr;64(4):E773-4; discussion E774
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  • [Title] Use of temozolomide in aggressive pituitary tumors: case report.
  • OBJECTIVE: The management of aggressive pituitary macroadenomas represents a challenge to neurosurgeons.
  • CLINICAL PRESENTATION: Three cases of patients with pituitary adenomas who underwent temozolomide treatment are presented.
  • The first 2 patients had corticotroph macroadenoma of the Crooke's cell variant.
  • The third patient had a glioblastoma multiforme with an incidental pituitary tumor.
  • CONCLUSION: The marked improvement in clinical state of the first 2 patients accompanied by radiological evidence of tumor shrinkage in all patients demonstrates the potential use of temozolomide in treating aggressive pituitary macroadenomas.
  • The usefulness of temozolomide in aggressive pituitary adenomas should be studied in larger trials.
  • [MeSH-major] Adenoma / drug therapy. Antineoplastic Agents, Alkylating / therapeutic use. Dacarbazine / analogs & derivatives. Pituitary Neoplasms / drug therapy

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  • (PMID = 19349807.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
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62. De Menis E, Roncaroli F, Calvari V, Chiarini V, Pauletto P, Camerino G, Cremonini N: Corticotroph adenoma of the pituitary in a patient with X-linked adrenal hypoplasia congenita due to a novel mutation of the DAX-1 gene. Eur J Endocrinol; 2005 Aug;153(2):211-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Corticotroph adenoma of the pituitary in a patient with X-linked adrenal hypoplasia congenita due to a novel mutation of the DAX-1 gene.
  • We report the occurrence of an ACTH-secreting adenoma in a patient with X-linked congenital adrenal hypoplasia.
  • DESIGN AND METHODS: Detailed clinical, radiological and pathological investigation of the pituitary adenoma.
  • ACTH was 24 980 pg/ml and nuclear magnetic resonance disclosed a huge pituitary adenoma.
  • Three transsphenoidal operations and radiotherapy were necessary to remove the tumor mass and control ACTH secretion.
  • Histologically, the adenoma was composed of chromophobic and basophilic neoplastic cells with positive immunostaining for ACTH.
  • CONCLUSIONS: This case suggests that in adrenal hypoplasia congenita the development of a pituitary adenoma should be considered when a sudden rise of ACTH occurs despite adequate steroid substitution.
  • [MeSH-major] Adenoma / complications. Adrenal Insufficiency / complications. Adrenal Insufficiency / genetics. DNA-Binding Proteins / genetics. Pituitary Neoplasms / complications. Receptors, Retinoic Acid / genetics. Repressor Proteins / genetics
  • [MeSH-minor] Adrenocorticotropic Hormone / metabolism. Adult. Chromosomes, Human, X. DAX-1 Orphan Nuclear Receptor. Family Health. Female. Frameshift Mutation. Humans. Magnetic Resonance Imaging. Male. Pituitary ACTH Hypersecretion / complications. Pituitary ACTH Hypersecretion / metabolism. Pituitary ACTH Hypersecretion / pathology

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  • (PMID = 16061826.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] eng
  • [Grant] Italy / Telethon / / B.38
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DAX-1 Orphan Nuclear Receptor; 0 / DNA-Binding Proteins; 0 / NR0B1 protein, human; 0 / Receptors, Retinoic Acid; 0 / Repressor Proteins; 9002-60-2 / Adrenocorticotropic Hormone
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63. van Rijn SJ, Grinwis GC, Penning LC, Meij BP: Expression of Ki-67, PCNA, and p27kip1 in canine pituitary corticotroph adenomas. Domest Anim Endocrinol; 2010 May;38(4):244-52
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  • [Title] Expression of Ki-67, PCNA, and p27kip1 in canine pituitary corticotroph adenomas.
  • Pituitary-dependent hypercortisolism (PDH), which is caused by adrenocorticotropic hormone (ACTH)-secreting pituitary adenomas, is a common endocrinopathy in dogs.
  • The aim of this study was to investigate the expression of the proliferation markers Ki-67 and proliferating cell nuclear antigen (PCNA) and the cell-cycle inhibitor p27kip1 in corticotroph adenomas in enlarged and non-enlarged pituitaries.
  • The expression of Ki-67, PCNA, and p27kip1 was analyzed by immunohistochemical staining of 17 pituitary adenoma samples harvested during pituitary surgery in dogs with PDH.
  • However, a trend toward significance was observed when comparing the expression of p27kip1 in enlarged pituitaries versus normal pituitary tissue.
  • It is concluded that Ki-67 and PCNA are not useful as proliferative markers for studying the pathobiology of pituitary corticotroph adenomas in dogs.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / veterinary. Cyclin-Dependent Kinase Inhibitor p27 / analysis. Dog Diseases / metabolism. Ki-67 Antigen / analysis. Pituitary Neoplasms / veterinary. Proliferating Cell Nuclear Antigen / analysis

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  • [Copyright] Copyright (c) 2009 Elsevier Inc. All rights reserved.
  • (PMID = 20022446.001).
  • [ISSN] 1879-0054
  • [Journal-full-title] Domestic animal endocrinology
  • [ISO-abbreviation] Domest. Anim. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Proliferating Cell Nuclear Antigen; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 581-05-5 / alpha-MSH; 9002-60-2 / Adrenocorticotropic Hormone
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64. Alexandraki KI, Grossman AB: Pituitary-targeted medical therapy of Cushing's disease. Expert Opin Investig Drugs; 2008 May;17(5):669-77
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  • [Title] Pituitary-targeted medical therapy of Cushing's disease.
  • BACKGROUND: The goals of ideal medical therapy for Cushing's disease should be to target the aetiology of the disorder, as is the case for surgery, which is the current 'gold standard' treatment.
  • However, no effective drug that directly and reliably targets the adrenocorticotropin-secreting pituitary adenoma has yet been found.
  • OBJECTIVE: To summarise pituitary-targeted medical treatment of Cushing's disease.
  • METHODS: Compounds with neuromodulatory properties and ligands of different nuclear hormone receptors involved in hypothalamo-pituitary regulation have been investigated.
  • RESULTS: The somatostatin analogue pasireotide and the dopamine agonist cabergoline, as well as their combination, show some therapeutic promise in the medical therapy of Cushing's disease.
  • CONCLUSION: Since a percentage of patients treated with surgery are not cured, or improve and subsequently relapse, there is an urgent need for effective medical therapies for this disorder.
  • [MeSH-major] Dopamine Agonists. Ergolines. Oligopeptides. Pituitary ACTH Hypersecretion / drug therapy. Pituitary Gland / drug effects. Somatostatin / analogs & derivatives

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  • [ErratumIn] Expert Opin Investig Drugs. 2008 Jul;17(7):1141
  • (PMID = 18447593.001).
  • [ISSN] 1744-7658
  • [Journal-full-title] Expert opinion on investigational drugs
  • [ISO-abbreviation] Expert Opin Investig Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Dopamine Agonists; 0 / Ergolines; 0 / Neurotransmitter Agents; 0 / Oligopeptides; 51110-01-1 / Somatostatin; 9002-60-2 / Adrenocorticotropic Hormone; 98H1T17066 / pasireotide; LL60K9J05T / cabergoline
  • [Number-of-references] 100
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65. Cho HY, Cho SW, Kim SW, Shin CS, Park KS, Kim SY: Silent corticotroph adenomas have unique recurrence characteristics compared with other nonfunctioning pituitary adenomas. Clin Endocrinol (Oxf); 2010 May;72(5):648-53
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  • [Title] Silent corticotroph adenomas have unique recurrence characteristics compared with other nonfunctioning pituitary adenomas.
  • OBJECTIVE: The prevalence of silent corticotroph adenomas (SCAs) is not rare among nonfunctioning pituitary adenomas (NFPAs); however, it is unknown whether the clinical significance of SCAs differs from that of NFPAs without ACTH immunoreactivity (non-SCAs).
  • MEASUREMENTS: We analysed whether clinical manifestations at diagnosis, postoperative recurrence rate and recurrence characteristics differed between SCA and non-SCA patients.
  • The mean age at the time of diagnosis was 44 years (range, 13-67 years) in the SCA group and 50 years (18-79 years) in the non-SCA group (P = 0.026), with respective follow-up periods of 5.2 (range, 1.0-16.0 years) and 4.2 years (0.5-16.1 years) (P = 0.255).
  • [MeSH-major] Adenoma / pathology. Adrenocorticotropic Hormone / analysis. Neoplasm Recurrence, Local. Pituitary Neoplasms / pathology

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  • (PMID = 19650787.001).
  • [ISSN] 1365-2265
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone
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66. Waugh MS, Soler AP, Robboy SJ: Silent corticotroph cell pituitary adenoma in a struma ovarii. Int J Gynecol Pathol; 2007 Jan;26(1):26-9
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  • [Title] Silent corticotroph cell pituitary adenoma in a struma ovarii.
  • This is the first report of a silent corticotroph cell pituitary adenoma arising in a struma ovarii.
  • The patient, a 79-year-old woman, was found to have an asymptomatic left-sided adnexal mass confirmed by vaginal sonography to be a complex cystic and solid tumor.
  • Pathological analysis demonstrated an 8-cm partially cystic struma ovarii in which there was a focus of predominantly basophilic adenohypophyseal cells arranged in a diffuse pattern, adjacent to mature neural tissue containing numerous Herring bodies.
  • The pituitary cells were predominantly immunoreactive for adrenocorticotropic hormone, in addition to synaptophysin.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / pathology. Corticotrophs / pathology. Struma Ovarii / pathology

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  • (PMID = 17197893.001).
  • [ISSN] 0277-1691
  • [Journal-full-title] International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists
  • [ISO-abbreviation] Int. J. Gynecol. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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67. Pecori Giraldi F, Pesce S, Maroni P, Pagliardini L, Lasio G, Losa M, Cavagnini F: Inhibitory effect of prepro-thyrotrophin-releasing hormone (178-199) on adrenocorticotrophic hormone secretion by human corticotroph tumours. J Neuroendocrinol; 2010 Apr;22(4):294-300
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  • [Title] Inhibitory effect of prepro-thyrotrophin-releasing hormone (178-199) on adrenocorticotrophic hormone secretion by human corticotroph tumours.
  • Prepro-thyrotrophin-releasing hormone (TRH) (178-199), a 22-amino acid cleavage product of the TRH prohormone, has been postulated to act as an adrenocorticotrophin hormone (ACTH)-release inhibitor.
  • Indeed, although in vitro evidence indicates that this peptide may inhibit basal and stimulated ACTH secretion in rodent anterior pituitary primary cultures and cell lines, not all studies concur and no study has as yet evaluated the effect of this peptide in Cushing's disease.
  • Twenty-four human ACTH-secreting pituitary tumours (13 macroadenomas, 11 microadenomas) were collected during surgery and incubated with 10 or 100 nm preproTRH(178-199).
  • ACTH secretion was assessed after 4 and 24 h of incubation by immunometric assay and expressed relative to levels observed in control, unchallenged wells (= 100%).
  • Parallel experiments were performed in rat anterior pituitary primary cultures.
  • A clear inhibition of ACTH secretion at 4 and 24 h was observed in 12 specimens (for 10 nm ppTRH: 70 +/- 4% control at 4 h and 83 +/- 5% control at 24 h; for 100 nm ppTRH: 70 +/- 4% control at 4 h and 85 +/- 5% control at 24 h), whereas a mild and short-lasting stimulatory effect was observed in three tumours and no changes in ACTH secretion in the remaining nine tumoural specimens.
  • Significant inhibition of ACTH secretion by preproTRH(178-199) in rat pituitary cultures was observed after 24 h of incubation.
  • The present study conducted in a large series of human corticotroph tumours shows that preproTRH(178-199) inhibits tumoural ACTH secretion in a sizable proportion of specimens, in close relation to the size of the tumour and its sensitivity to glucocorticoid negative feedback.
  • This appears a promising avenue of research and further studies are warranted to explore the full scope of preproTRH(178-199) as a regulator of ACTH secretion.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / secretion. Adenoma / secretion. Adrenocorticotropic Hormone / secretion. Peptide Fragments / pharmacology. Protein Precursors / pharmacology. Thyrotropin-Releasing Hormone / pharmacology
  • [MeSH-minor] Animals. Cell Culture Techniques. Cells, Cultured. Corticotropin-Releasing Hormone / pharmacology. Dexamethasone / pharmacology. Dose-Response Relationship, Drug. Down-Regulation / drug effects. Drug Evaluation, Preclinical. Female. Hormone Antagonists / pharmacology. Humans. Male. Pituitary Gland, Anterior / drug effects. Pituitary Gland, Anterior / metabolism. Rats

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  • (PMID = 20136686.001).
  • [ISSN] 1365-2826
  • [Journal-full-title] Journal of neuroendocrinology
  • [ISO-abbreviation] J. Neuroendocrinol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hormone Antagonists; 0 / Peptide Fragments; 0 / Protein Precursors; 122018-92-2 / prepro-thyrotropin-releasing hormone (178-199); 5Y5F15120W / Thyrotropin-Releasing Hormone; 7S5I7G3JQL / Dexamethasone; 9002-60-2 / Adrenocorticotropic Hormone; 9015-71-8 / Corticotropin-Releasing Hormone
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68. Pecori Giraldi F, Bucciarelli LG, Saccani A, Scacchi M, Pesce S, Losa M, Cavagnini F: Ghrelin stimulates adrenocorticotrophic hormone (ACTH) secretion by human ACTH-secreting pituitary adenomas in vitro. J Neuroendocrinol; 2007 Mar;19(3):208-12
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ghrelin stimulates adrenocorticotrophic hormone (ACTH) secretion by human ACTH-secreting pituitary adenomas in vitro.
  • Ghrelin is a brain-gut peptide with wide-ranging endocrine, metabolic, cardiovascular and neural effects.
  • Ghrelin, like its synthetic counterparts, the growth hormone (GH) secretagogues, has been shown to markedly stimulate adrenocorticotrophic hormone (ACTH) and cortisol secretion in humans and the ACTH-releasing effect of GH secretagogues is even greater in patients with pituitary ACTH-secreting tumours.
  • The aim of the present study was to evaluate the effect of ghrelin on ACTH secretion by human pituitary corticotroph tumours in vitro to test the functionality of this circuit.
  • Nine ACTH-secreting pituitary tumours (four microadenomas, five macroadenomas) were collected during surgery and incubated with 10-100 nM human ghrelin or with 10 nM human corticotrophin-releasing hormone (CRH).
  • Control experiments were performed in rat anterior pituitary primary cultures.
  • ACTH secretion was assessed after 4 h and 24 h incubation by immunometric assay.
  • After 4 h of incubation with ghrelin, medium ACTH concentrations were two- to ten-fold higher compared to ACTH concentrations in unstimulated wells.
  • The ACTH-releasing effect of ghrelin was significantly less than the response elicited by 10 nM CRH (up to 40-fold) Similar results were obtained after 24 h of incubation and a superimposable response pattern was observed in rat anterior pituitary primary cultures.
  • The present study demonstrates that the endogenous GH secretagogue, ghrelin, stimulates ACTH secretion directly from human tumoural corticotrophs, as well as from normal rat pituitary, and indicates that the marked ACTH release elicited by ghrelin in patients with Cushing's disease in vivo is due, at least in part, to its action on the pituitary tumour.
  • Moreover, these data uphold the concept of a functional intratumoural ghrelin paracrine circuit in human corticotroph adenomas.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / secretion. Adenoma / secretion. Adrenocorticotropic Hormone / secretion. Corticotrophs / secretion. Peptide Hormones / physiology
  • [MeSH-minor] Adult. Animals. Corticotropin-Releasing Hormone / physiology. Female. Ghrelin. Humans. In Vitro Techniques. Male. Middle Aged. Pituitary ACTH Hypersecretion / metabolism. Pituitary Gland, Anterior / metabolism. Rats

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  • (PMID = 17280594.001).
  • [ISSN] 0953-8194
  • [Journal-full-title] Journal of neuroendocrinology
  • [ISO-abbreviation] J. Neuroendocrinol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Ghrelin; 0 / Peptide Hormones; 9002-60-2 / Adrenocorticotropic Hormone; 9015-71-8 / Corticotropin-Releasing Hormone
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69. Giacomini D, Páez-Pereda M, Theodoropoulou M, Labeur M, Refojo D, Gerez J, Chervin A, Berner S, Losa M, Buchfelder M, Renner U, Stalla GK, Arzt E: Bone morphogenetic protein-4 inhibits corticotroph tumor cells: involvement in the retinoic acid inhibitory action. Endocrinology; 2006 Jan;147(1):247-56
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bone morphogenetic protein-4 inhibits corticotroph tumor cells: involvement in the retinoic acid inhibitory action.
  • The molecular mechanisms governing the pathogenesis of ACTH-secreting pituitary adenomas are still obscure.
  • In this study, we report that bone morphogenetic protein-4 (BMP-4) is expressed in the corticotrophs of human normal adenohypophysis and its expression is reduced in corticotrophinomas obtained from Cushing's patients compared with the normal pituitary.
  • BMP-4 treatment of AtT-20 mouse corticotrophinoma cells has an inhibitory effect on ACTH secretion and cell proliferation.
  • AtT-20 cells stably transfected with a dominant-negative form of the BMP-4 signal cotransducer Smad-4 or the BMP-4 inhibitor noggin have increased tumorigenicity in nude mice, showing that BMP-4 has an inhibitory role on corticotroph tumorigenesis in vivo.
  • Because the activation of the retinoic acid receptor has an inhibitory action on Cushing's disease progression, we analyzed the putative interaction of these two pathways.
  • Indeed, retinoic acid induces both BMP-4 transcription and expression and its antiproliferative action is blocked in Smad-4dn- and noggin-transfected Att-20 cells that do not respond to BMP-4.
  • This new mechanism is a potential target for therapeutic approaches for Cushing's disease.
  • [MeSH-major] Adenoma / pathology. Bone Morphogenetic Proteins / pharmacology. Bone Morphogenetic Proteins / physiology. Cushing Syndrome / pathology. Pituitary Neoplasms / pathology. Tretinoin / pharmacology
  • [MeSH-minor] Animals. Bone Morphogenetic Protein 4. Cell Division / drug effects. Cell Line, Tumor. Humans. Immunohistochemistry. Mice. Pituitary Gland / pathology. Pituitary Gland / physiology. Reference Values


70. Erickson D, Scheithauer B, Atkinson J, Horvath E, Kovacs K, Lloyd RV, Young WF Jr: Silent subtype 3 pituitary adenoma: a clinicopathologic analysis of the Mayo Clinic experience. Clin Endocrinol (Oxf); 2009 Jul;71(1):92-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Silent subtype 3 pituitary adenoma: a clinicopathologic analysis of the Mayo Clinic experience.
  • BACKGROUND: Macroadenomas represent 50% of pituitary tumours and are often (30%) nonfunctioning.
  • Their immunophenotype suggests differentiation toward a specific pituitary cell line.
  • A substantial proportion of tumours with particularly aggressive behaviour are so called 'silent subtype 3 adenoma'.
  • Its diagnosis requires ultrastructural confirmation.
  • Although once included among silent corticotroph adenomas, this aggressive, morphologically distinctive tumour is now recognized as a major form of plurihormonal adenoma and, in fact, some patients might present with clinical hormonal excess.
  • The cytogenesis and pathobiology of silent subtype 3 adenomas is unsettled.
  • DESIGN: This retrospective, single institution study found 27 confirmed examples of silent subtype 3 adenoma, a frequency of 0.9% of adenomas.
  • RESULTS: The study group was comprised of 16 men (59%) and 11 women (41%); two patients (7%) had definitive diagnosis of multiple endocrine neoplasia type 1 (MEN1).
  • Most tumours were plurihormonal, featuring immunoreactivity for PRL (17), GH (15), TSH (16) or ACTH (3); only one lesion was immunonegative.
  • CONCLUSION: Silent subtype 3 adenoma, a plurihormonal tumour, is rare and aggressive in nature.
  • This adenoma must be considered in the differential of often clinically nonfunctioning but plurihormonal adenomas featuring variable cytologic atypia.
  • Electron microscopy is required for confirmation of the diagnosis.
  • The cytogenesis of silent subtype 3 adenoma remains unsettled.
  • [MeSH-major] Pituitary Neoplasms / pathology

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  • (PMID = 19170710.001).
  • [ISSN] 1365-2265
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hormones
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71. Vila G, Papazoglou M, Stalla J, Theodoropoulou M, Stalla GK, Holsboer F, Paez-Pereda M: Sonic hedgehog regulates CRH signal transduction in the adult pituitary. FASEB J; 2005 Feb;19(2):281-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sonic hedgehog regulates CRH signal transduction in the adult pituitary.
  • It is known to be involved in pituitary development, but its role in the adult pituitary has not been investigated.
  • Here, we show Shh and Gli1 immunoreactivity in adult human corticotroph cells.
  • Administration of Shh (5 microg/ml) alone and in combination with corticotrophin-releasing hormone (CRH; 100 nM) in dispersed rat anterior pituitary and AtT-20 mouse corticotrophinoma cells increased corticotrophin (ACTH) secretion and pro-opiomelanocortin (POMC) promoter activity.
  • Shh and CRH act additively in increasing CRH receptor 1 (CRH-R1).
  • Taken together, our results demonstrate a new role for Shh and Gli1 in corticotroph function and provide a new link between Shh and CRH signaling pathways.
  • [MeSH-major] Corticotropin-Releasing Hormone / physiology. Pituitary Gland / chemistry. Pituitary Gland / metabolism. Signal Transduction / physiology. Trans-Activators / physiology
  • [MeSH-minor] Adrenocorticotropic Hormone / secretion. Adult. Animals. Cell Line, Tumor. Cells, Cultured. Hedgehog Proteins. Humans. Kruppel-Like Transcription Factors. Male. Mice. Pro-Opiomelanocortin / genetics. Rats. Rats, Sprague-Dawley. Transcription Factors / antagonists & inhibitors. Transcription Factors / metabolism. Transcription, Genetic / physiology

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  • (PMID = 15572433.001).
  • [ISSN] 1530-6860
  • [Journal-full-title] FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • [ISO-abbreviation] FASEB J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / GLI1 protein, human; 0 / Gli protein, mouse; 0 / Gli protein, rat; 0 / Hedgehog Proteins; 0 / Kruppel-Like Transcription Factors; 0 / SHH protein, human; 0 / Trans-Activators; 0 / Transcription Factors; 66796-54-1 / Pro-Opiomelanocortin; 9002-60-2 / Adrenocorticotropic Hormone; 9015-71-8 / Corticotropin-Releasing Hormone
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72. Tateno T, Izumiyama H, Doi M, Yoshimoto T, Shichiri M, Inoshita N, Oyama K, Yamada S, Hirata Y: Differential gene expression in ACTH -secreting and non-functioning pituitary tumors. Eur J Endocrinol; 2007 Dec;157(6):717-24
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  • [Title] Differential gene expression in ACTH -secreting and non-functioning pituitary tumors.
  • OBJECTIVE: Differential expression of several genes between ACTH-secreting pituitary tumors causing Cushing' disease (CD), silent corticotroph adenoma (SCA), and non-functioning pituitary tumors (NFT) was investigated.
  • DESIGN AND METHODS: We used tissue specimens from 35 pituitary tumors (12 CD, 8 SCA, and 15 NFT).
  • Steady-state mRNA levels of the genes related to proopiomelanocortin (POMC) transcription, synthesis, processing, and secretion, such as neurogenic differentiation 1 (NeuroD1), T-box 19 (Tpit), corticotropin releasing hormone receptor (CRHR), vasopressin receptor 1b (V1bR), prohormone convertase (PC) 1/3 and PC2, 11beta-hydroxysteroid dehydrogenase (11beta-HSD) type 1 and type 2, glucocorticoid receptor alpha (GRalpha), annexin A1, histone deacetylase 2 (HDAC2), and BRM/SWI2-related gene 1, were determined by real-time RT-PCR.
  • In conclusion, our study demonstrated that the genes related to transcription, synthesis, processing, and secretion of POMC are differentially regulated in ACTH-secreting pituitary tumors causing CD and SCA compared with those in NFT.

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  • (PMID = 18057378.001).
  • [ISSN] 1479-683X
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / CRF receptor type 1; 0 / Homeodomain Proteins; 0 / NEUROD1 protein, human; 0 / RNA, Messenger; 0 / Receptors, Corticotropin-Releasing Hormone; 0 / Receptors, Glucocorticoid; 0 / Receptors, Vasopressin; 0 / T-Box Domain Proteins; 0 / TBX19 protein, human; 0 / glucocorticoid receptor alpha; 66796-54-1 / Pro-Opiomelanocortin; 9002-60-2 / Adrenocorticotropic Hormone; EC 1.1.1.146 / 11-beta-Hydroxysteroid Dehydrogenases; EC 3.4.21.94 / Proprotein Convertase 2
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73. van Aken MO, Feelders RA, van der Lely AJ, Romijn JA, Lamberts SW, de Herder WW: [Cushing's syndrome. II. New forms of treatment]. Ned Tijdschr Geneeskd; 2006 Oct 28;150(43):2365-9
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  • [Title] [Cushing's syndrome. II. New forms of treatment].
  • Several new therapeutic options both medicinal and surgical, have emerged for the treatment of Cushing's syndrome.
  • In Cushing's disease caused by an adrenocorticotropin (ACTH) secreting pituitary adenoma, the introduction ofendoscopic pituitary surgery offers better visualization of the sella than does the traditional explorative surgery.
  • These agents may also be effective for the medicinal treatment of ectopic ACTH-secretion.
  • The primary treatment for ACTH-independent Cushing's syndrome is laparoscopic adrenalectomy.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / therapy. Adenoma / therapy. Cushing Syndrome / therapy
  • [MeSH-minor] Adrenalectomy. Adrenergic Antagonists / therapeutic use. Humans. Pituitary Gland / surgery. Treatment Outcome

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  • [CommentIn] Ned Tijdschr Geneeskd. 2006 Oct 28;150(43):2345-9 [17100122.001]
  • [CommentIn] Ned Tijdschr Geneeskd. 2007 Feb 3;151(5):330; author reply 331 [17326480.001]
  • (PMID = 17100127.001).
  • [ISSN] 0028-2162
  • [Journal-full-title] Nederlands tijdschrift voor geneeskunde
  • [ISO-abbreviation] Ned Tijdschr Geneeskd
  • [Language] dut
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Adrenergic Antagonists
  • [Number-of-references] 24
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74. Matsuno A: [Recent trends in the pathophysiology and treatment of pituitary adenomas]. Brain Nerve; 2009 Aug;61(8):957-62
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  • [Title] [Recent trends in the pathophysiology and treatment of pituitary adenomas].
  • Recent molecular pathological investigations have elucidated the cytodifferentiation of pituitary cells and identified several transcriptional factors that regulate this cytodifferentiation of pituitary cells.
  • The patterns of cytodifferentiation are closely related to the pathogenesis of pituitary adenomas.
  • Meanwhile, the role of hypothalamic hormones in the development of pituitary adenomas has recently attracted the attention of investigators.
  • The expression of growth hormone-releasing hormone and corticotrophin releasing hormone in corticotroph adenomas have been demonstrated in somatotroph adenomas and corticotropin adenomas, respectively.
  • This finding indicates that the endogenous expression of hypothalamic hormones and their receptors in human pituitary adenoma cells has ample significance in the autocrine or paracrine regulation of pituitary hormone production and tumor extension induced by hypothalamic hormones produced by adenoma cells.
  • The recent progress in surgical techniques for treatment of pituitary adenomas has provided several alternatives: transsphenoidal surgery vs. transcranial surgery, sublabial approach vs. endonasal approach, and microsurgery vs. endoscopic surgery.
  • There have also been developments in the medical treatment of pituitary adenomas.
  • The frequently used dopamine agonist, cabergoline, is very effective for treating prolactin-producing adenoma.
  • Long-acting octreotide and pegvisomant are now available for the treatment of growth hormone producing adenoma.
  • Cabergoline is also used for growth hormone producing adenoma.
  • Temozolomide has recently been used for atypical adenomas or pituitary carcinomas.
  • Adult growth hormone deficiency sometimes occurs in postoperative patients with pituitary adenomas.
  • [MeSH-major] Adenoma / etiology. Adenoma / therapy. Pituitary Neoplasms / etiology. Pituitary Neoplasms / therapy
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Corticotropin-Releasing Hormone. Dacarbazine / analogs & derivatives. Dacarbazine / therapeutic use. Ergolines / therapeutic use. Growth Hormone-Releasing Hormone. Human Growth Hormone / analogs & derivatives. Human Growth Hormone / therapeutic use. Humans. Hypothalamic Hormones. Incidental Findings. Neurosurgical Procedures / methods. Neurosurgical Procedures / trends. Octreotide / therapeutic use. Prolactinoma. Receptors, Neuropeptide. Receptors, Pituitary Hormone-Regulating Hormone

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  • (PMID = 19697885.001).
  • [ISSN] 1881-6096
  • [Journal-full-title] Brain and nerve = Shinkei kenkyū no shinpo
  • [ISO-abbreviation] Brain Nerve
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Ergolines; 0 / Hypothalamic Hormones; 0 / Receptors, Neuropeptide; 0 / Receptors, Pituitary Hormone-Regulating Hormone; 0 / pegvisomant; 0 / somatotropin releasing hormone receptor; 12629-01-5 / Human Growth Hormone; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; 9015-71-8 / Corticotropin-Releasing Hormone; 9034-39-3 / Growth Hormone-Releasing Hormone; LL60K9J05T / cabergoline; RWM8CCW8GP / Octreotide
  • [Number-of-references] 32
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75. Siddiqui AA, Bashir SH: Giant pituitary macroadenoma at the age of 4 months: case report and review of the literature. Childs Nerv Syst; 2006 Mar;22(3):290-4
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  • [Title] Giant pituitary macroadenoma at the age of 4 months: case report and review of the literature.
  • CASE REPORT: Adrenocorticotropic hormone (ACTH)-secreting pituitary adenoma is extremely rare.
  • We report the youngest patient of Cushing's disease due to ACTH-secreting pituitary macroadenoma at the age of 4 months.
  • Serum cortisol level was 97 microg/dl, with increased secretion of urinary free cortisol; plasma ACTH level was 353 pg/ml.
  • Magnetic resonance imaging of the brain showed a large contrast-enhancing solid mass sitting in the sellar region, with suprasellar and lateral extension.
  • Surgical resection was done, and immunohistochemistry confirmed the diagnosis of ACTH-secreting pituitary adenoma.
  • CONCLUSION: Cushing's disease due to ACTH-secreting pituitary macroadenoma is a possible diagnosis in early infancy.
  • This surgical morbidity is possibly attributed to difficult peroperative hemostasis due to vasculopathy in Cushing's disease, which leads to excessive blood loss, adverse hemodynamic changes, myocardial dysfunction and disseminated intravascular coagulopathy.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / surgery. Adenoma / surgery. Cushing Syndrome / surgery. Disseminated Intravascular Coagulation / etiology. Postoperative Complications / etiology

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  • (PMID = 16047217.001).
  • [ISSN] 0256-7040
  • [Journal-full-title] Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery
  • [ISO-abbreviation] Childs Nerv Syst
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76. Iván G, Szigeti-Csúcs N, Oláh M, Nagy GM, Góth MI: Treatment of pituitary tumors: dopamine agonists. Endocrine; 2005 Oct;28(1):101-10
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  • [Title] Treatment of pituitary tumors: dopamine agonists.
  • In the hypothalamopituitary system its function is a dominant and tonic inhibitory regulation of pituitary hormone secretion including prolactin- and proopiomelanocortin-derived hormones.
  • It is well known that dopamine agonists, such as bromocriptine, pergolide, quinagolide, cabergoline, and lisuride, can inhibit PRL secretion by binding to the D(2) dopamine receptors located on normal as well as tumorous pituitary cells.
  • Moreover, they can effectively decrease excessive PRL secretion as well as the size of the tumor in patients having prolactinoma.
  • Furthermore, dopamine agonists can also be used in other pituitary tumors.
  • The major requirement for its use is that the tumor cells should express D(2) receptors.
  • Therefore, in addition to prolactinomas, targets of dopamine agonist therapy are somatotroph tumors, nonfunctioning pituitary tumors, corticotroph pituitary tumors, Nelson's syndrome, gonadotropinomas, and thyrotropin-secreting pituitary tumors.
  • It is also an option for the treatment of pituitary disease during pregnancy.
  • Differences between the effectiveness and the resistance of different dopaminergic agents as well as the future perspectives of them in the therapy of pituitary tumors are discussed.
  • [MeSH-major] Adenoma / drug therapy. Dopamine Agonists / pharmacology. Pituitary Neoplasms / drug therapy

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  • (PMID = 16311416.001).
  • [ISSN] 1355-008X
  • [Journal-full-title] Endocrine
  • [ISO-abbreviation] Endocrine
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dopamine Agonists; 0 / Ergolines; 0 / Receptors, Dopamine; 3A64E3G5ZO / Bromocriptine; LL60K9J05T / cabergoline; VTD58H1Z2X / Dopamine
  • [Number-of-references] 71
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77. Tani Y, Inoshita N, Sugiyama T, Kato M, Yamada S, Shichiri M, Hirata Y: Upregulation of CDKN2A and suppression of cyclin D1 gene expressions in ACTH-secreting pituitary adenomas. Eur J Endocrinol; 2010 Oct;163(4):523-9
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  • [Title] Upregulation of CDKN2A and suppression of cyclin D1 gene expressions in ACTH-secreting pituitary adenomas.
  • OBJECTIVE: Cushing's disease (CD) is usually caused by ACTH-secreting pituitary microadenomas, while silent corticotroph adenomas (SCA) are macroadenomas without Cushingoid features.
  • However, the molecular mechanism(s) underlying their different tumor growth remains unknown.
  • The aim of the current study was to evaluate and compare the gene expression profile of cell cycle regulators and cell growth-related transcription factors in CD, SCA, and non-functioning adenomas (NFA).
  • DESIGN AND METHODS: Tumor tissue specimens resected from 43 pituitary tumors were studied: CD (n=10), SCA (n=11), and NFA (n=22).
  • The gene expressions of cyclins D1, E1, and B1, but not of A1, in CD were significantly suppressed than those in NFA.
  • The gene expressions of E2F1, RB1, BUB1, BUBR1, ETS1, and ETS2 did not differ between each group.
  • Thus, it is suggested that upregulated CDKN2A with the concomitant downregulated cyclin gene family is partly involved in the small size of ACTH-secreting adenoma.


78. Suzuki K, Hattori Y, Aoki C, Nakano A, Tomizawa A, Kase H, Kasai K: An ACTH-secreting pituitary adenoma within the sphenoid sinus. Intern Med; 2010;49(8):763-6
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  • [Title] An ACTH-secreting pituitary adenoma within the sphenoid sinus.
  • She was found to have a markedly elevated plasma ACTH-cortisol level.
  • Magnetic resonance imaging (MRI) revealed a mass in the left sphenoidal sinus, which had become enlarged to a point where it could not be removed by transsphenoidal surgery.
  • We decided to proceed with radiation therapy to shrink the tumor.
  • We describe a rare case of an ACTH-secreting pituitary adenoma within the sphenoid sinus.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / diagnosis. Paranasal Sinus Neoplasms / diagnosis. Sphenoid Sinus / pathology

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  • (PMID = 20424367.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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79. de Bruin C, Hanson JM, Meij BP, Kooistra HS, Waaijers AM, Uitterlinden P, Lamberts SW, Hofland LJ: Expression and functional analysis of dopamine receptor subtype 2 and somatostatin receptor subtypes in canine cushing's disease. Endocrinology; 2008 Sep;149(9):4357-66
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  • [Title] Expression and functional analysis of dopamine receptor subtype 2 and somatostatin receptor subtypes in canine cushing's disease.
  • Cushing's disease (CD) is a severe disorder characterized by chronic hypercortisolism due to an ACTH-secreting pituitary adenoma.
  • Finding an effective and safe medical treatment for CD may improve long-term clinical outcome.
  • The recent demonstration of expression of somatostatin receptor subtypes (mainly sst5) and dopamine receptor subtype 2 (D2) in human corticotroph adenomas offers the possibility for medical treatment of CD with novel somatostatin analogs and dopamine agonists.
  • Interestingly, CD is a frequent disorder in dogs with striking clinical similarities with CD in humans.
  • Therefore, we investigated the expression and functional role of D2 and somatostatin receptors in corticotroph adenoma cells from 13 dogs with active CD that underwent therapeutic hypophysectomy and normal anterior pituitary cells from five dogs.
  • Quantitative RT-PCR and immunohistochemistry revealed that both in CD and normal anterior pituitary, sst2 was the predominant receptor subtype expressed, whereas D2 was modestly expressed and sst5 was expressed only at very low levels.
  • In primary cultures of canine adenomas (n = 7), the sst2-preferring agonist octreotide also showed the strongest ACTH-suppressive effects.
  • In conclusion, canine corticotroph adenomas provide an interesting model to study CD, but differences in somatostatin and dopamine receptor expression between humans and dogs should be taken into account when using dogs with CD as a model to evaluate efficacy of novel somatostatin analogs and dopamine agonists for human CD.
  • [MeSH-major] Dog Diseases / genetics. Pituitary ACTH Hypersecretion / genetics. Receptors, Dopamine D2 / genetics. Receptors, Dopamine D2 / physiology. Receptors, Somatostatin / genetics. Receptors, Somatostatin / physiology
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / genetics. ACTH-Secreting Pituitary Adenoma / metabolism. ACTH-Secreting Pituitary Adenoma / pathology. Adenoma / genetics. Adenoma / metabolism. Adenoma / pathology. Animals. Cells, Cultured. Dexamethasone / pharmacology. Dogs. Female. Follow-Up Studies. Gene Expression Regulation, Neoplastic / drug effects. Male. Protein Isoforms / genetics. Protein Isoforms / metabolism. RNA, Messenger / metabolism

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  • (PMID = 18483151.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / Receptors, Dopamine D2; 0 / Receptors, Somatostatin; 7S5I7G3JQL / Dexamethasone
  • [Other-IDs] NLM/ PMC2553383
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80. Bertagna X, Guignat L, Groussin L, Bertherat J: Cushing's disease. Best Pract Res Clin Endocrinol Metab; 2009 Oct;23(5):607-23
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cushing's disease.
  • Cushing's syndrome refers to the clinical manifestations induced by chronic exposure to excess glucocorticoids.
  • There are three pathological conditions that can result in the chronic overproduction of endogenous cortisol in man: the most frequent is Cushing's disease where adrenocorticotropic hormone (ACTH) is overproduced by a pituitary corticotroph adenoma, rarely ACTH can be produced in an 'ectopic' manner by a non-pituitary tumour, finally cortisol can be directly over-secreted by one or (rarely) the two adrenals that have become tumourous, either benign or malignant.
  • The positive diagnosis of Cushing's syndrome requires that chronic hypercortisolism is unequivocally demonstrated biologically, using 24-h urinary cortisol, late-evening plasma or salivary cortisol, midnight 1-mg or the classic 48-h-low-dose dexamethasone suppression test, etc., all with essentially the same diagnosis potencies.
  • The search for the responsible tumour then relies on the assessment of the corticotroph function, and imaging: suppressed ACTH plasma levels indicate an 'adrenal' Cushing, and the responsible unilateral adrenocortical tumour is always visible at computed tomography (CT) scan, whereas its benign or malignant nature may be difficult to diagnose before surgery.
  • Imaging can suspect bilateral 'adrenal' Cushing, when the two adrenals are small, as in the primary pigmented nodular adrenal dysplasia associated with Carney complex, or enlarged, as in the ACTH-independent macronodular adrenocortical hyperplasia.
  • Measurable or increased ACTH plasma levels indicate either Cushing's disease or the ectopic ACTH syndrome.
  • When the dynamics of the corticotroph function (high-dose dexamethasone suppression test, the CRH test) are equivocal, and/or the imaging is non-contributive, it may be difficult to distinguish between the two.
  • This is the situation where sampling ACTH plasma levels in the inferior petrosal sinus may be necessary.
  • The best treatment option of Cushing's disease is when the responsible corticotroph adenoma can be entirely removed by the trans-sphenoidal approach, with sufficient skill to preserve the normal anterior pituitary function.
  • When it fails, all other options directed towards the pituitary (radiation therapies), or the adrenals (medications or surgery), have numerous side effects.
  • There is at present no recognised efficient medical treatment towards the corticotroph adenoma -still an orphan disease.
  • [MeSH-major] Pituitary ACTH Hypersecretion / etiology
  • [MeSH-minor] Algorithms. Cushing Syndrome / diagnosis. Cushing Syndrome / etiology. Diagnosis, Differential. Diagnostic Errors. Diagnostic Techniques, Endocrine. Humans. Prognosis

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  • (PMID = 19945026.001).
  • [ISSN] 1878-1594
  • [Journal-full-title] Best practice & research. Clinical endocrinology & metabolism
  • [ISO-abbreviation] Best Pract. Res. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 74
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81. Bondioni S, Mantovani G, Polentarutti N, Ambrosi B, Loli P, Peverelli E, Lania AG, Beck-Peccoz P, Spada A: Evaluation of proopiomelanocortin mRNA in the peripheral blood from patients with Cushing's syndrome of different origin. J Endocrinol Invest; 2007 Nov;30(10):828-32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evaluation of proopiomelanocortin mRNA in the peripheral blood from patients with Cushing's syndrome of different origin.
  • ACTH-dependent Cushing's syndrome is due to ACTH overproduction originating from a pituitary corticotroph adenoma (Cushing's disease) or from ectopic tumors (ectopic ACTH syndrome).
  • Due to difficulties in the differential diagnosis between these two forms of hypercortisolism it would be important to have molecular tools able to discriminate the two conditions.
  • In order to analyse the presence of different POMC transcripts, we extracted total RNA from peripheral lymphocytes of 10 patients with Cushing's disease, 10 with ectopic Cushing syndrome, and 20 controls as well as from pituitary tissues (2 ACTH-omas and a normal pituitary polyA+ sample).
  • Northern blot analysis correctly revealed a 1072 nt mRNA molecule in pituitary ACTH-oma and in the normal pituitary polyA+ RNA samples, whereas neither this molecule nor other alternative transcripts were detected in blood samples from patients and controls.
  • This study further underlines the need for alternative approaches in the diagnosis of ACTH-dependent Cushing's syndrome.
  • [MeSH-major] ACTH Syndrome, Ectopic / diagnosis. ACTH-Secreting Pituitary Adenoma / diagnosis. Adenoma / diagnosis. Biomarkers, Tumor / genetics. Cushing Syndrome / diagnosis. Pro-Opiomelanocortin / genetics
  • [MeSH-minor] Blotting, Northern. Diagnosis, Differential. Humans. RNA, Messenger / blood. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 18075284.001).
  • [ISSN] 1720-8386
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / RNA, Messenger; 66796-54-1 / Pro-Opiomelanocortin
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82. Dehdashti AR, Gentili F: Current state of the art in the diagnosis and surgical treatment of Cushing disease: early experience with a purely endoscopic endonasal technique. Neurosurg Focus; 2007;23(3):E9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Current state of the art in the diagnosis and surgical treatment of Cushing disease: early experience with a purely endoscopic endonasal technique.
  • OBJECT: Transsphenoidal pituitary surgery is the primary therapy for Cushing disease because of its potential to produce lasting remission without the need for long-term drug or hormone replacement therapy.
  • The authors evaluated the current role of pure endoscopic endonasal pituitary surgery in the treatment of Cushing disease.
  • METHODS: Twenty-five patients underwent pure endoscopic surgery for confirmed Cushing disease.
  • Final histological results were consistent with adrenocorticotropin hormone (ACTH)-secreting adenoma in 20 patients.
  • Three patients presented with new anterior pituitary deficiency, but no one had permanent diabetes insipidus.
  • Treatment failure was attributable to involvement of the cavernous sinus in two patients, incomplete tumor removal in one, negative exploration in one, and nodular corticotroph hyperplasia of the pituitary gland in one.
  • CONCLUSIONS: Early results indicated that endoscopic endonasal surgery is a safe and effective treatment for ACTH-producing adenomas.
  • Further studies with a larger number of patients and longer follow-ups are required to determine whether this more minimally invasive pure endoscopic approach should become the standard of care for the surgical treatment of Cushing disease.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / surgery. Adenoma / surgery. Endoscopy. Paranasal Sinuses / surgery. Pituitary ACTH Hypersecretion / diagnosis. Pituitary ACTH Hypersecretion / surgery

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  • (PMID = 17961027.001).
  • [ISSN] 1092-0684
  • [Journal-full-title] Neurosurgical focus
  • [ISO-abbreviation] Neurosurg Focus
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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83. Mancini T, Porcelli T, Giustina A: Treatment of Cushing disease: overview and recent findings. Ther Clin Risk Manag; 2010;6:505-16
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of Cushing disease: overview and recent findings.
  • Endogenous Cushing syndrome is an endocrine disease caused by excessive secretion of adrenocorticotropin hormone in approximately 80% of cases, usually by a pituitary corticotroph adenoma (Cushing disease [CD]).
  • It is a heterogeneous disorder requiring a multidisciplinary and individualized approach to patient management.
  • Generally, the treatment of choice is the surgical removal of the pituitary tumor by transsphenoidal approach, performed by an experienced surgeon.
  • Drug treatment has been targeted at the hypothalamic or pituitary level, at the adrenal gland, and also at the glucocorticoid receptor level.
  • Medical therapy can be also useful in patients with CD while waiting for pituitary radiotherapy to take effect, which can take up to 10 years or more.
  • So far, results of medical treatment of CD have not been particularly relevant; however, newer tools promise to change this scenario.

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  • (PMID = 21063461.001).
  • [ISSN] 1178-203X
  • [Journal-full-title] Therapeutics and clinical risk management
  • [ISO-abbreviation] Ther Clin Risk Manag
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] New Zealand
  • [Other-IDs] NLM/ PMC2963160
  • [Keywords] NOTNLM ; Cushing disease / dopamine agonists / glucocorticoids / hypopituitarism / ketoconazole / rosiglitazone / somatostatin analogs
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84. Kidambi S, Raff H, Findling JW: Limitations of nocturnal salivary cortisol and urine free cortisol in the diagnosis of mild Cushing's syndrome. Eur J Endocrinol; 2007 Dec;157(6):725-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Limitations of nocturnal salivary cortisol and urine free cortisol in the diagnosis of mild Cushing's syndrome.
  • OBJECTIVE: Cushing's syndrome (CS) is difficult to diagnose due to its nonspecific presentation.
  • However, its performance in mild CS has not been reported.
  • We present 11 cases of CS with normal or mildly elevated UFC in whom NSC was helpful in making a diagnosis.
  • Imaging studies included magnetic resonance imaging (MRI) of pituitary or computer tomography scan of abdomen.
  • Out of eleven patients, six had an abnormality in the pituitary gland found by MRI and two out of eleven had adrenal masses.
  • The remaining three had normal pituitary MRI but had inferior petrosal sinus (IPS) sampling indicating Cushing's disease.
  • All patients had appropriate surgery, and histopathology of all except one was suggestive of either a cortisol-producing adrenal adenoma or an ACTH-secreting pituitary adenoma.
  • Multiple samples (urine/saliva) and DST are needed to make the diagnosis of mild CS.

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  • (PMID = 18057379.001).
  • [ISSN] 1479-683X
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 7S5I7G3JQL / Dexamethasone; WI4X0X7BPJ / Hydrocortisone
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85. Taoda T, Hara Y, Takekoshi S, Itoh J, Teramoto A, Osamura RY, Tagawa M: Effect of mitotane on pituitary corticotrophs in clinically normal dogs. Am J Vet Res; 2006 Aug;67(8):1385-94
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  • [Title] Effect of mitotane on pituitary corticotrophs in clinically normal dogs.
  • OBJECTIVE: To evaluate the effects of mitotane administration on the function and morphology of pituitary corticotrophs in clinically normal dogs.
  • In both groups, ACTH stimulation testing and corticotrophin-releasing hormone (CRH) stimulation testing were performed.
  • Magnetic resonance imaging (MRI) of the pituitary gland and brain was performed in mitotane treatment group dogs before and after administration of mitotane.
  • After CRH stimulation testing and MRI, dogs were euthanatized and the pituitary gland and adrenal glands were excised for gross and histologic examination.
  • RESULTS: ACTH concentrations in mitotane treatment group dogs were significantly higher than in the control group dogs following CRH stimulation.
  • Magnetic resonance imaging revealed that pituitary glands were significantly larger in treatment group dogs after administration of mitotane, compared with before administration.
  • Immunohistochemistry revealed hypertrophy of corticotrophs in pituitary glands of mitotane treatment group dogs.
  • In instances of corticotroph adenoma, hypertrophy of individual corticotrophs induced by mitotane may greatly facilitate enlargement of the pituitary gland and increases in ACTH secretion.
  • [MeSH-major] Adrenocorticotropic Hormone / metabolism. Corticotropin-Releasing Hormone / metabolism. Health. Mitotane / pharmacology. Pituitary Gland / drug effects. Pituitary Gland / metabolism

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  • (PMID = 16881851.001).
  • [ISSN] 0002-9645
  • [Journal-full-title] American journal of veterinary research
  • [ISO-abbreviation] Am. J. Vet. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 78E4J5IB5J / Mitotane; 9002-60-2 / Adrenocorticotropic Hormone; 9015-71-8 / Corticotropin-Releasing Hormone
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86. Tateno T, Izumiyama H, Doi M, Akashi T, Ohno K, Hirata Y: Defective expression of prohormone convertase 1/3 in silent corticotroph adenoma. Endocr J; 2007 Dec;54(5):777-82
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  • [Title] Defective expression of prohormone convertase 1/3 in silent corticotroph adenoma.
  • Silent corticotroph adenoma (SCA) is defined as an ACTH-producing pituitary tumor not associated with clinical and endocrine feartures of Cushing's syndrome, but its underlying molecular mechanism(s) remains unknown thus far.
  • We tested the hypothesis that reduced expression of prohormone convertase (PC) 1/3 responsible for proteolytic processing of proopiomelanocortin (POMC) in SCA may lead to production of unprocessed, biologically inactive POMC and/or precursor of ACTH.
  • Among 30 non-functioning pituitary macroadenomas (NFA) examined, we found 6 SCAs by immunohistochemical study using anti-ACTH antibody.
  • Preoperative endocrine and diagnostic image tests did not reveal any differences between SCA and the remaining NFA except for the higher recurrence rate of SCA.
  • Our data suggest that defective PC1/3 expression may lead to preferential production of unprocessed, biologically inactive ACTH variants in SCA.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / genetics. Adenoma / genetics. Proprotein Convertase 1 / genetics

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  • (PMID = 17917309.001).
  • [ISSN] 1348-4540
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Protein Isoforms; 66796-54-1 / Pro-Opiomelanocortin; 9002-60-2 / Adrenocorticotropic Hormone; EC 3.4.21.93 / Proprotein Convertase 1
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87. Pecori Giraldi F, Andrioli M, De Marinis L, Bianchi A, Giampietro A, De Martin M, Sacco E, Scacchi M, Pontecorvi A, Cavagnini F: Significant GH deficiency after long-term cure by surgery in adult patients with Cushing's disease. Eur J Endocrinol; 2007 Feb;156(2):233-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Significant GH deficiency after long-term cure by surgery in adult patients with Cushing's disease.
  • OBJECTIVE: Impaired GH secretion usually accompanies Cushing's syndrome and a variable proportion of patients reportedly fail to recover normal GH secretion after successful treatment.
  • The aim of the present study is to evaluate GH secretory status after long-term cure of Cushing's disease achieved by surgery alone.
  • DESIGN AND METHODS: We studied 34 patients (27 females and 7 males, age range 21-68 years) formerly affected by Cushing's disease.
  • Patients were studied 2-20 years (median 3.3 years) following remission of hypercortisolism; all patients underwent transsphenoidal surgery with the removal of an ACTH-secreting adenoma; repeat pituitary surgery for relapse was performed in two patients while bilateral adrenalectomy was necessary in two patients.
  • CONCLUSIONS: This study demonstrates the presence of GH deficiency in a high percentage of patients with Cushing's disease after long-term remission of hypercortisolism obtained by surgery alone.
  • This finding is significant as it highlights that even the most favourable therapeutical course, i.e. remission achieved by surgery alone, is accompanied by impaired GH secretion.
  • Assessment of GH secretion is therefore recommended for all patients cured from Cushing's disease, even if not submitted to radiotherapy.
  • Studies on the clinical impact of GH deficiency and the use of GH replacement therapy seem warranted in patients cured from Cushing's disease.

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  • (PMID = 17287413.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I; 9034-39-3 / Growth Hormone-Releasing Hormone; 94ZLA3W45F / Arginine
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88. Raitila A, Georgitsi M, Karhu A, Tuppurainen K, Mäkinen MJ, Birkenkamp-Demtröder K, Salmenkivi K, Orntoft TF, Arola J, Launonen V, Vahteristo P, Aaltonen LA: No evidence of somatic aryl hydrocarbon receptor interacting protein mutations in sporadic endocrine neoplasia. Endocr Relat Cancer; 2007 Sep;14(3):901-6
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  • Germline mutations in the aryl hydrocarbon receptor interacting protein (AIP) gene were recently observed in patients with pituitary adenoma predisposition (PAP).
  • Though AIP mutation-positive individuals with prolactin-, mixed growth hormone/prolactin-, and ACTH-producing pituitary adenomas as well as non-secreting pituitary adenomas have been reported, most mutation-positive patients have had growth hormone-producing adenomas diagnosed at relatively young age.
  • Pituitary adenomas are also component tumors of some familial endocrine neoplasia syndromes such as multiple endocrine neoplasia type 1 (MEN1) and Carney complex (CNC).
  • Genes underlying MEN1 and CNC are rarely mutated in sporadic pituitary adenomas, but more often in other lesions contributing to these two syndromes.
  • Thus far, the occurrence of somatic AIP mutations has not been studied in endocrine tumors other than pituitary adenomas.
  • Here, we have analyzed 32 pituitary adenomas and 79 other tumors of the endocrine system for somatic AIP mutations by direct sequencing.
  • However, two out of nine patients with prolactin-producing adenoma were shown to harbor a Finnish founder mutation (Q14X) with a complete loss of the wild-type allele in the tumors.
  • These results are in agreement with previous studies in that prolactin-producing adenomas are component tumors in PAP.
  • The data also support the previous finding that somatic AIP mutations are not common in pituitary adenomas and suggest that such mutations are rare in other endocrine tumors as well.
  • [MeSH-major] Adenoma / genetics. Carcinoma / genetics. Endocrine Gland Neoplasms / genetics. Mutation. Proteins / genetics

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  • (PMID = 17914118.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / Proteins; 0 / aryl hydrocarbon receptor-interacting protein
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89. Thodou E, Argyrakos T, Kontogeorgos G: Galectin-3 as a marker distinguishing functioning from silent corticotroph adenomas. Hormones (Athens); 2007 Jul-Sep;6(3):227-32
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  • [Title] Galectin-3 as a marker distinguishing functioning from silent corticotroph adenomas.
  • OBJECTIVE: Galectin-3 (Gal-3) belongs to the family of carbohydrate-binding proteins with high affinity for galactoside and is involved in many biological processes including cell growth and differentiation, cell adhesion, tumor progression, apoptosis and metastasis.
  • The aim of this study was to disclose differences in the expression of Gal-3 in silent and functioning corticotroph pituitary adenomas.
  • DESIGN: We examined 30 pituitary adenomas (19 functioning corticotroph, 11 silent corticotroph adenomas).
  • Two prolactinomas and 2 functioning somatotroph adenomas served as positive controls.
  • The independent variables t-test was used for comparison of the mean expression of Gal-3 in the two different corticotroph adenoma subgroups.
  • RESULTS: Eighteen of the functioning corticotroph adenomas (94.73%) were positive for Gal-3 with a cytoplasmic and focally membranous distribution; two cases also exhibited nuclear expression, whereas 9 of the silent corticotroph adenomas (81.81%) had zero or<1% expression of Gal-3 (p=0.001).
  • CONCLUSIONS: Gal-3 is highly expressed in functioning corticotroph adenomas of the pituitary gland, while silent adenomas exhibit very focal to null expression of Gal-3.
  • This observation can be used in the pathological diagnosis to separate functioning from silent corticotroph adenomas of the pituitary.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / diagnosis. Adenoma / diagnosis. Biomarkers, Tumor / metabolism. Galectin 3 / metabolism
  • [MeSH-minor] Humans. Immunohistochemistry. Pituitary Gland / metabolism

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  • (PMID = 17724007.001).
  • [ISSN] 1109-3099
  • [Journal-full-title] Hormones (Athens, Greece)
  • [ISO-abbreviation] Hormones (Athens)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Galectin 3
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90. Pawlikowski M, Gruszka A, Kurnatowska I, Winczyk K, Kunert-Radek J, Radek A: Proliferating cell nuclear antigen (PCNA) expression in pituitary adenomas: relationship to the endocrine phenotype of adenoma. Folia Histochem Cytobiol; 2006;44(1):37-41
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  • [Title] Proliferating cell nuclear antigen (PCNA) expression in pituitary adenomas: relationship to the endocrine phenotype of adenoma.
  • The expression of proliferating cell nuclear antigen (PCNA) correlates to cell proliferation and for this reason it is commonly considered as one of proliferation markers.
  • Since proliferation rate is an important factor determining the tumor aggressiveness, the evaluation of PCNA index (the percentage of PCNA-immunopositive nuclei in the investigated tumor sample) is suggested as useful in predicting pituitary adenoma outcome.
  • Seventy three unselected, surgically removed pituitary adenomas were immunostained with antibodies against the pituitary hormones or their subunits and against the proliferating cell nuclear antigen (PCNA).
  • The highest PCNA index was found in ACTH-immunopositive tumors without the manifestation of the Cushing's disease ("silent" corticotropinomas).
  • This value was significantly different in comparison to other adenoma subtypes including corticotropinomas manifesting themselves by Cushing's disease.
  • The lowest PCNA index was noticed in monohormonal GH-secreting tumors.
  • The adenomas which express more than one hormone (plurihormonal adenomas) seem to have a higher PCNA indices than monohormonal ones; the difference was significant in the case of mono- and plurihormonal prolactinomas.
  • These findings suggest that the proliferative potential of pituitary adenomas is related to the tumor recurrence and hormone expression.

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  • (PMID = 16584090.001).
  • [ISSN] 0239-8508
  • [Journal-full-title] Folia histochemica et cytobiologica
  • [ISO-abbreviation] Folia Histochem. Cytobiol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Follicle Stimulating Hormone, Human; 0 / Gonadotropins; 0 / Proliferating Cell Nuclear Antigen; 9002-60-2 / Adrenocorticotropic Hormone; 9002-62-4 / Prolactin; 9002-67-9 / Luteinizing Hormone
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91. Sahdev A, Reznek RH, Evanson J, Grossman AB: Imaging in Cushing's syndrome. Arq Bras Endocrinol Metabol; 2007 Nov;51(8):1319-28
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  • [Title] Imaging in Cushing's syndrome.
  • Once the diagnosis of Cushing's syndrome (CS) has been established, the main step is to differentiate between ACTH dependent and independent disease.
  • In adults, 80% of CS is due to ACTH-dependent causes and 20% due to adrenal causes.
  • ACTH-secreting neoplasms cause ACTH-dependent CS.
  • These are usually anterior pituitary microadenomas, which result in the classic Cushing's disease.
  • Non-pituitary ectopic sources of ACTH, such as a small-cell lung carcinoma or carcinoid tumours, are the source of the remainder of ACTH-dependent disease.
  • Imaging is essential for determining the source of ACTH in ectopic ACTH production, locating the pituitary tumours and distinguishing adrenal adenomas, carcinomas and hyperplasias.
  • In our chapter we review the adrenal appearances in ACTH-dependent and ACTH-independent CS.
  • We also include a discussion on the use of MRI and CT for the detection and management of pituitary ACTH secreting adenomas.
  • CT of the chest, abdomen and pelvis with intravenous injection of contrast medium is the most sensitive imaging modality for the identification of the ectopic ACTH source and detecting adrenal pathology.
  • MRI is used for characterising adrenal adenomas, problem solving in difficult cases and for detecting ACTH-secreting pituitary adenomas.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / diagnosis. Cushing Syndrome / diagnosis. Pituitary Gland / pathology. Pituitary Neoplasms / diagnosis
  • [MeSH-minor] ACTH Syndrome, Ectopic / diagnosis. Adenoma / diagnosis. Adenoma / radiography. Adrenal Gland Neoplasms / diagnosis. Adrenal Gland Neoplasms / radiography. Carcinoma / diagnosis. Carcinoma / radiography. Humans. Hyperplasia / diagnosis. Hyperplasia / radiography. Lung Neoplasms / diagnosis. Lung Neoplasms / secretion. Magnetic Resonance Imaging. Tomography, X-Ray Computed

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  • (PMID = 18209870.001).
  • [ISSN] 0004-2730
  • [Journal-full-title] Arquivos brasileiros de endocrinologia e metabologia
  • [ISO-abbreviation] Arq Bras Endocrinol Metabol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Brazil
  • [Number-of-references] 36
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92. Hernández I, Espinosa-de-los-Monteros AL, Mendoza V, Cheng S, Molina M, Sosa E, Mercado M: Ectopic ACTH-secreting syndrome: a single center experience report with a high prevalence of occult tumor. Arch Med Res; 2006 Nov;37(8):976-80
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  • [Title] Ectopic ACTH-secreting syndrome: a single center experience report with a high prevalence of occult tumor.
  • BACKGROUND: Differentiation between the two forms of ACTH-dependent Cushing's syndrome is a challenging task.
  • Although the majority of these cases will be diagnosed as Cushing's disease secondary to an ACTH-secreting pituitary adenoma, 10-15% result from the ectopic ACTH secretion syndrome (EAS), which is usually due to neuroendocrine tumors.
  • The latter included a standard biochemical assessment (urinary free cortisol, low- and high-dose dexamethasone suppression tests), petrosal sinus sampling when indicated and imaging techniques such as pituitary MRI, total body CT and somatostatin receptor scintigraphy.
  • RESULTS: The ectopic nature of the ACTH hypersecretion was confirmed with inferior petrosal sinus samplings in all cases.
  • CT scanning localized a putative tumor in 6/8 patients, whereas octreotide scintigraphy was positive in only five.
  • However, upon performing thoracotomy, a documented ACTH-secreting bronchial carcinoid tumor was found in only four patients.
  • CONCLUSIONS: EAS is a rare cause of ACTH-dependent Cushing's syndrome.
  • [MeSH-major] ACTH Syndrome, Ectopic / diagnosis. ACTH-Secreting Pituitary Adenoma / diagnosis. Adenoma / diagnosis. Adenoma / therapy
  • [MeSH-minor] Adrenalectomy. Cushing Syndrome / diagnosis. Diagnosis, Differential. Female. Humans. Magnetic Resonance Imaging. Male. Tomography, X-Ray Computed. Treatment Outcome

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  • (PMID = 17045113.001).
  • [ISSN] 0188-4409
  • [Journal-full-title] Archives of medical research
  • [ISO-abbreviation] Arch. Med. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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93. Hanson JM, Mol JA, Leegwater PA, Bilodeau S, Drouin J, Meij BP: Expression and mutation analysis of Tpit in the canine pituitary gland and corticotroph adenomas. Domest Anim Endocrinol; 2008 Apr;34(3):217-22
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  • [Title] Expression and mutation analysis of Tpit in the canine pituitary gland and corticotroph adenomas.
  • Pituitary-dependent hyperadrenocorticism (PDH) in dogs is caused by a pituitary corticotroph adenoma.
  • Although PDH is a common disorder in dogs, little is known about the underlying pathogenesis.
  • In the pituitary glands of humans and mice, the pro-opiomelanocortin (POMC)-expressing cell lineages, the corticotrophs and melanotrophs, have a specific marker in common, the T-box transcription factor Tpit (Tbx19), which is obligate for POMC expression.
  • Tpit also regulates the late differentiation of the corticotrophs and melanotrophs, and therefore may contribute to the pathogenesis of the corticotroph adenomas.
  • The aim of this study was to perform an expression and mutation analysis of Tpit in the normal canine pituitary and in corticotroph adenomas.
  • The distribution of the Tpit protein in the pituitary gland was studied with immunohistochemistry and the expression of the gene with RT-PCR.
  • Tpit was expressed in corticotroph and melanotroph cells of the normal and adenomatous canine pituitary, and remained present in non-adenomatous corticotrophs of pituitaries from PDH dogs.
  • No tumor-specific mutation in the Tpit cDNA from the corticotroph adenomas was found.
  • It is concluded that Tpit can be used as a reliable marker for the corticotroph and melanotroph cells in the canine pituitary tissue and that mutations in the Tpit gene are unlikely to play a major role in the pathogenesis of canine corticotroph adenomas.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / veterinary. Adenoma / veterinary. Dog Diseases / genetics. Pituitary Gland / chemistry. Pituitary Neoplasms / veterinary. T-Box Domain Proteins / genetics

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  • (PMID = 17544240.001).
  • [ISSN] 0739-7240
  • [Journal-full-title] Domestic animal endocrinology
  • [ISO-abbreviation] Domest. Anim. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / T-Box Domain Proteins; 9007-49-2 / DNA
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94. Alarifi A, Alzahrani AS, Salam SA, Ahmed M, Kanaan I: Repeated remissions of Cushing's disease due to recurrent infarctions of an ACTH-producing pituitary macroadenoma. Pituitary; 2005;8(2):81-7
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  • [Title] Repeated remissions of Cushing's disease due to recurrent infarctions of an ACTH-producing pituitary macroadenoma.
  • Infarction of prolactin-secreting or growth hormone-secreting pituitary adenomas is not unusual.
  • However, Infarction of ACTH-secreting adenomas has rarely been reported.
  • Cyclical course of Cushing's syndrome alternating with adrenal insufficiency due to recurrent infarction of an ACTH-secreting pituitary adenoma has not been reported.
  • We report here a 20-year-old lady who presented with florid signs of Cushing's syndrome but was found to have adrenal insufficiency on biochemical evaluation.
  • Magnetic resonance imaging (MRI) of the pituitary gland showed that she had infarction of an ACTH-secreting macroadenoma.
  • Over the next 6 years, her disease ran a cyclical course characterized by periods of hypercortisolism alternating with adrenal insufficiency due to repeated episodes of infarctions of the ACTH-secreting pituitary macroadenoma with corresponding changes in the pituitary adenoma on serial MRIs.
  • The case alerts clinicians to this possibility when a patient presents with clinical picture of Cushing's syndrome but has adrenal insufficiency on biochemical testing.
  • It also suggests that silent or subclinical infarction of pituitary adenomas is not uncommon and is probably under diagnosed.
  • [MeSH-major] Adenoma / blood supply. Adrenocorticotropic Hormone / secretion. Infarction / physiopathology. Pituitary ACTH Hypersecretion / physiopathology. Pituitary Neoplasms / blood supply

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  • (PMID = 16195779.001).
  • [ISSN] 1386-341X
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
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95. Cooper O, Ben-Shlomo A, Bonert V, Bannykh S, Mirocha J, Melmed S: Silent corticogonadotroph adenomas: clinical and cellular characteristics and long-term outcomes. Horm Cancer; 2010 Apr;1(2):80-92
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  • [Title] Silent corticogonadotroph adenomas: clinical and cellular characteristics and long-term outcomes.
  • Silent corticotrophins adenomas (SCAs) are clinically silent and non-secreting but immunostain positively for ACTH.
  • We hypothesize that SCAs comprise both corticotroph and gonadotroph characteristics.
  • We compared preoperative and postoperative clinical results and tumor cytogenesis in 25 SCAs and 84 nonfunctioning adenomas in 109 consecutive patients diagnosed pre-operatively with nonfunctioning pituitary adenomas.
  • Pathologic outcomes were expression of relevant pituitary hormones, tissue-specific transcription factors, and electron microscopy features.
  • Preoperative SCA presentation was similar to that observed for nonfunctioning adenomas.
  • However, SCAs recurred postoperatively at a median of 3 years vs. 8 years for nonfunctioning adenomas (p<0.0001).
  • Fifty-four percent of patients with SCAs had new onset postoperative hypopituitarism vs. 17% of nonfunctioning adenomas (p<0.025).
  • SCAs (n=18) were immunopositive for ACTH, cytoplasmic and nuclear SF-1, NeuroD1, DAX-1, and alpha-gonadotropin subunit, but Tpit negative, and co-expression of tumor ACTH with either SF-1 or LH was detected.
  • In contrast, functional corticotroph adenomas (n=11) were immunopositive for ACTH, nuclear SF-1, NeuroD1, and Tpit, but negative for DAX-1, a gonadotroph cell transcription factor.
  • Gonadotroph adenomas (n=23) were immunonegative for ACTH and Tpit but positive for nuclear SF-1, NeuroD1, and DAX-1.
  • SCA electron microscopy demonstrated ultrastructural features consistent with corticotroph and gonadotroph cells.
  • As SCAs exhibit features consistent with both corticotroph and gonadotroph cytologic origin, we propose a pathologic and clinically distinct classification of SCAs as silent corticogonadotroph adenomas.

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  • (PMID = 20717480.001).
  • [ISSN] 1868-8500
  • [Journal-full-title] Hormones & cancer
  • [ISO-abbreviation] Horm Cancer
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / T32 DK007770-08; United States / NCI NIH HHS / CA / R01 CA075979-08; United States / NIDDK NIH HHS / DK / T32 DK007770; United States / NIDDK NIH HHS / DK / T32 DK07770; United States / NIDDK NIH HHS / DK / DK007770-08; United States / NCI NIH HHS / CA / CA 075979; United States / NCI NIH HHS / CA / R01 CA075979; United States / NCI NIH HHS / CA / CA075979-08
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gonadotropins
  • [Keywords] NOTNLM ; Corticotroph adenoma / Gonadotroph adenoma / Nonfunctioning adenoma / Pituitary adenoma
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96. Teshima T, Hara Y, Takekoshi S, Nezu Y, Harada Y, Yogo T, Teramoto A, Osamura RY, Tagawa M: Trilostane-induced inhibition of cortisol secretion results in reduced negative feedback at the hypothalamic-pituitary axis. Domest Anim Endocrinol; 2009 Jan;36(1):32-44
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Trilostane-induced inhibition of cortisol secretion results in reduced negative feedback at the hypothalamic-pituitary axis.
  • Cushing's disease caused by pituitary corticotroph adenoma in dogs is usually treated by medical treatment, and the efficacy of this treatment has been reported.
  • The purpose of this study was to investigate the effect of reduced negative feedback through the inhibition of cortisol secretion by daily trilostane administration on the pituitary-adrenal axis in clinically normal dogs.
  • After the initiation of trilostane administration, plasma adrenocorticotropic hormone (ACTH) concentrations were increased remarkably.
  • As assessed by magnetic resonance imaging (MRI) during administration, the pituitary became enlarged.
  • After trilostane administration, the cytoplasmic areas of the pituitary corticotrophs were increased and the ratio of pituitary corticotrophs to all cells in the anterior lobe was greater in the trilostane-treated dogs than that in untreated animals.
  • Using real-time PCR quantification, the expression of proopiomelanocortin (POMC) mRNA in the pituitary and ACTH receptor (ACTH-R) mRNA in the adrenal gland was greater in the dogs treated with trilostane than in untreated dogs.
  • These results indicate that reduced negative feedback induced hyperfunction of the pituitary corticotrophs and pituitary enlargement in healthy dogs.
  • These changes suggest that the inhibition of cortisol secretion by trilostane may increase the risk for accelerating the growth of corticotroph adenomas in dogs with Cushing's disease.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Dihydrotestosterone / analogs & derivatives. Dogs. Hydrocortisone / antagonists & inhibitors. Hypothalamus / drug effects. Pituitary Gland / drug effects
  • [MeSH-minor] Adrenal Glands / chemistry. Adrenal Glands / drug effects. Adrenal Glands / pathology. Adrenocorticotropic Hormone / blood. Animals. Corticotrophs / drug effects. Corticotrophs / ultrastructure. Feedback, Physiological / drug effects. Female. Hyperplasia. Magnetic Resonance Imaging. Male. Pro-Opiomelanocortin / genetics. RNA, Messenger / analysis. Receptors, Corticotropin / genetics

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  • (PMID = 19041802.001).
  • [ISSN] 1879-0054
  • [Journal-full-title] Domestic animal endocrinology
  • [ISO-abbreviation] Domest. Anim. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / RNA, Messenger; 0 / Receptors, Corticotropin; 08J2K08A3Y / Dihydrotestosterone; 66796-54-1 / Pro-Opiomelanocortin; 9002-60-2 / Adrenocorticotropic Hormone; L0FPV48Q5R / trilostane; WI4X0X7BPJ / Hydrocortisone
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97. Parenti G, Nassi R, Silvestri S, Bianchi S, Valeri A, Manca G, Mangiafico S, Ammannati F, Serio M, Mannelli M, Peri A: Multi-step approach in a complex case of Cushing's syndrome and medullary thyroid carcinoma. J Endocrinol Invest; 2006 Feb;29(2):177-81
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Multi-step approach in a complex case of Cushing's syndrome and medullary thyroid carcinoma.
  • The diagnosis of Cushing's syndrome (CS) may sometimes be cumbersome.
  • In particular, in ACTH-dependent CS it may be difficult to distinguish between the presence of an ACTH-secreting pituitary adenoma and ectopic ACTH and/or CRH secretion.
  • We report here the case of a 54-yr-old man affected by ACTH-dependent CS in association with a left adrenal adenoma and medullary thyroid carcinoma (MTC).
  • It was then decided to remove the left adenomatous adrenal gland.
  • This case well depicts the complexity of the diagnostic workout, which is needed sometimes to correctly diagnose and treat CS, and suggests that monolateral adrenalectomy may represent, at least temporarily, a reasonable therapeutic option in occult ACTH-dependent hypercortisolism.
  • [MeSH-major] Carcinoma, Medullary / diagnosis. Cushing Syndrome / diagnosis. Thyroid Neoplasms / diagnosis

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  • (PMID = 16610247.001).
  • [ISSN] 0391-4097
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 9007-12-9 / Calcitonin
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98. Pecori Giraldi F, Scaroni C, Arvat E, Martin M, Giordano R, Albiger N, Leao AA, Picu A, Mantero F, Cavagnini F: Effect of protracted treatment with rosiglitazone, a PPARgamma agonist, in patients with Cushing's disease. Clin Endocrinol (Oxf); 2006 Feb;64(2):219-24
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of protracted treatment with rosiglitazone, a PPARgamma agonist, in patients with Cushing's disease.
  • OBJECTIVE: Cushing's disease, hypercortisolism due to a pituitary ACTH-secreting tumour, is a highly morbid illness as yet without effective medical therapy.
  • Recent studies have demonstrated that peroxisome proliferator-activated receptor gamma (PPARgamma) agonists effectively suppress ACTH secretion in a murine tumoral corticotroph cell line, but the few studies conducted so far in patients with ACTH-secreting pituitary adenomas have yielded variable results.
  • DESIGN: Ten patients with Cushing's disease were treated with 4-16 mg rosiglitazone p.o. daily for 1-8 months (median 3 months) and plasma ACTH and cortisol, urinary free cortisol (UFC), as well as para