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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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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. 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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3. Vilar L, Naves LA, Azevedo MF, Arruda MJ, Arahata CM, Moura E Silva L, Agra R, Pontes L, Montenegro L, Albuquerque JL, Canadas V: Effectiveness of cabergoline in monotherapy and combined with ketoconazole in the management of Cushing's disease. Pituitary; 2010 Jun;13(2):123-9
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  • [Title] Effectiveness of cabergoline in monotherapy and combined with ketoconazole in the management of Cushing's disease.
  • The expression of dopamine receptor subtypes has been reported in corticotroph adenomas, and this finding support the possibility for medical treatment of Cushing's disease (CD) with dopamine agonists when conventional treatment has failed.
  • In the remaining patients UFC levels did not normalize but a significant reduction ranging from to 44.4 to 51.7% was achieved.
  • Moreover, the addition of relatively low doses of ketoconazole led to normalization of UFC in about two-thirds of patients not achieving a full response to cabergoline.
  • [MeSH-major] Ergolines / therapeutic use. Ketoconazole / therapeutic use. Pituitary ACTH Hypersecretion / drug therapy

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  • (PMID = 19943118.001).
  • [ISSN] 1573-7403
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ergolines; LL60K9J05T / cabergoline; R9400W927I / Ketoconazole; WI4X0X7BPJ / Hydrocortisone
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4. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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5. 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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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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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  • [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. Tateno T, Kato M, Tani Y, Oyama K, Yamada S, Hirata Y: Differential expression of somatostatin and dopamine receptor subtype genes in adrenocorticotropin (ACTH)-secreting pituitary tumors and silent corticotroph adenomas. Endocr J; 2009;56(4):579-84
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  • [Title] Differential expression of somatostatin and dopamine receptor subtype genes in adrenocorticotropin (ACTH)-secreting pituitary tumors and silent corticotroph adenomas.
  • Somatostatin analogs and dopamine agonists are clinically used for medical therapy of functioning pituitary tumors, such as growth hormone- and prolactin-secreting tumors, however, their effects on ACTH-secreting tumors are controversial.
  • This study was aimed to determine whether somatostatin receptor (SSTR) subtype (1-5) and dopamine receptor type 2 (D2R) are differentially expressed in pituitary tumors causing Cushing's disease (CD), silent corticotroph adenoma (SCA), and non-functioning pituitary tumor (NFT).
  • Tissue specimens were obtained from 35 pituitary tumors during transsphenoidal surgery.
  • Both SSTR1 and 2 mRNA levels in SCA were greater than CD, while SSTR1 mRNA levels, but not SSTR2, in SCA were also greater than NFT.
  • SSTR5 mRNA levels in CD were greater than SCA, but did not differ between NFT and SCA.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / genetics. Adenoma / genetics. Pituitary ACTH Hypersecretion / metabolism. Pituitary Neoplasms / genetics. Receptors, Dopamine D2 / genetics. Receptors, Somatostatin / physiology

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  • (PMID = 19318729.001).
  • [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 / Receptors, Dopamine D2; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 0 / somatostatin receptor 5; 0 / somatostatin receptor type 1; 9002-60-2 / Adrenocorticotropic Hormone
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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. 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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15. Hofland LJ, van der Hoek J, Feelders R, van der Lely AJ, de Herder W, Lamberts SW: Pre-clinical and clinical experiences with novel somatostatin ligands: advantages, disadvantages and new prospects. J Endocrinol Invest; 2005;28(11 Suppl International):36-42
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  • GH-secreting pituitary adenomas preferentially express SSTR2 and SSTR5, prolactinomas SSTR1 and SSTR5, and corticotroph adenomas express SSTR2 (low number) and predominantly SSTR5s.
  • In patients with GEP neuroendocrine tumors, both somatostatin-analogs effectively suppress the production of bioactive peptides and hormones by the tumor cells, resulting in an important improvement of the related clinical symptomatology.
  • In vitro studies using human pituitary adenoma cells demonstrate a more profound inhibition of GH, PRL and ACTH secretion by somatostatin-analogs targeting both SSTR2s and SSTR5s, compared with SSTR2-preferential somatostatin-analogs.
  • This likely reflects the SSTR subtype expression pattern in the adenoma cells.
  • [MeSH-minor] Acromegaly / drug therapy. Adenoma / drug therapy. Animals. Carcinoma, Neuroendocrine / drug therapy. Endocrine Gland Neoplasms / drug therapy. Gene Expression. Humans. Ligands. Neurosecretory Systems. Pituitary ACTH Hypersecretion / drug therapy. Pituitary Neoplasms / drug therapy. Receptors, Somatostatin / drug effects. Receptors, Somatostatin / genetics. Receptors, Somatostatin / physiology

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  • (PMID = 16625843.001).
  • [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 / Ligands; 0 / Receptors, Somatostatin; 51110-01-1 / Somatostatin
  • [Number-of-references] 40
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16. 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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17. de Bruin C, Meij BP, Kooistra HS, Hanson JM, Lamberts SW, Hofland LJ: Cushing's disease in dogs and humans. Horm Res; 2009 Jan;71 Suppl 1:140-3
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  • [Title] Cushing's disease in dogs and humans.
  • BACKGROUND: Cushing's disease (CD) is a common endocrinological disorder in dogs with an estimated incidence of 1 to 2 cases/1,000 dogs/year.
  • Canine CD may therefore serve as an animal model for human CD, especially since therapeutic canine hypophysectomy can generate substantial amounts of primary corticotroph adenoma tissue for in vitro research purposes.
  • In a recent study, we found that dopamine (DA) D(2) and somatostatin (SS) receptor subtypes are well expressed in canine corticotroph adenomas, but there are some distinct differences compared with the expression profile observed in human CD.
  • CASE REPORT: This case involves an 8-year-old female dog that developed signs of exercise intolerance, muscle weakness and polyuria/polydipsia due to an adrenocorticotropic hormone-secreting pituitary adenoma.
  • [MeSH-major] Dog Diseases / radiography. Pituitary ACTH Hypersecretion / radiography. Pituitary ACTH Hypersecretion / veterinary

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  • [Copyright] Copyright 2009 S. Karger AG, Basel.
  • (PMID = 19153526.001).
  • [ISSN] 1423-0046
  • [Journal-full-title] Hormone research
  • [ISO-abbreviation] Horm. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
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18. 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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19. 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
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20. Banasiak MJ, Malek AR: Nelson syndrome: comprehensive review of pathophysiology, diagnosis, and management. Neurosurg Focus; 2007;23(3):E13
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  • [Title] Nelson syndrome: comprehensive review of pathophysiology, diagnosis, and management.
  • Nelson syndrome (NS) is a rare clinical manifestation of an enlarging pituitary adenoma that can occur following bilateral adrenal gland removal performed for the treatment of Cushing disease.
  • It is characterized by excess adreno-corticotropin secretion and hyperpigmentation of the skin and mucus membranes.
  • The authors present a comprehensive review of the pathophysiology, diagnosis, and management of NS.
  • Corticotroph adenomas in NS remain challenging tumors that can lead to significant rates of morbidity and mortality.
  • Although the primary treatment for each tumor type may vary, it is important to consider all of the available options and select the one that is most appropriate for the individual case, particularly in cases of lesions resistant to intervention.


21. Villa C, Magri F, Morbini P, Falchetti A, Scagnelli P, Lovati E, Locatelli D, Canevari FR, Necchi V, Gabellieri E, Guabello G, Chiovato L, Solcia E: Silent familial isolated pituitary adenomas: histopathological and clinical case report. Endocr Pathol; 2008;19(1):40-6
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  • [Title] Silent familial isolated pituitary adenomas: histopathological and clinical case report.
  • Familial isolated pituitary adenoma (FIPA) is a rare condition independent of Carney Complex or MEN1.
  • An international multicenter study recently described 28 nonfunctioning pituitary adenomas in 26 families with only two homogeneous nonsecreting phenotype families consistent of silent GH and silent gonadotroph adenomas, respectively.
  • We present the clinical, genetic, and morphological analysis of two silent pituitary adenomas occurring in a man and his daughter, and discuss the differential diagnosis associated with their histological, immunohistochemical, and ultrastructural features.
  • Tissue samples obtained after paraseptal trans-sphenoidal surgery were studied by immunohistochemistry for adenohypophyseal hormones, low molecular weight cytokeratins (CAM 5.2), proliferation markers, and anterior pituitary transcription factors (Pit-1 and SF-1) and by electron microscopy for secretory granules.
  • The clinical, histological, and immunohistochemical features of the lesions posed a differential diagnosis between a null cell adenoma and a silent corticotroph adenoma (Type II); on the basis of immunohistochemical stains for cytokeratin and adenohypophysis cell lineage markers, tumor behavior and ultrastructural studies we concluded for the second.
  • The reported cases represent an as yet undescribed example of homogeneous family with silent corticotroph adenomas (Type II).
  • Our observations support the trend for more aggressive behavior in nonsecreting FIPAs as compared with sporadic adenomas.
  • [MeSH-major] Adenoma / genetics. Multiple Endocrine Neoplasia Type 1 / genetics. Pituitary Neoplasms / genetics
  • [MeSH-minor] Aged. DNA, Neoplasm / genetics. Humans. Immunohistochemistry. Ki-67 Antigen / analysis. Male. Mutation. Pedigree

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  • (PMID = 18317953.001).
  • [ISSN] 1559-0097
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Ki-67 Antigen
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22. 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


23. Chacko G, Chacko AG, Lombardero M, Mani S, Seshadri MS, Kovacs K, Scheithauer BW: Clinicopathologic correlates of giant pituitary adenomas. J Clin Neurosci; 2009 May;16(5):660-5
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  • [Title] Clinicopathologic correlates of giant pituitary adenomas.
  • Giant adenomas comprise a clinical/therapeutic subset of pituitary adenomas that pose a surgical challenge.
  • The study population consisted of 28 patients who had giant pituitary adenomas, which are defined as tumors with a diameter greater than 5cm.
  • Clinically, five tumors (18%) were endocrinologically functional and 23 (82%) were not.
  • During surgery, one tumor was radically excised, four were subtotally excised, 12 were partially excised, and 11 were biopsied.
  • All of the tumors showed typical histological features of pituitary adenoma.
  • Of the 23 clinically non-functional adenomas, 18 were gonadotrophic tumors, four were null cell adenomas and one was a silent corticotroph adenoma.
  • The present study found giant adenomas to be invasive but slow growing, histologically benign and often gonadotrophic in subtype.
  • [MeSH-major] Adenoma / pathology. Adenoma / therapy. Pituitary Neoplasms / pathology. Pituitary Neoplasms / therapy
  • [MeSH-minor] Adolescent. Adrenocorticotropic Hormone / metabolism. Adult. Antigens, CD34 / metabolism. Female. Follow-Up Studies. Humans. Ki-67 Antigen / metabolism. Magnetic Resonance Imaging / methods. Male. Middle Aged. Neoplasm Invasiveness. Retrospective Studies. Treatment Outcome. Young Adult

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  • (PMID = 19285407.001).
  • [ISSN] 0967-5868
  • [Journal-full-title] Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
  • [ISO-abbreviation] J Clin Neurosci
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Ki-67 Antigen; 9002-60-2 / Adrenocorticotropic Hormone
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24. 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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25. 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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26. 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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27. 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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28. Trapani F, Del Basso De Caro ML, Insabato L, Papparella S, Paciello O: Type II muscle fibers atrophy associated with silent corticotroph adenoma in a dog. Folia Histochem Cytobiol; 2010 Sep 30;48(3):403-6
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  • [Title] Type II muscle fibers atrophy associated with silent corticotroph adenoma in a dog.
  • The Silent Corticotroph Adenoma (SCA) is a pituitary adenoma variant characterized by the immunoreactivity for adrenocorticotropic hormone (ACTH) and related peptides, without the clinical signs of Cushing's disease.
  • SCA has been postulated to either secrete structurally abnormal ACTH that is inactive but detectable by immunohistochemistry or radioimmunoassay, or to secrete ACTH intermittently or at low levels continuously.
  • Excess of ACTH has been associated to type II muscle atrophy.
  • We describe a case of type II muscle fibers atrophy associated with silent corticotroph adenoma in a dog.
  • The tumour showed a trabecular growth pattern and immunohistochemical analysis demonstrated the presence of cytoplasmic immunoreactivity for ACTH.
  • The muscle atrophy was considered to be related to an excess of inactive ACTH.

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  • (PMID = 21071346.001).
  • [ISSN] 1897-5631
  • [Journal-full-title] Folia histochemica et cytobiologica
  • [ISO-abbreviation] Folia Histochem. Cytobiol.
  • [Language] ENG
  • [Publication-type] Case Reports; Comparative Study; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; EC 1.3.99.1 / Succinate Dehydrogenase; EC 1.6.- / NADH Tetrazolium Reductase
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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. 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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31. 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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32. Remick AK, Wood CE, Cann JA, Gee MK, Feiste EA, Kock ND, Cline JM: Histologic and immunohistochemical characterization of spontaneous pituitary adenomas in fourteen cynomolgus macaques (Macaca fascicularis). Vet Pathol; 2006 Jul;43(4):484-93
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  • [Title] Histologic and immunohistochemical characterization of spontaneous pituitary adenomas in fourteen cynomolgus macaques (Macaca fascicularis).
  • Pituitary adenomas were identified in 14 of 491 (2.9%) cynomolgus macaques evaluated from 1994 to 2004.
  • Seven of the pituitary adenomas caused gross enlargement of the pituitary gland that was visible on postmortem examination, whereas the remaining 7 were multifocal microadenomas identified on histologic examination.
  • A total of 35 adenomas were identified in the 14 macaques, 6 of which were being treated for diabetes mellitus.
  • Mean (+/- SD) pituitary weight was 0.31 +/- 0.42 g, compared with 0.07 +/- 0.02 g for 430 historical control animals (P < 0.0001).
  • Immunohistochemical staining for follicle-stimulating hormone, luteinizing hormone, prolactin, human growth hormone, thyroid-stimulating hormone, and adrenocorticotropic hormone was applied to pituitary tissue from all cases.
  • Immunostaining revealed 22 of 35 (62.9%) lactotroph adenomas, 5 of 35 (14.3%) plurihormonal cell adenomas, 3 of 35 (8.6%) corticotroph adenomas, 2 of 35 (5.7%) null cell adenomas, 1 of 35 (2.9%) somatotroph adenomas, 1 of 35 (2.9%) mixed corticotroph-somatotroph adenomas, 1 of 35 (2.9%) mixed lactotroph-corticotroph adenomas, 0 of 35 gonadotroph adenomas, and 0 of 35 thyrotroph adenomas.
  • This study represents the first extensive retrospective case series performed to evaluate the histologic and immunohistochemical characteristics of pituitary adenomas in cynomolgus macaques.
  • Our findings indicated that macaque pituitary adenomas frequently had mixed histologic appearance and hormone expression, and that, similar to human pituitary adenomas, prolactin-secreting neoplasms were the most prevalent type.
  • [MeSH-major] Macaca fascicularis. Monkey Diseases / pathology. Pituitary Neoplasms / veterinary. Prolactinoma / veterinary

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  • (PMID = 16846990.001).
  • [ISSN] 0300-9858
  • [Journal-full-title] Veterinary pathology
  • [ISO-abbreviation] Vet. Pathol.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / T32 RR07009
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 12629-01-5 / Human Growth Hormone; 9002-60-2 / Adrenocorticotropic Hormone; 9002-62-4 / Prolactin; 9002-67-9 / Luteinizing Hormone; 9002-68-0 / Follicle Stimulating Hormone; 9002-71-5 / Thyrotropin
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33. 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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34. 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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35. 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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36. 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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37. 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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38. 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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  • [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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39. 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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40. Hosoyama T, Nishijo K, Garcia MM, Schaffer BS, Ohshima-Hosoyama S, Prajapati SI, Davis MD, Grant WF, Scheithauer BW, Marks DL, Rubin BP, Keller C: A Postnatal Pax7 Progenitor Gives Rise to Pituitary Adenomas. Genes Cancer; 2010 Apr 1;1(4):388-402
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  • [Title] A Postnatal Pax7 Progenitor Gives Rise to Pituitary Adenomas.
  • Pituitary adenomas are classified into functioning and nonfunctioning (silent) tumors on the basis of hormone secretion.
  • However, the mechanism of tumorigenesis and the cell of origin for pituitary adenoma subtypes remain to be elucidated.
  • Employing a tamoxifen-inducible mouse model, we demonstrate that a novel postnatal Pax7(+) progenitor cell population in the pituitary gland gives rise to silent corticotroph macro-adenomas when the retinoblastoma tumor suppressor is conditionally deleted.
  • While Pax transcriptional factors are critical for embryonic patterning as well as postnatal stem cell renewal for many organs, we have discovered that Pax7 marks a restricted cell population in the postnatal pituitary intermediate lobe.
  • This Pax7(+) early progenitor cell population is overlapping but ontologically downstream of the Nestin(+) pituitary stem cell population, yet upstream of another newly discovered Myf6(+) late progenitor cell population.
  • Interestingly, the Pax7(+) progenitor cell population is evolutionarily conserved in primates and humans, and Pax7 expression is maintained not only in murine tumors but also in human functioning and silent corticotropinomas.
  • Taken together, our results strongly suggest that human silent corticotroph adenomas may in fact arise from a Pax7 lineage of the intermediate lobe, a region of the human pituitary bearing closer scientific interest as a reservoir of pituitary progenitor cells.

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  • (PMID = 20811506.001).
  • [ISSN] 1947-6019
  • [Journal-full-title] Genes & cancer
  • [ISO-abbreviation] Genes Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA133229-03; United States / NCRR NIH HHS / RR / P41 RR012553; United States / NCI NIH HHS / CA / R01 CA133229
  • [Publication-type] JOURNAL ARTICLE
  • [Publication-country] United States
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41. 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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42. Al Brahim NY, Rambaldini G, Ezzat S, Asa SL: Complex endocrinopathies in MEN-1: diagnostic dilemmas in endocrine oncology. Endocr Pathol; 2007;18(1):37-41
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  • Patients with endocrine tumors often have delayed diagnosis because of the nonspecific and often subtle signs and symptoms.
  • In patients with multiple endocrine neoplasia syndromes, diagnosis and clinicopathologic correlations can be even more challenging.
  • We report a patient with multiple endocrine neoplasia type 1 (MEN-1) and a highly complex clinical story associated with multiple atypical lesions including two pituitary adenomas, a gonadotroph macroadenoma and a corticotroph microadenoma with Crooke's hyaline change and ectopic production of corticotropin-releasing hormone (CRH) from a thymic endocrine carcinoma.
  • This case illustrates a number of clinically relevant challenges, including the diagnosis of pituitary adenomas in MEN-1, the difficulty in diagnosing Cushing's disease, and the large differential of pituitary pathologies in this disorder, double pituitary adenomas and other decoy lesions in Cushing's disease, the pathophysiology of Crooke's hyaline change in the pituitary, and the various causes of Cushing's syndrome associated with MEN-1.
  • [MeSH-major] Multiple Endocrine Neoplasia Type 1 / pathology. Pituitary ACTH Hypersecretion / pathology. Pituitary Neoplasms / pathology. Thymus Neoplasms / pathology
  • [MeSH-minor] Humans. Hyalin / metabolism. Male. Middle Aged. Pituitary Gland / metabolism. Pituitary Gland / pathology. Treatment Outcome

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  • (PMID = 17652799.001).
  • [ISSN] 1046-3976
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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43. 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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44. 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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45. 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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46. 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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47. Meinardi JR, Wolffenbuttel BH, Dullaart RP: Cyclic Cushing's syndrome: a clinical challenge. Eur J Endocrinol; 2007 Sep;157(3):245-54
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  • [Title] Cyclic Cushing's syndrome: a clinical challenge.
  • Cyclic Cushing's syndrome (CS) is a rare disorder, characterized by repeated episodes of cortisol excess interspersed by periods of normal cortisol secretion.
  • Our review of 65 reported cases demonstrates that cyclic CS originates in 54% of cases from a pituitary corticotroph adenoma, in 26% from an ectopic ACTH-producing tumour and in about 11% from an adrenal tumour, the remainder being unclassified.
  • When cyclic CS is biochemically confirmed, further imaging and laboratory studies are guided by the presence or absence of ACTH dependency.
  • In cases of suspected ectopic ACTH production, specific biochemical testing for carcinoids or neuroendocrine tumours is required, including measurements of serotonin in platelets and/or urine, chromogranin A and calcitonin.

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  • (PMID = 17766705.001).
  • [ISSN] 0804-4643
  • [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] WI4X0X7BPJ / Hydrocortisone
  • [Number-of-references] 108
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48. 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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  • [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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49. 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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50. 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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51. 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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  • [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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52. Roccabianca P, Rondena M, Paltrinieri S, Pocacqua V, Scarpa P, Faverzani S, Scanziani E, Caniatti M: Multiple endocrine neoplasia type-I-like syndrome in two cats. Vet Pathol; 2006 May;43(3):345-52
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  • The MEN-1 syndrome is associated with menin gene mutations that induce various combinations of parathyroid, pituitary, and pancreatic endocrine tumors in humans.
  • Two male, Domestic Shorthair cats developed symmetric alopecia, insulin-resistant diabetes mellitus, and pituitary-dependent hyperadrenocorticism at 12 and 13 years of age.
  • Multiple invasive pancreatic beta cell carcinomas, pituitary corticotroph adenomas, and thyroid C-cell and parathyroid chief cell hyperplasia were diagnosed on the basis of results of gross, histologic, and immunohistochemical findings in both cats.
  • The combination of lesions observed was consistent with the diagnosis of MEN-1-like syndrome in both cats.

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  • (PMID = 16672581.001).
  • [ISSN] 0300-9858
  • [Journal-full-title] Veterinary pathology
  • [ISO-abbreviation] Vet. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Complementary; 0 / Proto-Oncogene Proteins
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53. 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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54. 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


55. 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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56. 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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57. Fazekas I, Hegedüs B, Bácsy E, Kerekes E, Slowik F, Balint K, Pásztor E: Characterization of human pituitary adenomas in cell cultures by light and electron microscopic morphology and immunolabeling. Folia Histochem Cytobiol; 2005;43(2):81-90
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  • [Title] Characterization of human pituitary adenomas in cell cultures by light and electron microscopic morphology and immunolabeling.
  • The morphology and hormone production of pituitary adenoma cell cultures were compared in order to highlight their characteristic in vitro features.
  • Cell suspensions were prepared from 494 surgical specimens.
  • The viability and detailed in vitro morphology of adenoma cells were found to be characteristic for the various types of pituitary tumors.
  • The sparsely granulated growth hormone, the corticotroph and the acidophil stem cell adenomas provided the highest ratio of viable cultures.
  • Both light microscopic and ultrastructural analyses proved that the primary cultures of adenoma cells retain their physiological features during in vitro cultivations.
  • These results prove that monolayer cultures of pituitary adenoma cells can contribute to the correct diagnosis and are valid model systems for various oncological and neuroendocrinological studies.

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  • (PMID = 16044945.001).
  • [ISSN] 0239-8508
  • [Journal-full-title] Folia histochemica et cytobiologica
  • [ISO-abbreviation] Folia Histochem. Cytobiol.
  • [Language] ENG
  • [Publication-type] Case Reports; Comparative Study; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 9002-62-4 / Prolactin; 9002-72-6 / Growth Hormone
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58. 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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59. 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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60. 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


61. 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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  • [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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62. Evang JA, Borota OC, Melum E, Holm R, Ramm-Pettersen J, Bollerslev J, Berg JP: HDAC2 expression and variable number of repeats in exon 1 of the HDAC2 gene in corticotroph adenomas. Clin Endocrinol (Oxf); 2010 Aug;73(2):229-35
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  • [Title] HDAC2 expression and variable number of repeats in exon 1 of the HDAC2 gene in corticotroph adenomas.
  • OBJECTIVES: Alterations in protein expression of histone deacetylase 2 (HDAC2) have been demonstrated in various neoplasms, and lack of nuclear expression of HDAC2 has previously been shown in some human and canine corticotroph adenomas.
  • This study aimed to examine HDAC2 expression in a Norwegian cohort of corticotroph adenomas, screen for exonic HDAC2 gene variants in the adenomas and correlate the results with clinical data.
  • PATIENTS AND DESIGN: Forty-four patients with verified Cushing's disease or Nelson's syndrome, positive ACTH staining and tissue available for immunohistochemistry and/or DNA sequencing were included.
  • RESULTS: Histone deacetylase 2 expression examined by immunohistochemistry was strongly reduced in 3/30 adenomas.
  • A previously unidentified insertion of three bases in a region coding for a polyserine cluster in exon 1 of the HDAC2 gene was identified in 6/32 adenomas.
  • The same insertion was also found in 28/94 of the controls (i.e., not significantly different from the patients).
  • CONCLUSIONS: Strongly reduced HDAC2 protein expression was confirmed in a small portion of corticotroph tumours.
  • Mutations in HDAC2 exons are unlikely to play an important role in the development of corticotroph adenomas.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / genetics. Adenoma / genetics. Histone Deacetylase 2 / genetics. Minisatellite Repeats

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  • (PMID = 20346000.001).
  • [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] EC 3.5.1.98 / HDAC2 protein, human; EC 3.5.1.98 / Histone Deacetylase 2
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63. 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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64. Teshima T, Hara Y, Shigihara K, Takekoshi S, Nezu Y, Harada Y, Yogo T, Teramoto A, Osamura RY, Tagawa M: Coexistence of corticotroph adenoma and thyrotroph hyperplasia in a dog. J Vet Med Sci; 2009 Jan;71(1):93-8
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  • [Title] Coexistence of corticotroph adenoma and thyrotroph hyperplasia in a dog.
  • Pituitary thyrotroph hyperplasia results from prolonged primary hypothyroidism in humans, mice and rats.
  • In dogs with Cushing's disease, many cases have low serum thyroid hormones concentrations due to euthyroid sick syndrome.
  • A 6-year-old castrated male Beagle diagnosed with Cushing's disease had a high serum thyroid stimulating hormone (TSH) concentration that was treated by hypophysectomy.
  • On histological examination, the resected pituitary gland contained both a corticotroph adenoma and thyrotroph hyperplasia.
  • The TSH-positive cell ratio in this case was greater than that of healthy Beagles.
  • In the present case, the pituitary thyrotroph hyperplasia was probably caused by primary hypothyroidism.
  • In conclusion, this Beagle is the first histological confirmation of the coexistence of a corticotroph adenoma and thyrotroph hyperplasia.

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  • (PMID = 19194082.001).
  • [ISSN] 0916-7250
  • [Journal-full-title] The Journal of veterinary medical science
  • [ISO-abbreviation] J. Vet. Med. Sci.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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65. 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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  • [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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66. 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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  • [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


67. Schaaf C, Shan B, Buchfelder M, Losa M, Kreutzer J, Rachinger W, Stalla GK, Schilling T, Arzt E, Perone MJ, Renner U: Curcumin acts as anti-tumorigenic and hormone-suppressive agent in murine and human pituitary tumour cells in vitro and in vivo. Endocr Relat Cancer; 2009 Dec;16(4):1339-50
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  • [Title] Curcumin acts as anti-tumorigenic and hormone-suppressive agent in murine and human pituitary tumour cells in vitro and in vivo.
  • Curcumin (diferuloylmethane) is the active ingredient of the spice plant Curcuma longa and has been shown to act anti-tumorigenic in different types of tumours.
  • Therefore, we have studied its effect in pituitary tumour cell lines and adenomas.
  • Proliferation of lactosomatotroph GH3 and somatotroph MtT/S rat pituitary cells as well as of corticotroph AtT20 mouse pituitary cells was inhibited by curcumin in monolayer cell culture and in colony formation assay in soft agar.
  • Fluorescence-activated cell sorting (FACS) analysis demonstrated curcumin-induced cell cycle arrest at G2/M.
  • Analysis of cell cycle proteins by immunoblotting showed reduction in cyclin D(1), cyclin-dependent kinase 4 and no change in p27(kip).
  • In endocrine pituitary tumour cell lines, GH, ACTH and prolactin production were inhibited by curcumin.
  • Studies in 25 human pituitary adenoma cell cultures have confirmed the anti-tumorigenic and hormone-suppressive effects of curcumin.
  • Altogether, the results described in this report suggest this natural compound as a good candidate for therapeutic use on pituitary tumours.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Curcumin / pharmacology. Pituitary Hormones / metabolism. Pituitary Neoplasms / drug therapy. Pituitary Neoplasms / pathology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Blotting, Western. Caspase 3 / metabolism. Cell Cycle / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Cyclin D1 / metabolism. Cyclin-Dependent Kinase 4 / metabolism. Flow Cytometry. Humans. Male. Mice. Mice, Nude. Rats

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  • (PMID = 19726538.001).
  • [ISSN] 1479-6821
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Pituitary Hormones; 136601-57-5 / Cyclin D1; EC 2.7.11.22 / Cyclin-Dependent Kinase 4; EC 3.4.22.- / Caspase 3; IT942ZTH98 / Curcumin
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68. 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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69. Kovacs K, Horvath E, Coire C, Cusimano M, Smyth H, Scheithauer BW, Lloyd RV: Pituitary corticotroph hyperplasia preceding adenoma in a patient with Nelson's syndrome. Clin Neuropathol; 2006 Mar-Apr;25(2):74-80
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  • [Title] Pituitary corticotroph hyperplasia preceding adenoma in a patient with Nelson's syndrome.
  • We report the case of a 42-year-old woman with Cushing's disease and Nelson's syndrome.
  • A detailed morphologic study demonstrated nodular hyperplasia of corticotroph cells but no adenoma.
  • Following a long-lasting remission (14 years), Cushing's disease recurred.
  • After an unsuccessful second transsphenoidal surgery, Cushing's disease persisted and both adrenals were removed (at the age of 34).
  • The pituitary tumor proved to be a corticotroph adenoma; it was removed by the transsphenoidal approach (at the age of 42).
  • Although in most patients Cushing's disease is due to an ACTH-secreting pituitary corticotroph adenoma which precedes the manifestation of Nelson's syndrome, our case indicates not only that corticotroph hyperplasia may cause Cushing's disease but that it may exist before the development of Nelson's syndrome after the removal of both adrenals.
  • Our study supports the view that protracted stimulation of corticotrophs resulting from the elimination of the negative inhibitory feedback effect by corticosteroids plays a role in adenoma initiation.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / etiology. Adenoma / etiology. Hyperplasia / complications. Nelson Syndrome / etiology. Pituitary ACTH Hypersecretion / complications

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  • (PMID = 16550740.001).
  • [ISSN] 0722-5091
  • [Journal-full-title] Clinical neuropathology
  • [ISO-abbreviation] Clin. Neuropathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
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70. 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.


71. Moyes VJ, Alusi G, Sabin HI, Evanson J, Berney DM, Kovacs K, Monson JP, Plowman PN, Drake WM: Treatment of Nelson's syndrome with temozolomide. Eur J Endocrinol; 2009 Jan;160(1):115-9
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  • A 64-year-old woman was previously treated for Cushing's disease with trans-sphenoidal surgery, external beam radiotherapy and bilateral adrenalectomy.
  • Progression of an aggressive corticotroph adenoma was evident 3 years post-adrenalectomy; involvement of the clivus was treated with surgery and gamma knife radiosurgery.
  • ACTH levels peaked at 2472 and 2265 pmol/l pre- and post-hydrocortisone respectively.
  • Treatment with temozolomide resulted in a significant improvement in symptoms, a reduction of plasma ACTH to 389 pmol/l and regression of tumour on magnetic resonance imaging scan after four cycles of treatment.

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  • (PMID = 18984772.001).
  • [ISSN] 1479-683X
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; 9002-60-2 / Adrenocorticotropic Hormone
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72. Bademci G: Pitfalls in the management of Cushing's disease. J Clin Neurosci; 2007 May;14(5):401-8; discussion 409
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  • [Title] Pitfalls in the management of Cushing's disease.
  • Cushing's disease is caused by functional corticotroph adenomas of the pituitary gland, most commonly noninvasive microadenomas.
  • Transsphenoidal microsurgery is an effective means of control for patients with adrenocorticotrophic hormone-producing microadenomas.
  • The major causes of surgical failure in the treatment of Cushing's disease lies in inadequate preoperative evaluation, unsuccessful identification of the adenoma and inexperience of the surgeon.
  • For optimal results in this rare disease, endocrinological, radiological and surgical procedures should be co-ordinated in a specialized center.
  • [MeSH-major] Pituitary ACTH Hypersecretion / therapy. Treatment Failure

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  • (PMID = 17386367.001).
  • [ISSN] 0967-5868
  • [Journal-full-title] Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
  • [ISO-abbreviation] J Clin Neurosci
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Scotland
  • [Number-of-references] 82
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73. 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
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 15
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74. Theodoropoulou M, Labeur M, Paez Pereda M, Haedo M, Perone MJ, Renner U, Arzt E, Stalla GK: Novel medical therapies for pituitary tumors. Front Horm Res; 2010;38:158-64
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Novel medical therapies for pituitary tumors.
  • Despite considerable progress, there is still no medical treatment available for some kinds of pituitary tumors, in particular hormone inactive adenomas and corticotroph pituitary tumors.
  • Surgical removal or at least debulking of the tumor is the only option to treat these kinds of tumors apart from rarely applied radiotherapy.
  • Moreover, treatment resistance is present in a considerable proportion of patients bearing pituitary tumors, for which medical treatment regimens are already available (prolactinomas, somatotroph adenomas).
  • Here, we summarize preclinical and clinical findings about the hormone and growth-suppressive action of various drugs, which will probably lead to novel future medical treatment concepts for pituitary tumors.
  • [MeSH-major] Pituitary Neoplasms / drug therapy

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  • [Copyright] Copyright (c) 2010 S. Karger AG, Basel.
  • (PMID = 20616507.001).
  • [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 / BIM 23A760; 0 / Dopamine Agonists; 51110-01-1 / Somatostatin; 5688UTC01R / Tretinoin; 82115-62-6 / Interferon-gamma; 98H1T17066 / pasireotide; VTD58H1Z2X / Dopamine
  • [Number-of-references] 32
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75. 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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76. Roussel-Gervais A, Bilodeau S, Vallette S, Berthelet F, Lacroix A, Figarella-Branger D, Brue T, Drouin J: Cooperation between cyclin E and p27(Kip1) in pituitary tumorigenesis. Mol Endocrinol; 2010 Sep;24(9):1835-45
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  • [Title] Cooperation between cyclin E and p27(Kip1) in pituitary tumorigenesis.
  • Cushing's disease is caused by glucocorticoid-resistant pituitary corticotroph adenomas.
  • We have previously identified the loss of nuclear Brg1 as one mechanism that may lead to partial glucocorticoid resistance: this loss is observed in about 33% of human corticotroph adenomas.
  • We now show that Brg1 loss of function correlates with cyclin E expression in corticotroph adenomas and with loss of the cell cycle inhibitor p27(Kip1) expression.
  • Because Brg1 is thought to have tumor suppressor activity, the present study was undertaken to understand the putative contribution of cyclin E derepression produced by loss of Brg1 expression on adenoma development.
  • Overexpression of cyclin E in pituitary proopiomelanocortin cells leads to abnormal reentry into cell cycle of differentiated proopiomelanocortin cells and to centrosome instability.
  • These alterations are consistent with the intermediate lobe hyperplasia and anterior lobe adenomas that were observed in these pituitaries.
  • When combined with the p27(Kip1) knockout, overexpression of cyclin E increased the incidence of pituitary tumors, their size, and their proliferation index.
  • These results suggest that cyclin E up-regulation and p27(Kip1) loss-of-function act cooperatively on pituitary adenoma development.
  • [MeSH-major] Cyclin E / metabolism. Cyclin-Dependent Kinase Inhibitor p27 / metabolism. Pituitary Neoplasms / metabolism. Precancerous Conditions / metabolism
  • [MeSH-minor] Animals. Biomarkers / metabolism. Cell Differentiation. Cell Proliferation. Centrosome / metabolism. DNA Helicases / metabolism. Gene Knockdown Techniques. Hyperplasia. Mice. Mice, Transgenic. Nuclear Proteins / metabolism. Phenotype. Pituitary ACTH Hypersecretion / complications. Pituitary ACTH Hypersecretion / metabolism. Pituitary ACTH Hypersecretion / pathology. Pituitary Gland / metabolism. Pituitary Gland / pathology. Pro-Opiomelanocortin / metabolism. Repressor Proteins. Transcription Factors / metabolism


77. 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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  • [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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78. Karavitaki N, Ansorge O, Wass JA: Silent corticotroph adenomas. Arq Bras Endocrinol Metabol; 2007 Nov;51(8):1314-8
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  • [Title] Silent corticotroph adenomas.
  • Silent corticotroph pituitary adenomas (SCA) are defined as pituitary adenomas showing positive staining for adrenocorticotrophic hormone in immunohistochemical studies, but not associated with perioperative clinical or laboratory features of hypercortisolaemia.
  • They account for 1.1-6% of surgically removed pituitary adenomas.
  • The lack of manifestations of cortisol excess has not been conclusively explained.
  • In surgical series, most tumours are macroadenomas with suprasellar extension present in 87-100% of the cases; this is in contrast to Cushing's disease, which is mostly attributed to microadenomas.
  • Attempts to identify predictors of recurrence have not been successful.
  • The development of florid pituitary Cushing's syndrome and local recurrence followed by metastatic disease (occasionally outside the central nervous system) have been rarely reported.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / pathology. Adenoma / pathology. Pituitary Neoplasms / pathology

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  • (PMID = 18209869.001).
  • [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
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone
  • [Number-of-references] 27
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79. 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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  • [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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80. 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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81. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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


82. Korbonits M, Carlsen E: Recent clinical and pathophysiological advances in non-functioning pituitary adenomas. Horm Res; 2009 Apr;71 Suppl 2:123-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Recent clinical and pathophysiological advances in non-functioning pituitary adenomas.
  • Pituitary adenomas are being recognized and diagnosed with increasing frequency.
  • One of the most common forms of pituitary lesion is the clinically non-functioning pituitary adenoma (NFPA), which is often diagnosed incidentally.
  • The vast majority of pituitary adenomas are sporadic, but familial adenomas can occur in the multiple pituitary adenoma type 1 syndrome, in Carney complex or in familial isolated pituitary adenoma.
  • Most often these are silent gonadotroph adenomas, with silent corticotroph or somatotroph adenomas occurring less frequently.
  • It is unclear why these silent adenomas do not release hormones at a clinically recognizable level, although it is probable that there is a continuum between fully functional and completely silent adenomas.
  • Temozolomide has been successfully used for the treatment of a few aggressive pituitary adenomas, and the response to this drug could be influenced by the expression of the DNA repair enzyme O-6-methylguanine DNA methyltransferase.
  • The early diagnosis, prediction of long-term outcome and treatment of NFPAs remain a challenge for endocrinologists.
  • [MeSH-major] Growth Hormone-Secreting Pituitary Adenoma. Prolactinoma
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / diagnosis. ACTH-Secreting Pituitary Adenoma / metabolism. ACTH-Secreting Pituitary Adenoma / pathology. ACTH-Secreting Pituitary Adenoma / therapy. Female. Humans. Male

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  • [Copyright] Copyright 2009 S. Karger AG, Basel.
  • (PMID = 19407508.001).
  • [ISSN] 1423-0046
  • [Journal-full-title] Hormone research
  • [ISO-abbreviation] Horm. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Number-of-references] 58
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83. Aznar Rodríguez S, Moreno Pérez O, Revert Marrahí P, Martínez Fuster S, Boix Carreño E, Picó Alfonso AM: Silent corticotroph adenomas of the pituitary gland: apropos of two cases. Endocrinol Nutr; 2008 Oct;55(8):367-71
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Silent corticotroph adenomas of the pituitary gland: apropos of two cases.
  • Clinically silent corticotroph adenomas are rare.
  • Given the absence of clinical and biochemical features of hypercortisolism, the definitive diagnosis is histological.

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  • [Copyright] Copyright © 2008 Sociedad Española de Endocrinología y Nutrición. Published by Elsevier Espana. All rights reserved.
  • (PMID = 22975601.001).
  • [ISSN] 1575-0922
  • [Journal-full-title] Endocrinología y nutrición : órgano de la Sociedad Española de Endocrinología y Nutrición
  • [ISO-abbreviation] Endocrinol Nutr
  • [Language] eng; spa
  • [Publication-type] Journal Article
  • [Publication-country] Spain
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84. 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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85. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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86. 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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87. 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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88. 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
  • [Publication-country] United States
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone
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89. 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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  • [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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90. Tauchmanovà L, Pivonello R, Di Somma C, Rossi R, De Martino MC, Camera L, Klain M, Salvatore M, Lombardi G, Colao A: Bone demineralization and vertebral fractures in endogenous cortisol excess: role of disease etiology and gonadal status. J Clin Endocrinol Metab; 2006 May;91(5):1779-84
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  • [Title] Bone demineralization and vertebral fractures in endogenous cortisol excess: role of disease etiology and gonadal status.
  • INTRODUCTION: The effects of endogenous cortisol (F) excess on bone mass and vertebral fractures have still not been thoroughly investigated.
  • Cushing's disease and adrenal and ectopic Cushing's syndrome.
  • MATERIALS AND METHODS: Eighty consecutive patients and 80 controls were prospectively enrolled: 37 patients (21 females) with pituitary ACTH-secreting adenoma, 18 (14 females) with adrenocortical adenoma, 15 (11 females) with adrenal carcinoma of mixed secretion, and 10 (three females) with ectopic ACTH secretion.
  • At diagnosis, bone mineral density (BMD) was determined by the dual-energy x-ray absorptiometry technique at the lumbar spine (L1-L4) and femoral neck; vertebral fractures were investigated by standard spinal radiographs.
  • RESULTS: When comparing the groups with different etiology of F excess, the patients with ectopic ACTH secretion had higher F and lower BMD values than the other subgroups.
  • Only multiple fractures were more frequent in patients with ectopic ACTH hypersecretion (P < 0.05).
  • The harmful effects of F excess at the spine were partly counterbalanced by the increased androgen production but were not affected by gonadal status in women.
  • [MeSH-minor] Adenoma / blood. Adolescent. Adrenal Gland Neoplasms / blood. Adrenocorticotropic Hormone / blood. Adult. Aged. Biomarkers. Body Mass Index. Carcinoma / blood. Case-Control Studies. Cross-Sectional Studies. Female. Humans. Male. Middle Aged. Prospective Studies. Risk Factors

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  • (PMID = 16522701.001).
  • [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 / Biomarkers; 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
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91. 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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92. Bush ZM, Lopes MB, Hussaini IM, Jane JA Jr, Laws ER Jr, Vance ML: Immunohistochemistry of COUP-TFI: an adjuvant diagnostic tool for the identification of corticotroph microadenomas. Pituitary; 2010;13(1):1-7
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  • [Title] Immunohistochemistry of COUP-TFI: an adjuvant diagnostic tool for the identification of corticotroph microadenomas.
  • Cushing's disease is caused by an ACTH-producing pituitary tumor, and accounts for 10-15% of pituitary tumors.
  • The majority of corticotroph tumors are microadenomas (<10 mm), and accurate histologic identification of these tumors can be challenging because of their small size and the presence of nests of normal corticotroph cells in the anterior pituitary.
  • Retinoic acid has been shown to inhibit ACTH production and induce apoptosis in corticotroph tumor cells.
  • The expression of the orphan nuclear receptor COUP-TFI antagonizes retinoic acid signaling and has been shown to be expressed in normal corticotroph cells, but absent in corticotroph tumor cell lines.
  • We analyzed 34 corticotroph tumor specimens by immunohistochemistry using a goat polyclonal IgG antibody with epitope mapping to the N-terminus of human COUP-TFI.
  • Segments of normal pituitary in each of the 34 specimens demonstrate COUP-TFI immunoreactivity in normal corticotroph cells.
  • Twenty-nine of 34 ACTH producing tumors were immunonegative for COUP-TFI.
  • Two tumors, measuring 9 and 11 mm, showed consistent (>90%) expression of COUP-TFI, and three adenomas (5, 11, and 18 mm) showed heterogenous (20-80%) expression of COUP-TFI.
  • Immunohistochemistry of COUP-TFI may be a useful adjuvant diagnostic tool in distinguishing corticotroph microadenomas from nests of normal corticotroph cells in the anterior pituitary.
  • Furthermore, this study identifies two unique corticotroph tumor populations which differ in their expression of COUP-TFI, the presence of which occurs more frequently in macroadenomas.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / diagnosis. Adenoma / diagnosis. COUP Transcription Factor I / analysis
  • [MeSH-minor] Diagnosis, Differential. Humans. Immunohistochemistry. Molecular Diagnostic Techniques. Retrospective Studies. Tissue Distribution

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  • (PMID = 19526345.001).
  • [ISSN] 1573-7403
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / 1-T32-DK-07646; United States / NIDDK NIH HHS / DK / T32 DK007646; United States / NCRR NIH HHS / RR / M01RR000847; United States / NIDDK NIH HHS / DK / 1-F32-DK082159-01; United States / NINDS NIH HHS / NS / 5R01NS035122-10
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / COUP Transcription Factor I
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93. Takayasu S, Iwasaki Y, Nigawara T, Asai M, Yoshida M, Kageyama K, Suda T: Involvement of nuclear factor-kB and Nurr-1 in cytokine-induced transcription of proopiomelanocortin gene in AtT20 corticotroph cells. Neuroimmunomodulation; 2010;17(2):88-96
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  • [Title] Involvement of nuclear factor-kB and Nurr-1 in cytokine-induced transcription of proopiomelanocortin gene in AtT20 corticotroph cells.
  • OBJECTIVE: The precise mechanism whereby proinflammatory cytokines activate the hypothalamo-pituitary-adrenal axis is still unclear.
  • METHODS: The mouse corticotropinoma cell line AtT20 was treated with tumor necrosis factor-alpha (TNF-alpha) or interleukin-1beta (IL-1beta).
  • Cotreatment of the cells with either of the cytokines and corticotropin-releasing hormone resulted in additive effects.
  • [MeSH-major] Cytokines / metabolism. Hypothalamo-Hypophyseal System / metabolism. NF-kappa B / genetics. Nuclear Receptor Subfamily 4, Group A, Member 2 / genetics. Pituitary Gland, Anterior / metabolism. Pro-Opiomelanocortin / genetics
  • [MeSH-minor] Adrenocorticotropic Hormone / metabolism. Adrenocorticotropic Hormone / secretion. Animals. Binding Sites / genetics. Cell Line. Dose-Response Relationship, Drug. Gene Expression Regulation / physiology. Immune System / cytology. Immune System / metabolism. Inflammation Mediators / metabolism. Inflammation Mediators / pharmacology. Interleukin-1beta / metabolism. Interleukin-1beta / pharmacology. Mice. Neurosecretory Systems / cytology. Neurosecretory Systems / metabolism. Pituitary-Adrenal System / cytology. Pituitary-Adrenal System / metabolism. RNA, Messenger / drug effects. RNA, Messenger / metabolism. Stress, Psychological / genetics. Stress, Psychological / metabolism. Stress, Psychological / physiopathology. Transcriptional Activation / physiology. Tumor Necrosis Factor-alpha / metabolism. Tumor Necrosis Factor-alpha / pharmacology. Up-Regulation / genetics

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  • [Copyright] Copyright 2009 S. Karger AG, Basel.
  • (PMID = 19923853.001).
  • [ISSN] 1423-0216
  • [Journal-full-title] Neuroimmunomodulation
  • [ISO-abbreviation] Neuroimmunomodulation
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Cytokines; 0 / Inflammation Mediators; 0 / Interleukin-1beta; 0 / NF-kappa B; 0 / Nuclear Receptor Subfamily 4, Group A, Member 2; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 66796-54-1 / Pro-Opiomelanocortin; 9002-60-2 / Adrenocorticotropic Hormone
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94. van der Hoek J, Lamberts SW, Hofland LJ: The somatostatin receptor subtype 5 in neuroendocrine tumours. Expert Opin Investig Drugs; 2010 Mar;19(3):385-99
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • AREAS COVERED IN THIS REVIEW: The scope of this review is primarily focused upon recent insights in sst(5)-receptor physiology, novel sst(5)-targeted treatment options predominantly directed towards pituitary adenomas, and gastroenteropancreatic neuroendocrine tumours.
  • WHAT THE READER WILL GAIN: An understanding of the potential that novel sst(5)-targeted SRIF analogues might have in the medical treatment of Cushing's disease and acromegaly, as demonstrated by translational research, based on pathophysiological data combined with results from clinical trials.
  • Finally, absence of sst(5) in corticotroph adenomas could be related to tumour aggressiveness in Cushing's disease.
  • [MeSH-minor] Adenoma / drug therapy. Adenoma / physiopathology. Animals. Drug Design. Gastrointestinal Neoplasms / drug therapy. Gastrointestinal Neoplasms / physiopathology. Humans. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / physiopathology. Pituitary Neoplasms / drug therapy. Pituitary Neoplasms / physiopathology

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  • (PMID = 20151855.001).
  • [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 / Receptors, Somatostatin; 0 / somatostatin receptor 5
  • [Number-of-references] 101
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95. Kowarik M, Onofri C, Colaco T, Stalla GK, Renner U: Platelet-derived growth factor (PDGF) and PDGF receptor expression and function in folliculostellate pituitary cells. Exp Clin Endocrinol Diabetes; 2010 Feb;118(2):113-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Platelet-derived growth factor (PDGF) and PDGF receptor expression and function in folliculostellate pituitary cells.
  • Homo- and heterodimers of platelet-derived growth factor-A (PDGF-A) and PDGF-B chains are involved through PDGF alpha- and beta-receptors in the growth regulation of multiple normal and tumoural cell types as well as in tumour neovascularization.
  • Since little information is available on the impact of PDGF/PDGF receptors in normal and adenomatous pituitary, we studied the expression and action of this growth factor system in a variety of pituitary tumour cell lines and in rat anterior pituitary cell cultures.
  • By RT-PCR, mRNA expression of PDGF-A and -B chains and of both receptors was found in rat pituitary and mouse folliculostellate TtT/GF pituitary tumour cells.
  • Rat somatotroph MtT-S and mouse corticotroph AtT20 tumor cells expressed only a part of the PDGF/PDGF receptor components whereas mouse gonadotroph alphaT3-1 and rat lactosomatotroph GH3 pituitary tumour cells contained neither PDGF nor PDGF receptors.
  • Both in rat pituitary cell cultures and in TtT/GF cells, PDGF-AB and -BB strongly enhanced VEGF-A secretion.
  • Its role in endocrine pituitary tumour cell lines and pituitary adenomas need to be clarified in future studies.
  • [MeSH-major] Pituitary Gland, Anterior / metabolism. Platelet-Derived Growth Factor / metabolism. Receptors, Platelet-Derived Growth Factor / metabolism
  • [MeSH-minor] Analysis of Variance. Animals. Blotting, Western. Cell Line, Tumor. Cell Proliferation / drug effects. Cells, Cultured. Gene Expression Regulation, Neoplastic / drug effects. Mice. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Phosphatidylinositol 3-Kinases / metabolism. Phosphorylation / drug effects. RNA, Messenger / genetics. RNA, Messenger / metabolism. Rats. Reverse Transcriptase Polymerase Chain Reaction. Vascular Endothelial Growth Factor A / secretion

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  • [Copyright] J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart. New York.
  • (PMID = 19373754.001).
  • [ISSN] 1439-3646
  • [Journal-full-title] Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association
  • [ISO-abbreviation] Exp. Clin. Endocrinol. Diabetes
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Platelet-Derived Growth Factor; 0 / RNA, Messenger; 0 / Vascular Endothelial Growth Factor A; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Receptors, Platelet-Derived Growth Factor
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96. Vassiliadi D, Tsagarakis S: Unusual causes of Cushing's syndrome. Arq Bras Endocrinol Metabol; 2007 Nov;51(8):1245-52
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  • [Title] Unusual causes of Cushing's syndrome.
  • Although in the majority of the patients with Cushing's syndrome (CS), hypercortisolism is due to ACTH hypersecretion by a pituitary tumour or to ectopic ACTH secretion from an extrapituitary neoplastic lesion or to autonomous cortisol secretion by an adrenal tumour, in occasional patients a much rarer entity may be the cause of the syndrome.
  • The following unusual forms of CS were identified: (i) ACTH hyperesecretion due to ectopic corticotroph adenomas in the parasellar region or the neurohypophysis, or as part of double adenomas, or gangliocytomas;.
  • (ii) ACTH hypersecretion due to ectopic CRH or CRH-like peptide secretion by various neoplasms;.
  • (iii) ACTH-independent cortisol hypersecretion from ectopic or bilateral adrenal adenomas;.
  • Such unusual presentations of CS illustrate why Cushing's syndrome represents one of the most puzzling endocrine syndromes.
  • [MeSH-minor] ACTH Syndrome, Ectopic / complications. Adrenal Gland Neoplasms / complications. Female. Glucocorticoids / adverse effects. Humans. Liver Neoplasms / complications. Megestrol Acetate / adverse effects. Ovarian Neoplasms / complications. Pituitary Neoplasms / complications. Ritonavir / adverse effects

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  • (PMID = 18209862.001).
  • [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
  • [Chemical-registry-number] 0 / Glucocorticoids; O3J8G9O825 / Ritonavir; TJ2M0FR8ES / Megestrol Acetate
  • [Number-of-references] 58
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97. Vila G, Theodoropoulou M, Stalla J, Tonn JC, Losa M, Renner U, Stalla GK, Paez-Pereda M: Expression and function of sonic hedgehog pathway components in pituitary adenomas: evidence for a direct role in hormone secretion and cell proliferation. J Clin Endocrinol Metab; 2005 Dec;90(12):6687-94
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression and function of sonic hedgehog pathway components in pituitary adenomas: evidence for a direct role in hormone secretion and cell proliferation.
  • Shh signaling is active in the corticotrophs of the adult pituitary gland, where it cross-talks with the CRH pathway and regulates ACTH secretion.
  • Because developmental pathways are involved in pituitary tumorigenesis, we hypothesized that Shh may be important in pituitary tumors.
  • OBJECTIVE: The objective of this study was to examine the expression and function of Shh-pathway components in pituitary adenomas.
  • METHODS: Using immunohistochemistry, we determined the expression of Shh and its receptors Patched 1 (Ptc1) and Patched 2 (Ptc2) in 55 human pituitary adenomas compared with the normal pituitary gland.
  • The AtT-20 and GH3 pituitary tumor cell lines were used as models for studying the role of Shh on cell proliferation and hormone secretion.
  • The effect of Shh on hormone secretion was confirmed in primary cultures of normal rat pituitaries and human pituitary tumors.
  • RESULTS: Ptc1 and Ptc2 were present, whereas Shh was down-regulated in pituitary adenomas and completely absent in Cushing tumors.
  • Shh inhibited cell proliferation in AtT-20 corticotrophinoma cells and the Shh-specific inhibitor cyclopamine increased proliferation in GH3 mammosomatotrophinoma cells.
  • On the other hand, exogenous administration of Shh increased hormone secretion from normal rat pituitaries, pituitary cell lines, and 10 different pituitary tumors.
  • CONCLUSIONS: Our results suggest that Shh might maintain pituitary cells in a nonproliferative state.
  • We conclude that Shh is a newly described hypophysiotropic cytokine and its down-regulation may be involved in the pathogenesis of pituitary adenomas.
  • [MeSH-major] Adenoma / metabolism. Adenoma / pathology. Hormones / secretion. Pituitary Neoplasms / metabolism. Pituitary Neoplasms / pathology. Trans-Activators / metabolism
  • [MeSH-minor] Adult. Aged. Cell Line, Tumor. Cell Proliferation / drug effects. Female. Hedgehog Proteins. Humans. Male. Membrane Proteins / metabolism. Middle Aged. Pituitary Gland / drug effects. Pituitary Gland / secretion. Receptors, Cell Surface / metabolism

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  • (PMID = 16159933.001).
  • [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] 0 / Hedgehog Proteins; 0 / Hormones; 0 / Membrane Proteins; 0 / Receptors, Cell Surface; 0 / SHH protein, human; 0 / Trans-Activators; 0 / patched receptors
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98. Drouin J, Bilodeau S, Vallette S: Of old and new diseases: genetics of pituitary ACTH excess (Cushing) and deficiency. Clin Genet; 2007 Sep;72(3):175-82
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Of old and new diseases: genetics of pituitary ACTH excess (Cushing) and deficiency.
  • The pituitary gland orchestrates our endocrine environment: it produces hormones in response to hypothalamic factors that integrate neural inputs and its activity is balanced by the feedback action of peripheral hormones.
  • Genetic analysis of pituitary function led to discovery of critical transcription factors that cause hormone deficiencies when mis-expressed.
  • This review will summarize recent findings that led to the first complete clinical description of inherited, isolated corticotropin (ACTH) deficiency (IAD) and to the first molecular mechanism for excessive ACTH production in Cushing's disease.
  • Indeed, mutations in TPIT, a positive or negative regulator of cell fates for different pituitary lineages, cause neonatal IAD, a condition considered anecdotic before discovery of this transcription factor.
  • Cushing's disease is caused by corticotroph adenomas that produce excess ACTH as a result of resistance to glucocorticoids (Gc).
  • Molecular investigation of the normal mechanism of Gc feedback led to identification of two essential proteins for pro-opiomelanocortin repression that are often mis-expressed in corticotroph adenomas thus providing a molecular explanation for Gc resistance.
  • These two proteins, Brg1 and histone deacetylase 2 (HDAC2), are involved in chromatin remodeling and may also participate in the tumorigenic process, as Brg1 is a tumor suppressor.
  • These recent advances have provided improved diagnosis and opened new perspectives for patient management and therapies.
  • [MeSH-major] Adrenocorticotropic Hormone / deficiency. Pituitary ACTH Hypersecretion / genetics
  • [MeSH-minor] Animals. DNA Helicases / physiology. Feedback, Physiological. Glucocorticoids / physiology. Histone Deacetylase 2. Histone Deacetylases / physiology. Homeodomain Proteins / genetics. Humans. Hypothalamo-Hypophyseal System / physiology. Nuclear Proteins / physiology. Pituitary-Adrenal System / physiology. Pro-Opiomelanocortin / metabolism. Receptors, Glucocorticoid / physiology. Repressor Proteins / physiology. T-Box Domain Proteins / genetics. Transcription Factors / physiology

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  • (PMID = 17718852.001).
  • [ISSN] 0009-9163
  • [Journal-full-title] Clinical genetics
  • [ISO-abbreviation] Clin. Genet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Glucocorticoids; 0 / Homeodomain Proteins; 0 / Nuclear Proteins; 0 / Receptors, Glucocorticoid; 0 / Repressor Proteins; 0 / T-Box Domain Proteins; 0 / TBX19 protein, human; 0 / Transcription Factors; 66796-54-1 / Pro-Opiomelanocortin; 9002-60-2 / Adrenocorticotropic Hormone; EC 3.5.1.98 / Histone Deacetylase 2; EC 3.5.1.98 / Histone Deacetylases; EC 3.6.1.- / SMARCA4 protein, human; EC 3.6.4.- / DNA Helicases
  • [Number-of-references] 41
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99. Kiehna EN, Keil M, Lodish M, Stratakis C, Oldfield EH: Pseudotumor cerebri after surgical remission of Cushing's disease. J Clin Endocrinol Metab; 2010 Apr;95(4):1528-32
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  • [Title] Pseudotumor cerebri after surgical remission of Cushing's disease.
  • CONTEXT: Pseudotumor cerebri has only been described after successful surgery for Cushing's disease (CD) in case reports.
  • All underwent resection of an ACTH-secreting adenoma, and postoperative serum cortisol reached a nadir of less than 2 microg/dl.
  • Three patients did not receive treatment, and their symptoms resolved over several months.
  • A patient exhibiting signs of intracranial hypertension after surgery for CD should undergo an evaluation for pseudotumor cerebri.

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  • (PMID = 20164289.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] ENG
  • [Grant] United States / NICHD NIH HHS / HD / Z01 HD000642; United States / NICHD NIH HHS / HD / Z01-HD-000642-04; United States / Intramural NIH HHS / /
  • [Publication-type] Case Reports; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Carbonic Anhydrase Inhibitors; 0 / Steroids; O3FX965V0I / Acetazolamide; WI4X0X7BPJ / Hydrocortisone
  • [Other-IDs] NLM/ PMC2853987
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100. Quentien MH, Barlier A, Franc JL, Pellegrini I, Brue T, Enjalbert A: Pituitary transcription factors: from congenital deficiencies to gene therapy. J Neuroendocrinol; 2006 Sep;18(9):633-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pituitary transcription factors: from congenital deficiencies to gene therapy.
  • Despite the existence of interspecies phenotypic variability, animal models have yielded valuable insights into human pituitary diseases.
  • Studies on Snell and Jackson mice known to have growth hormone, prolactin and thyroid-stimulating hormone deficiencies involving the hypoplastic pituitary gland have led to identifying alterations of the pituitary specific POU homeodomain Pit-1 transcription factor gene.
  • Terminal differentiation of lactotroph cells and direct regulation of the prolactin gene both require interactions between Pit-1 and cell type specific partners, including panpituitary transcriptional regulators such as Pitx1 and Pitx2.
  • Synergistic activation of the prolactin promoter by Pitx factors and Pit-1 is involved not only in basal condition, but also in responsiveness to forskolin, thyrotrophin-releasing-hormone and epidermal growth factor.
  • In corticotroph cells, Pitx1 interacts with Tpit.
  • This finding supports the idea that Tpit plays an essential role in the differentiation of the pro-opiomelanocortin pituitary lineage.
  • The effects of Pit-1 are not restricted to hormone gene regulation because this factor also contributes to cell division and protects the cell from programmed cell death.
  • Lentiviral vectors expressing a Pit-1 dominant negative mutant induced time- and dose-dependent cell death in somatotroph and lactotroph adenomas in vitro.
  • Gene transfer by lentiviral vectors should provide a promising step towards developing an efficient specific therapeutic approach by which a gene therapy programme for treating human pituitary adenomas could be based.
  • [MeSH-major] Gene Expression Regulation / physiology. Genetic Therapy. Pituitary Diseases / genetics. Pituitary Gland, Anterior / metabolism. Pituitary Hormones / metabolism. Transcription Factor Pit-1 / metabolism
  • [MeSH-minor] Animals. Gene Transfer Techniques. Growth Hormone / metabolism. Homeodomain Proteins / genetics. Homeodomain Proteins / metabolism. Humans. Mice, Neurologic Mutants. Mutation / genetics. Pituitary Neoplasms / genetics. Pituitary Neoplasms / physiopathology. Pituitary Neoplasms / therapy. Prolactin / metabolism. T-Box Domain Proteins. Thyrotropin / metabolism. Transcription Factors / genetics. Transcription Factors / metabolism

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  • (PMID = 16879162.001).
  • [ISSN] 0953-8194
  • [Journal-full-title] Journal of neuroendocrinology
  • [ISO-abbreviation] J. Neuroendocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Pituitary Hormones; 0 / T-Box Domain Proteins; 0 / TBX19 protein, human; 0 / Transcription Factor Pit-1; 0 / Transcription Factors; 184787-43-7 / homeobox protein PITX2; 9002-62-4 / Prolactin; 9002-71-5 / Thyrotropin; 9002-72-6 / Growth Hormone
  • [Number-of-references] 98
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