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1. 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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2. 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


3. Dovio A, Allasino B, Palmas E, Ventura M, Pia A, Saba L, Aroasio E, Terzolo M, Angeli A: Increased osteoprotegerin levels in Cushing's syndrome are associated with an adverse cardiovascular risk profile. J Clin Endocrinol Metab; 2007 May;92(5):1803-8
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  • [Title] Increased osteoprotegerin levels in Cushing's syndrome are associated with an adverse cardiovascular risk profile.
  • CONTEXT: Patients with Cushing's syndrome (CS) have a mortality rate four times higher than age- and sex-matched subjects, mainly due to cardiovascular events.
  • Serum osteoprotegerin (OPG) levels are increased in patients with cardiovascular disease and/or excess bone resorption.
  • Twenty-six patients had pituitary-dependent CS; five patients had CS caused by ectopic ACTH secretion; and 17 patients had adrenal-dependent CS, accounted for by cortisol-secreting adenoma (n = 9), ACTH-independent macronodular bilateral adrenal hyperplasia (n = 4), or World Health Organization stage II cortisol-secreting carcinoma (n = 4).
  • RESULTS: Serum OPG (but not sRANKL) levels were significantly higher in CS patients than in controls (P < 0.01).
  • Serum OPG levels were higher in patients with pituitary-dependent CS in comparison with adrenal-dependent CS.
  • [MeSH-minor] Absorptiometry, Photon. Adrenal Glands / physiopathology. Adrenocorticotropic Hormone / blood. Adult. Aged. Cross-Sectional Studies. Female. Humans. Hydrocortisone / blood. Male. Metabolic Syndrome X / metabolism. Middle Aged. Pituitary Function Tests. Pituitary Gland / physiopathology. Receptor Activator of Nuclear Factor-kappa B / blood. Risk

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  • (PMID = 17327380.001).
  • [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 / Osteoprotegerin; 0 / Receptor Activator of Nuclear Factor-kappa B; 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
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4. Woo YS, Isidori AM, Wat WZ, Kaltsas GA, Afshar F, Sabin I, Jenkins PJ, Monson JP, Besser GM, Grossman AB: Clinical and biochemical characteristics of adrenocorticotropin-secreting macroadenomas. J Clin Endocrinol Metab; 2005 Aug;90(8):4963-9
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  • [Title] Clinical and biochemical characteristics of adrenocorticotropin-secreting macroadenomas.
  • CONTEXT: Cushing's disease as a result of a pituitary macroadenoma is an uncommon cause of Cushing's syndrome, and reports in the published literature are few and of limited size.
  • OBJECTIVE: Our objective was to establish the clinical and biochemical characteristics of macroadenomas associated with Cushing's disease compared with a large cohort of microadenomas and to assess their response to therapy.
  • PATIENTS: Patients had Cushing's disease presenting with a pituitary macroadenoma, in comparison with a large group of microadenoma patients.
  • MAIN OUTCOME MEASURES: Outcome measures included basal and dynamically responsive plasma ACTH and cortisol levels and response to treatment.
  • RESULTS: We identified 18 patients with Cushing's disease secondary to a macroadenoma; basal 0900 h plasma ACTH was 135.8 +/- 32.5 and 45.0 +/- 4.3 ng/liter (mean +/- SEM), respectively, in macroadenomas and microadenomas (P = 0.013).
  • Testing with high-dose dexamethasone showed less suppression in the macroadenomas (57.6 +/- 8.7% vs. 74.4 +/- 2.1%; P = 0.02) and an attenuated ACTH response to CRH.
  • CONCLUSIONS: Pituitary macroadenomas causing Cushing's disease have biochemical features largely distinct from patients harboring microadenomas but represent one end of a continuum.
  • [MeSH-major] Adenoma / metabolism. Adrenal Gland Neoplasms / metabolism. Adrenocorticotropic Hormone / secretion. Pituitary ACTH Hypersecretion / metabolism
  • [MeSH-minor] Adult. Combined Modality Therapy. Female. Humans. Hydrocortisone / blood. Magnetic Resonance Imaging. Male. Middle Aged. Neoplasm Invasiveness. Retrospective Studies. Tomography, X-Ray Computed. Treatment Outcome

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  • (PMID = 15886242.001).
  • [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] 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
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5. Minniti G, Brada M: Radiotherapy and radiosurgery for Cushing's disease. Arq Bras Endocrinol Metabol; 2007 Nov;51(8):1373-80
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  • [Title] Radiotherapy and radiosurgery for Cushing's disease.
  • Patients with residual or recurrent Cushing's disease receive external beam radiotherapy (RT) with the aim of achieving long-term tumour control and normalization of elevated hormone levels.
  • On the basis of the available literature, fractionated conventional and stereotactic radiotherapy offer effective treatment for Cushing's disease not controlled with surgery alone.
  • The lower efficacy and higher toxicity of single fraction treatment suggest that SRS is not the appropriate therapy for the majority of patients with Cushing's disease.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma. Adenoma. Pituitary ACTH Hypersecretion. Radiosurgery. Radiotherapy, Conformal
  • [MeSH-minor] Humans. Neoplasm Recurrence, Local. Neoplasm, Residual / radiotherapy

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  • (PMID = 18209876.001).
  • [ISSN] 0004-2730
  • [Journal-full-title] Arquivos brasileiros de endocrinologia e metabologia
  • [ISO-abbreviation] Arq Bras Endocrinol Metabol
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Brazil
  • [Number-of-references] 52
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6. Mantovani G, Lania AG, Bondioni S, Peverelli E, Pedroni C, Ferrero S, Pellegrini C, Vicentini L, Arnaldi G, Bosari S, Beck-Peccoz P, Spada A: Different expression of protein kinase A (PKA) regulatory subunits in cortisol-secreting adrenocortical tumors: relationship with cell proliferation. Exp Cell Res; 2008 Jan 1;314(1):123-30
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  • [Title] Different expression of protein kinase A (PKA) regulatory subunits in cortisol-secreting adrenocortical tumors: relationship with cell proliferation.
  • The four regulatory subunits (R1A, R1B, R2A, R2B) of protein kinase A (PKA) are differentially expressed in several cancer cell lines and exert distinct roles in growth control.
  • Mutations of the R1A gene have been found in patients with Carney complex and in a minority of sporadic primary pigmented nodular adrenocortical disease (PPNAD).
  • The aim of this study was to evaluate the expression of PKA regulatory subunits in non-PPNAD adrenocortical tumors causing ACTH-independent Cushing's syndrome and to test the impact of differential expression of these subunits on cell growth.
  • Immunohistochemistry demonstrated a defective expression of R2B in all cortisol-secreting adenomas (n=16) compared with the normal counterpart, while both R1A and R2A were expressed at high levels in the same tissues.
  • The R2-selective cAMP analogue 8-Cl-cAMP dose-dependently inhibited Y-1 cell proliferation and induced apoptosis, while the R1-selective cAMP analogue 8-HA-cAMP stimulated cell proliferation.
  • Finally, R2B gene silencing induced up-regulation of R1A protein, associated with an increase in cell proliferation.
  • In conclusion, we propose that a high R1/R2 ratio favors the proliferation of well differentiated and hormone producing adrenocortical cells, while unbalanced expression of these subunits is not required for malignant transformation.
  • [MeSH-major] Adrenal Cortex Neoplasms / enzymology. Adrenal Cortex Neoplasms / genetics. Adrenocortical Adenoma / enzymology. Adrenocortical Adenoma / genetics. Cell Proliferation / drug effects. Cyclic AMP-Dependent Protein Kinases / genetics. Hydrocortisone / secretion
  • [MeSH-minor] 8-Bromo Cyclic Adenosine Monophosphate / analogs & derivatives. 8-Bromo Cyclic Adenosine Monophosphate / pharmacology. Base Sequence / genetics. Carcinoma / enzymology. Carcinoma / genetics. Carcinoma / secretion. Cell Line, Tumor. Cell Transformation, Neoplastic / genetics. Cyclic AMP-Dependent Protein Kinase RIIbeta Subunit / genetics. Cyclic AMP-Dependent Protein Kinase RIIbeta Subunit / metabolism. Cyclic AMP-Dependent Protein Kinase RIalpha Subunit / genetics. Cyclic AMP-Dependent Protein Kinase RIalpha Subunit / metabolism. Dose-Response Relationship, Drug. Gene Expression Regulation, Enzymologic / genetics. Gene Expression Regulation, Neoplastic / genetics. Gene Silencing / physiology. Humans. Up-Regulation / genetics

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  • (PMID = 17904549.001).
  • [ISSN] 0014-4827
  • [Journal-full-title] Experimental cell research
  • [ISO-abbreviation] Exp. Cell Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclic AMP-Dependent Protein Kinase RIIbeta Subunit; 0 / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit; 23583-48-4 / 8-Bromo Cyclic Adenosine Monophosphate; 41941-56-4 / 8-chloro-cyclic adenosine monophosphate; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; WI4X0X7BPJ / Hydrocortisone
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7. Swords FM, Monson JP, Besser GM, Chew SL, Drake WM, Grossman AB, Plowman PN: Gamma knife radiosurgery: a safe and effective salvage treatment for pituitary tumours not controlled despite conventional radiotherapy. Eur J Endocrinol; 2009 Dec;161(6):819-28
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  • [Title] Gamma knife radiosurgery: a safe and effective salvage treatment for pituitary tumours not controlled despite conventional radiotherapy.
  • OBJECTIVE: We report the use of 'gamma knife' (GK) radiosurgery in 25 patients with pituitary adenomas not cured despite conventional therapy, including external beam radiotherapy.
  • PATIENTS AND METHODS: All patients had previously received conventional radiotherapy for a mean of 11.8 years prior to receiving GK; 23 out of 25 had also undergone pituitary surgery on at least one occasion.
  • Seventeen had hyperfunctioning adenomas that still required medical therapy without an adequate biochemical control--ten somatotroph adenomas, six corticotroph adenomas and one prolactinoma, while eight patients had non-functioning pituitary adenomas (NFPAs).
  • A total of 75% NFPAs showed disease stabilisation or shrinkage post GK.
  • The results in corticotroph adenomas were variable.
  • Prior to GK, 72% of the patients were panhypopituitary, and 42% of the remainder have developed new anterior pituitary hormone deficiencies to date.
  • CONCLUSIONS: These data indicate that GK is a safe and effective adjunctive treatment for patients with NFPAs and acromegaly not satisfactorily controlled with surgery and radiotherapy.

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  • (PMID = 19773368.001).
  • [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] 12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I
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8. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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


9. Starke RM, Williams BJ, Vance ML, Sheehan JP: Radiation therapy and stereotactic radiosurgery for the treatment of Cushing's disease: an evidence-based review. Curr Opin Endocrinol Diabetes Obes; 2010 Aug;17(4):356-64
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  • [Title] Radiation therapy and stereotactic radiosurgery for the treatment of Cushing's disease: an evidence-based review.
  • PURPOSE OF REVIEW: The indications, efficacy, and safety of radiation therapy and stereotactic radiosurgery for Cushing's disease are evaluated.We queried PubMed using the terms, 'Cushing's disease', 'radiotherapy', and 'radiosurgery', then evaluated each study for the number of patients, method of radiation delivery, type of radiation therapy or radiosurgical device used, treatment parameters (e.g. maximal dose, tumor margin dose), length of follow-up, tumor-control rate, complications, rate of hormone normalization, newly onset loss of pituitary function, and method used to assess endocrine remission.
  • The reported rates of tumor-volume control following radiotherapy and radiosurgery vary considerably from 66-100%.
  • Although post-treatment hypopituitarism and disease recurrence were uncommon, they did occur, and this underscores the necessity for long-term follow-up in these patients.
  • SUMMARY: Radiosurgery and, in the modern era, less commonly, radiation therapy, offer both well tolerated and reasonably effective treatment for recurrent or residual Cushing's adenomas.
  • [MeSH-major] Pituitary ACTH Hypersecretion / radiotherapy. Pituitary ACTH Hypersecretion / surgery. Radiosurgery / methods. Radiotherapy / methods
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / radiotherapy. ACTH-Secreting Pituitary Adenoma / surgery. Adenoma / radiotherapy. Adenoma / surgery. Evidence-Based Practice / methods. Evidence-Based Practice / trends. Humans. Preoperative Care / methods. Treatment Outcome

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  • (PMID = 20531182.001).
  • [ISSN] 1752-2978
  • [Journal-full-title] Current opinion in endocrinology, diabetes, and obesity
  • [ISO-abbreviation] Curr Opin Endocrinol Diabetes Obes
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 95
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10. Burdman JA, Pauni M, Heredia Sereno GM, Bordón AE: Estrogen receptors in human pituitary tumors. Horm Metab Res; 2008 Aug;40(8):524-7
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  • [Title] Estrogen receptors in human pituitary tumors.
  • The relationship between the presence of estrogen receptors in pituitary adenomas and the post surgical evolution of the patients in order to find another prognostic parameter for these tumors have been studied to improve the treatment selection.
  • Estrogen receptors were studied by immunocytochemistry in histological sections of paraffin embedded 42 pituitary adenomas.
  • As expected, the higher concentration (60%) was found in prolactin secreting adenomas, although we found estrogen receptors in one somatotroph and in one nonsecreting.
  • The results of this work suggest that the determination of estrogen receptors in pituitary tumors might help as a prognostic factor in these adenomas.
  • [MeSH-major] Adenoma / metabolism. Pituitary Neoplasms / metabolism. Receptors, Estrogen / metabolism
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / metabolism. Adult. Female. Growth Hormone-Secreting Pituitary Adenoma / metabolism. Humans. Immunohistochemistry. Male. Middle Aged. Prognosis. Prolactinoma / metabolism

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  • (PMID = 18398784.001).
  • [ISSN] 0018-5043
  • [Journal-full-title] Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et métabolisme
  • [ISO-abbreviation] Horm. Metab. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Receptors, Estrogen
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11. Lad SP, Patil CG, Laws ER Jr, Katznelson L: The role of inferior petrosal sinus sampling in the diagnostic localization of Cushing's disease. Neurosurg Focus; 2007;23(3):E2
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  • [Title] The role of inferior petrosal sinus sampling in the diagnostic localization of Cushing's disease.
  • Cushing's syndrome can present a complex problem of differential diagnosis.
  • Of cases in which hypercortisolemia results from an adrenocorticotropic hormone (ACTH)-dependent process, approximately 80% are due to a pituitary adenoma (Cushing's disease [CD]), 10% are due to adrenal lesions, and the remaining 10% are secondary to ectopic ACTH secretion.
  • For patients with CD, surgical removal of the pituitary adenoma is the treatment of choice.
  • Thus, localization of the source of ACTH secretion is critical in guiding timely treatment decisions.
  • Inferior petrosal sinus sampling (IPSS) is considered to be the gold standard for confirming the origin of ACTH secretion in patients with Cushing's syndrome.
  • A number of other techniques are discussed including sampling from the cavernous sinus, the jugular vein, and multiple sites to aid the diagnosis and lateralization of ACTH-producing pituitary adenomas.
  • [MeSH-major] Petrosal Sinus Sampling / methods. Pituitary ACTH Hypersecretion / diagnosis

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  • (PMID = 17961020.001).
  • [ISSN] 1092-0684
  • [Journal-full-title] Neurosurgical focus
  • [ISO-abbreviation] Neurosurg Focus
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone
  • [Number-of-references] 46
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12. 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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13. Sheehan JM, Douds GL, Hill K, Farace E: Transsphenoidal surgery for pituitary adenoma in elderly patients. Acta Neurochir (Wien); 2008 Jun;150(6):571-4; discussion 574
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  • [Title] Transsphenoidal surgery for pituitary adenoma in elderly patients.
  • BACKGROUND: As the population continues to age, the number of elderly patients with symptomatic pituitary tumours will continue to increase.
  • Little information exists as to the safety of pituitary surgery in this patient population.
  • Eight patients had new hormonal deficits post-operatively (1 ACTH, 3 TSH, 2 ACTH/TSH, 2 vasopressin).
  • Surgical removal of pituitary adenomas should be considered the mainstay of treatment in elderly patients in whom treatment is necessary.
  • [MeSH-major] Adenoma / surgery. Endoscopy / methods. Microsurgery / methods. Pituitary Neoplasms / surgery. Postoperative Complications / etiology. Sphenoid Sinus / surgery
  • [MeSH-minor] Age Factors. Aged. Aged, 80 and over. Female. Follow-Up Studies. Growth Hormone-Secreting Pituitary Adenoma / diagnosis. Growth Hormone-Secreting Pituitary Adenoma / surgery. Humans. Image Processing, Computer-Assisted. Magnetic Resonance Imaging. Male. Risk Factors


14. Ben-Shlomo A, Wawrowsky KA, Proekt I, Wolkenfeld NM, Ren SG, Taylor J, Culler MD, Melmed S: Somatostatin receptor type 5 modulates somatostatin receptor type 2 regulation of adrenocorticotropin secretion. J Biol Chem; 2005 Jun 24;280(25):24011-21
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  • [Title] Somatostatin receptor type 5 modulates somatostatin receptor type 2 regulation of adrenocorticotropin secretion.
  • Somatostatin inhibits adrenocorticotropin (ACTH) secretion from pituitary tumor cells.
  • Octreotide and somatostatin-28 cell membrane binding affinities correlated with their respective SST2-selective peptide ligand.
  • Although octreotide had similar inhibiting potency (picomolar) for cAMP accumulation and ACTH secretion as an SST2-selective agonist, somatostatin-28 exhibited a higher potency (femtomolar).
  • SST2 internalization was visualized with SST2-selective agonist at lower concentrations than for octreotide or somatostatin-28, whereas SST5 did not internalize.
  • This may explain superior somatostatin-28 potency and provides a rationale for somatostatin ligand design to treat ACTH-secreting pituitary tumors.
  • [MeSH-minor] Adenoma / secretion. Animals. Base Sequence. Blotting, Western. Cell Line, Tumor. DNA Primers. Immunoprecipitation. Mice. Microscopy, Confocal. Microscopy, Fluorescence. Pituitary Neoplasms / secretion

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  • (PMID = 15857828.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 0 / somatostatin receptor 5; 9002-60-2 / Adrenocorticotropic Hormone
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15. Ballian N, Androulakis II, Chatzistefanou K, Samara C, Tsiveriotis K, Kaltsas GA: Optic neuropathy following radiotherapy for Cushing's disease: case report and literature review. Hormones (Athens); 2010 Jul-Sep;9(3):269-73
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  • [Title] Optic neuropathy following radiotherapy for Cushing's disease: case report and literature review.
  • Radiation-induced optic neuropathy is a rare adverse effect of radiotherapy applied for the treatment of pituitary adenomas.
  • We report a patient with a recurrent adrenocorticotrophin secreting pituitary adenoma who received external beam irradiation after failing surgical and medical therapy.
  • Despite treatment with glucocorticoids and hyperbaric oxygen, her vision did not improve.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / radiotherapy. Adenoma / radiotherapy. Optic Nerve Diseases / etiology. Pituitary ACTH Hypersecretion / radiotherapy. Radiation Injuries / etiology

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  • (PMID = 20688625.001).
  • [ISSN] 1109-3099
  • [Journal-full-title] Hormones (Athens, Greece)
  • [ISO-abbreviation] Hormones (Athens)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Glucocorticoids
  • [Number-of-references] 31
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16. Utz A, Biller BM: The role of bilateral inferior petrosal sinus sampling in the diagnosis of Cushing's syndrome. Arq Bras Endocrinol Metabol; 2007 Nov;51(8):1329-38
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  • [Title] The role of bilateral inferior petrosal sinus sampling in the diagnosis of Cushing's syndrome.
  • Adrenocorticotropin hormone (ACTH)-dependent Cushing's syndrome is most often due to a pituitary corticotroph adenoma, with ectopic ACTH-secreting tumors representing approximately 15% of cases.
  • BIPSS is an interventional radiology procedure in which ACTH levels obtained from venous drainage very near the pituitary gland are compared to peripheral blood levels before and after corticotropin hormone (CRH) stimulation.
  • A gradient between these two locations indicates pituitary Cushing's, whereas the absence of a gradient suggests ectopic Cushing's.
  • Accurate BIPSS results require hypercortisolemia to suppress normal corticotroph ACTH production and hypercortisolemia at the time of the BIPSS to assure excessive ACTH secretion.
  • In some cases, intrapituitary gradients from side-to-side can be helpful to localize small corticotroph adenomas within the sella.
  • [MeSH-major] ACTH Syndrome, Ectopic / diagnosis. Cushing Syndrome / diagnosis. Petrosal Sinus Sampling
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / blood. ACTH-Secreting Pituitary Adenoma / diagnosis. ACTH-Secreting Pituitary Adenoma / secretion. Adenoma / blood. Adenoma / diagnosis. Adenoma / secretion. Adrenocorticotropic Hormone / blood. Corticotropin-Releasing Hormone. Diagnosis, Differential. Humans. Pituitary Neoplasms / blood. Pituitary Neoplasms / diagnosis. Pituitary Neoplasms / secretion. Sensitivity and Specificity

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  • (PMID = 18209871.001).
  • [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; 9015-71-8 / Corticotropin-Releasing Hormone
  • [Number-of-references] 37
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17. Sinha S, Sharma BS: Giant pituitary adenomas--an enigma revisited. Microsurgical treatment strategies and outcome in a series of 250 patients. Br J Neurosurg; 2010 Feb;24(1):31-9
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  • [Title] Giant pituitary adenomas--an enigma revisited. Microsurgical treatment strategies and outcome in a series of 250 patients.
  • BACKGROUND: Giant pituitary adenomas (> 4 cm) are a surgical challenge.
  • METHODS: Two hundred and fifty patients with giant pituitary adenomas were managed surgically at our center over last 13 years.
  • Among functioning adenomas, 63 patients (25.4%) had prolactinomas and 45 patients (18%) had GH-secreting adenomas; while 3 patients each had LH and ACTH- secreting adenomas.
  • The maximum tumor diameter varied from 4 to 10.5 cm, with mean diameter of 5.4 cm.
  • 23 patients (9.2%) underwent re-exploration either because of postoperative apoplexy or residual tumor.
  • Overall, near total (>90%) tumor excision could be achieved in 74%, with improved vision in 53% and good outcome in 75% patients.
  • CONCLUSIONS: The main goal of surgical treatment of giant pituitary adenoma is maximum possible tumor extirpation with minimal side effects, which can be achieved by careful preoperative planning of operative approach, based on directions of tumor extensions and invasiveness.
  • Maximal surgical removal of giant adenomas offers best chances to control tumor growth when followed with adjuvant medical and radiation therapies.
  • [MeSH-major] Adenoma / surgery. Microsurgery / methods. Pituitary Neoplasms / surgery

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  • (PMID = 20158350.001).
  • [ISSN] 1360-046X
  • [Journal-full-title] British journal of neurosurgery
  • [ISO-abbreviation] Br J Neurosurg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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18. Kelly DF: Transsphenoidal surgery for Cushing's disease: a review of success rates, remission predictors, management of failed surgery, and Nelson's Syndrome. Neurosurg Focus; 2007;23(3):E5
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  • [Title] Transsphenoidal surgery for Cushing's disease: a review of success rates, remission predictors, management of failed surgery, and Nelson's Syndrome.
  • Cushing's disease is a serious endocrinopathy that, if left untreated, is associated with significant morbidity and mortality rates.
  • After diagnostic confirmation of Cushing's disease has been made, transsphenoidal adenomectomy is the treatment of choice.
  • The management of Nelson's Syndrome often requires both transsphenoidal surgery and radio-therapy to gain disease control.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / surgery. Adenoma / surgery. Neurosurgical Procedures / methods. Pituitary ACTH Hypersecretion / surgery. Sphenoid Sinus / surgery

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  • (PMID = 17961026.001).
  • [ISSN] 1092-0684
  • [Journal-full-title] Neurosurgical focus
  • [ISO-abbreviation] Neurosurg Focus
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 76
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19. Pisarek H, Pawlikowski M, Kunert-Radek J, Radek M: Expression of somatostatin receptor subtypes in human pituitary adenomas -- immunohistochemical studies. Endokrynol Pol; 2009 Jul-Aug;60(4):240-51
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  • [Title] Expression of somatostatin receptor subtypes in human pituitary adenomas -- immunohistochemical studies.
  • BACKGROUND: The highly variable expression of SSTR subtypes in pituitary adenomas (PA) may partially explain why the subgroup of somatotropinomas or other adenomas do not respond to the therapeutic action of currently used long-acting somatostatin analogues like octreotide or lanreotide.
  • RESULTS: The pattern of SSTR immunostaining (estimated according to the percentage frequency of appearance) was in acromegaly: SSTR 5 > SSTR 1 > SSTR 2A = SSTR 3 > SSTR 2B, in prolactinomas: SSTR 2B = SSTR 3 = SSTR 5 > SSTR 1 = SSTR 2A, in gonadotropinomas: SSTR 3 > SSTR 2B > SSTR 1 = SSTR 2A > SSTR 5, in corticotropinomas: SSTR 2A > SSTR 1 = SSTR 3 > SSTR 5 > SSTR 2B.
  • In PA immunonegative for pituitary hormones, we noticed only a weak staining of all receptor subtypes including SSTR 4.
  • In plurihormonal adenomas with positive GH phenotype the staining pattern was: SSTR 5 > SSTR 1 = SSTR 2B and in plurihormonal PA with negative GH phenotype: SSTR 1 = SSTR 5 > SSTR 2A = SSTR 2B = SSTR 3.
  • In plurihormonal adenoma with ACTH immunopositivity, the staining pattern was: SSTR = SSTR 2A = SSTR 3 = SSTR 5.
  • SSTR 1 and SSTR 5 were the most frequent subtypes of somatostatin receptor in plurihormonal adenomas without ACTH expression.
  • Apart from applying SSTR 2 and SSTR 5-preferring octreotide and lanreotide - newly synthesized multiligand analogues, such as SOM 230, KE 108, or other SST selective analogues, may represent a further useful approach for the treatment, especially in cases other than somatotropinoma or thyrotropinoma.
  • [MeSH-major] Adenoma / metabolism. Pituitary Neoplasms / metabolism. Receptors, Somatostatin / metabolism

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  • (PMID = 19753537.001).
  • [ISSN] 0423-104X
  • [Journal-full-title] Endokrynologia Polska
  • [ISO-abbreviation] Endokrynol Pol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Peptides, Cyclic; 0 / Protein Isoforms; 0 / Receptors, Somatostatin; 0G3DE8943Y / lanreotide; 51110-01-1 / Somatostatin; RWM8CCW8GP / Octreotide
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20. Castillo VA, Gallelli MF: Corticotroph adenoma in the dog: pathogenesis and new therapeutic possibilities. Res Vet Sci; 2010 Feb;88(1):26-32
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  • [Title] Corticotroph adenoma in the dog: pathogenesis and new therapeutic possibilities.
  • The corticotrophinoma, causing pituitary dependent hypercortisolism, represents the highest percentage of pituitary tumours in the dog.
  • It is not clear either what factors are involved in the tumour genesis; nevertheless, firm candidates are the Rb1 gene, proteins p27, p21 and p16, as are also defects in the glucocorticoid receptor and Nur77/Nurr1.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / veterinary. Adenoma / veterinary. Dog Diseases / etiology

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  • [Copyright] Copyright 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19733374.001).
  • [ISSN] 1532-2661
  • [Journal-full-title] Research in veterinary science
  • [ISO-abbreviation] Res. Vet. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 95
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21. de Bruin C, Pereira AM, Feelders RA, Romijn JA, Roelfsema F, Sprij-Mooij DM, van Aken MO, van der Lelij AJ, de Herder WW, Lamberts SW, Hofland LJ: Coexpression of dopamine and somatostatin receptor subtypes in corticotroph adenomas. J Clin Endocrinol Metab; 2009 Apr;94(4):1118-24
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  • [Title] Coexpression of dopamine and somatostatin receptor subtypes in corticotroph adenomas.
  • CONTEXT: Previous studies have demonstrated the expression of somatostatin receptor subtypes (mainly sst(5)) and dopamine (DA) receptor subtypes (mainly D(2)) in smaller series of human corticotroph adenomas.
  • In line with these findings, sst(5) and D(2)-targeting agents have already been used clinically in patients with Cushing's disease (CD) and have shown promising results in subsets of patients.
  • To what extent these receptor subtypes are coexpressed within individual adenomas, is not known however.
  • OBJECTIVE: The aim of the study was to investigate the (co-)expression of both sst and DA receptors in a large series of human corticotroph adenomas.
  • DESIGN: We performed in vitro analysis of corticotroph adenoma tissue obtained via transsphenoidal adenomectomy.
  • PATIENTS: Adenoma tissue from 30 patients with CD was analyzed in this study.
  • RESULTS: Analyzed by quantitative RT-PCR, D(2) and sst(5) were significantly (co-) expressed in the majority (60%) of adenomas, whereas 23% of adenomas only expressed D(2), but not sst(5).
  • The remaining 17% of adenomas did not significantly express either sst(5) or D(2).
  • Corticotroph adenomas with invasive growth invariably showed loss of sst(5) and D(2) expression.
  • CONCLUSIONS: Sst(5) and especially D(2) are highly expressed in the majority of human corticotroph adenomas, with coexpression of sst(5) and D(2) being a common phenomenon.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / genetics. Adenoma / genetics. Receptors, Dopamine / genetics. Receptors, Somatostatin / genetics

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  • (PMID = 19141584.001).
  • [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
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Receptors, Dopamine; 0 / Receptors, Dopamine D2; 0 / Receptors, Somatostatin
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22. Timmers HJ, van Ginneken EM, Wesseling P, Sweep CG, Hermus AR: A patient with recurrent hypercortisolism after removal of an ACTH-secreting pituitary adenoma due to an adrenal macronodule. J Endocrinol Invest; 2006 Nov;29(10):934-9
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  • [Title] A patient with recurrent hypercortisolism after removal of an ACTH-secreting pituitary adenoma due to an adrenal macronodule.
  • A 41-yr-old female was referred for signs and symptoms of Cushing's syndrome.
  • Cortisol was not suppressed by 1 mg dexamethasone (0.41 micromol/l).
  • Midnight cortisol and ACTH were 0.44 micromol/l and 18 pmol/l, respectively.
  • A magnetic resonance imaging (MRI) revealed a pituitary lesion of 7 mm.
  • ACTH and cortisol levels were unaltered by administration of human CRH and high-dose dexamethasone.
  • Inferior sinus petrosus sampling showed CRH-stimulated ACTH levels of 128.4 (left sinus) vs a peripheral level of 19.2 pmol/l, indicating Cushing's disease.
  • After 4 months of pre-treatment with metyrapone and dexamethasone, endoscopic transsphenoidal resection of an ACTH-positive pituitary adenoma was performed.
  • ACTH levels decreased to 2.6 pmol/l and fasting cortisol was 0.35 micromol/l.
  • Despite clinical regression of Cushing's syndrome and normalization of urinary cortisol, cortisol was not suppressed by 1 mg dexamethasone (0.30 micromol/l).
  • Ten months post-operatively, signs and symptoms of Cushing's syndrome reoccurred.
  • A high dose dexamethasone test according to Liddle resulted in undetectable ACTH, but no suppression of cortisol levels, pointing towards adrenal-dependent Cushing's syndrome.
  • This case illustrates, that longstanding ACTH stimulation by a pituitary adenoma can induce unilateral macronodular adrenal hyperplasia with autonomous cortisol production.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / surgery. Adenoma / surgery. Adrenal Glands / metabolism. Adrenal Glands / pathology. Cushing Syndrome / etiology
  • [MeSH-minor] Adrenocorticotropic Hormone / blood. Adult. Female. Humans. Hydrocortisone / blood. Hyperplasia / complications. Hyperplasia / diagnosis. Hyperplasia / metabolism. Hyperplasia / pathology. Pituitary ACTH Hypersecretion / complications. Pituitary ACTH Hypersecretion / metabolism. Pituitary ACTH Hypersecretion / pathology. Recurrence

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  • (PMID = 17185905.001).
  • [ISSN] 1720-8386
  • [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] 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
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23. Hanson JM, Mol JA, Meij BP: Expression of leukemia inhibitory factor and leukemia inhibitory factor receptor in the canine pituitary gland and corticotrope adenomas. Domest Anim Endocrinol; 2010 May;38(4):260-71
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  • [Title] Expression of leukemia inhibitory factor and leukemia inhibitory factor receptor in the canine pituitary gland and corticotrope adenomas.
  • Leukemia inhibitory factor (LIF) is a pleiotropic cytokine of the IL-6 family that activates the hypothalamic-pituitary-adrenal axis and promotes corticotrope cell differentiation during development.
  • The aim of this study was to investigate the expression of LIF and its receptor (LIFR) in the canine pituitary gland and in corticotrope adenomas, and to perform a mutation analysis of LIFR.
  • Using immunohistochemistry, immunofluorescence, and quantitative expression analysis, LIF and LIFR expression were studied in pituitary glands of control dogs and in specimens of corticotrope adenoma tissue collected through hypophysectomy in dogs with pituitary-dependent hypercortisolism (PDH, Cushing's disease).
  • In the control pituitary tissues and corticotrope adenomas, there was a low magnitude of LIF expression.
  • The LIFR, however, was highly expressed and co-localized with ACTH(1-24) expression.
  • Cytoplasmatic immunoreactivity of LIFR was preserved in corticotrope adenomas and adjacent nontumorous cells of pars intermedia.
  • Surprisingly, nuclear to perinuclear immunoreactivity for LIFR was present in nontumorous pituitary cells of the pars distalis in 10 of 12 tissue specimens from PDH dogs.
  • These data show that LIFR is highly co-expressed with adrenocorticotropic hormone (ACTH) and alpha-melanocyte-stimulating hormone (alpha-MSH) in the canine pituitary gland and in corticotrope adenomas.
  • Nuclear immunoreactivity for LIFR in nontumorous cells of the pars distalis may indicate the presence of a corticotrope adenoma.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / veterinary. Dog Diseases / metabolism. Leukemia Inhibitory Factor / analysis. Pituitary Gland / chemistry. Pituitary Neoplasms / veterinary. Receptors, OSM-LIF / analysis
  • [MeSH-minor] Animals. Cell Nucleus / chemistry. Cosyntropin / analysis. Cytoplasm / chemistry. DNA, Complementary / analysis. Dogs. Female. Fluorescent Antibody Technique. Immunohistochemistry. Male. Mutation. Polymerase Chain Reaction. Sequence Analysis, DNA. alpha-MSH / analysis

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  • [Copyright] Copyright (c) 2009 Elsevier Inc. All rights reserved.
  • (PMID = 20036483.001).
  • [ISSN] 1879-0054
  • [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 / DNA, Complementary; 0 / Leukemia Inhibitory Factor; 0 / Receptors, OSM-LIF; 16960-16-0 / Cosyntropin; 581-05-5 / alpha-MSH
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24. Ebisawa T, Tojo K, Tajima N, Kamio M, Oki Y, Ono K, Sasano H: Immunohistochemical analysis of 11-beta-hydroxysteroid dehydrogenase type 2 and glucocorticoid receptor in subclinical Cushing's disease due to pituitary macroadenoma. Endocr Pathol; 2008;19(4):252-60
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  • [Title] Immunohistochemical analysis of 11-beta-hydroxysteroid dehydrogenase type 2 and glucocorticoid receptor in subclinical Cushing's disease due to pituitary macroadenoma.
  • Subclinical Cushing's disease (SCD) is characterized by lack of clinically evident Cushingoid features, despite abnormal hypersecretion of ACTH.
  • Nearly half the cases of SCD are due to macroadenomas, and in the majority of them, ACTH secretion is not inhibited even by high-dose dexamethasone.
  • Impaired glucocorticoid (GC) action may be correlated with the proliferation and development of pituitary macroadenomas causing SCD.
  • In this study, immunohistochemical analysis of the resected tumors were performed to evaluate the expression of 11beta-hydroxysteroid dehydrogenase type 2 (11betaHSD2) and glucocorticoid receptor (GR) in pituitary tissues obtained from two SCD (macroadenomas), eight Cushing's disease (CD) (microadenomas), nine acromegaly, and nine normal pituitary (NP).
  • [MeSH-major] 11-beta-Hydroxysteroid Dehydrogenase Type 2 / metabolism. ACTH-Secreting Pituitary Adenoma / metabolism. Adenoma / metabolism. Pituitary ACTH Hypersecretion / metabolism. Receptors, Glucocorticoid / metabolism
  • [MeSH-minor] Acromegaly / metabolism. Acromegaly / pathology. Adolescent. Adrenocorticotropic Hormone / metabolism. Adult. Aged. Female. Humans. Immunohistochemistry / methods. Male. Middle Aged. Pituitary Gland / metabolism. Pituitary Gland / pathology. Young Adult

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  • (PMID = 19048413.001).
  • [ISSN] 1046-3976
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Glucocorticoid; 9002-60-2 / Adrenocorticotropic Hormone; EC 1.1.1.146 / 11-beta-Hydroxysteroid Dehydrogenase Type 2
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25. Batista DL, Zhang X, Gejman R, Ansell PJ, Zhou Y, Johnson SA, Swearingen B, Hedley-Whyte ET, Stratakis CA, Klibanski A: The effects of SOM230 on cell proliferation and adrenocorticotropin secretion in human corticotroph pituitary adenomas. J Clin Endocrinol Metab; 2006 Nov;91(11):4482-8
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  • [Title] The effects of SOM230 on cell proliferation and adrenocorticotropin secretion in human corticotroph pituitary adenomas.
  • CONTEXT: There is no tumor-directed medical therapy available for Cushing's disease.
  • OBJECTIVE: The objective was to determine the in vitro effect of the somatostatin analog pasireotide (SOM230) on cell proliferation in human corticotroph tumors.
  • DESIGN/METHODS: Expression of somatostatin receptors (SSTR 1-5) was determined by quantitative RT-PCR in 13 human corticotroph tumors and by immunohistochemistry (IHC) in 12 of the 13 tumors.
  • SOM230 effects on cell proliferation and ACTH release were evaluated in vitro using primary cultures of six of the 13 human corticotroph adenomas.
  • RESULTS: In our series, we found expression of SSTR subtypes 1, 2, 4, and 5 in human corticotroph tumors by quantitative RT-PCR.
  • Significant suppression of cell proliferation was observed in all tumors cultured (percent suppression range: 10-70%; P = 0.045-0.001).
  • SOM230 inhibited ACTH secretion in five of the six tumors cultured (percent suppression range: 23-56%; P = 0.042-0.001).
  • CONCLUSION: Corticotroph tumors express multiple SSTR subtypes.
  • SOM230 significantly suppressed cell proliferation and ACTH secretion in primary cultures of human corticotroph tumors.
  • These in vitro results support the hypothesis that SOM230 may have a role in the medical therapy of corticotroph tumors.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / drug therapy. Adenoma / drug therapy. Adrenocorticotropic Hormone / secretion. Cell Proliferation / drug effects. Somatostatin / analogs & derivatives
  • [MeSH-minor] Adolescent. Adult. Child. Female. Humans. Immunohistochemistry. In Vitro Techniques. Male. Middle Aged. Pituitary ACTH Hypersecretion / drug therapy. RNA, Messenger / metabolism. Receptors, Somatostatin / metabolism. Tumor Cells, Cultured

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  • (PMID = 16940446.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Receptors, Somatostatin; 51110-01-1 / Somatostatin; 9002-60-2 / Adrenocorticotropic Hormone; 98H1T17066 / pasireotide
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26. Rudnik A, Kos-Kudła B, Larysz D, Zawadzki T, Bazowski P: Endoscopic transsphenoidal treatment of hormonally active pituitary adenomas. Neuro Endocrinol Lett; 2007 Aug;28(4):438-44
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  • [Title] Endoscopic transsphenoidal treatment of hormonally active pituitary adenomas.
  • AIM OF THE STUDY: The paper presents endoscopic surgical technique used in the treatment of hormonally active pituitary adenomas and assessment of the method in terms of its effectiveness and safety.
  • MATERIAL AND METHODS: In 217 cases the surgery was performed due to pituitary adenomas applying the technique developed by Jho and Carrau, with our own modifications.
  • 70 patients were treated for hormonally active adenomas.
  • The group consisted of 36 somatotrophic adenomas, 21 prolactinomas and 13 corticotrophic adenomas.
  • RESULTS: Biochemical and neurosurgical criteria for complete resection were obtained in 21 (58.3%) of 36 patients with all somatotrophic adenomas.
  • Of the 13 patients with Cushing's disease 11 (84.6%) were cured.
  • In the postoperative course only 2 (2.8%) patients suffered liquorrhoeas and new anterior lobe pituitary insufficiency was noted in 8 (11.4%) cases.
  • CONCLUSIONS: Endoscopic technique is an effective method of treatment of hormonally active pituitary adenomas.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / surgery. Adenoma / surgery. Endoscopy / methods. Growth Hormone-Secreting Pituitary Adenoma / surgery. Neurosurgical Procedures / methods. Pituitary Neoplasms / surgery. Prolactinoma / surgery

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  • (PMID = 17693972.001).
  • [ISSN] 0172-780X
  • [Journal-full-title] Neuro endocrinology letters
  • [ISO-abbreviation] Neuro Endocrinol. Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Sweden
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27. 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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28. Johnson MD, Fan X, Bourne P, Walters D: Neuronal differentiation and expression of neural epitopes in pituitary adenomas. J Histochem Cytochem; 2007 Dec;55(12):1265-71
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  • [Title] Neuronal differentiation and expression of neural epitopes in pituitary adenomas.
  • Neural transdifferentiation is increasingly recognized in neural crest and neural stem cell tumors.
  • Neuronal differentiation has been anecdotally described primarily in somatotroph cell adenomas associated with acromegaly, but its prevalence in adenomas and relationship to adenoma type has not been completely established.
  • In this study we performed a retrospective morphological and immunohistochemical analysis of neurofilament, phosphoneurofilament, Neu-N, class III tubulin, and Hu in WHO grade I pituitary adenomas.
  • Limited numbers of cells with neuronal features and neuron-associated epitopes may be more common in pituitary adenomas than previously recognized.
  • These may occur in many forms of adenomas including somatotroph, lactotroph, mixed somatotroph and lactotroph, null cell/gonadotroph cell and, rarely, corticotroph cell adenomas.
  • [MeSH-major] Adenoma / metabolism. Biomarkers, Tumor / biosynthesis. Epitopes. Neurons / metabolism. Pituitary Neoplasms / metabolism
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / metabolism. ACTH-Secreting Pituitary Adenoma / pathology. Adult. Aged. Aged, 80 and over. Antibodies. Cell Differentiation. Female. Gonadotrophs / metabolism. Gonadotrophs / pathology. Human Growth Hormone / metabolism. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Staging. Prolactin / metabolism. Prolactinoma / metabolism. Prolactinoma / pathology. Retrospective Studies

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  • (PMID = 17875653.001).
  • [ISSN] 0022-1554
  • [Journal-full-title] The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society
  • [ISO-abbreviation] J. Histochem. Cytochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Biomarkers, Tumor; 0 / Epitopes; 12629-01-5 / Human Growth Hormone; 9002-62-4 / Prolactin
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29. Teshima T, Hara Y, Takekoshi S, Teramoto A, Osamura RY, Tagawa M: Expression of genes related to corticotropin production and glucocorticoid feedback in corticotroph adenomas of dogs with Cushing's disease. Domest Anim Endocrinol; 2009 Jan;36(1):3-12
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  • [Title] Expression of genes related to corticotropin production and glucocorticoid feedback in corticotroph adenomas of dogs with Cushing's disease.
  • Cushing's disease caused by pituitary corticotroph adenoma is a common endocrine disease in dogs.
  • A characteristic biochemical feature of corticotroph adenomas is their relative resistance to negative feedback by glucocorticoids.
  • In this study, we examined gene expression related to adrenocorticotropic hormone (ACTH) production and secretion, and the negative feedback by glucocorticoids in canine corticotroph adenoma.
  • We used resected corticotroph adenomas from 10 dogs with Cushing's disease.
  • In order to investigate the alteration of gene expression between corticotroph adenoma and normal corticotrophic cells, ACTH-positive cells in the anterior lobe were microdissected using a laser-capture microdissection system, and mRNA levels of proopiomelanocortin (POMC), corticotropin releasing hormone receptor 1 (CRHR1), glucocorticoid receptor (GR), mineralocorticoid receptor (MR), and 11 beta hydroxysteroid dehydrogenase (11HSD) type 1 and type 2 were determined using real-time RT-PCR.
  • POMC, CRHR1, and 11HSD2 mRNA levels in corticotroph adenoma were greater than those in normal corticotrophic cells (POMC, 5.5-fold; CRHR1, 4.9-fold; 11HSD2, 4.2-fold, P<0.01, respectively).
  • MR and 11HSD1 mRNA levels in corticotroph adenoma were lower than those in normal corticotrophic cells (MR, 2.2-fold; 11HSD1, 2.9-fold, P<0.01, respectively).
  • GR mRNA levels did not differ between corticotroph adenoma and normal corticotrophic cells.
  • Our results may help to understand the increased ACTH production and the resistance to negative feedback suppression by glucocorticoids in canine corticotroph adenomas.
  • These changes in gene expression may have a role in the growth of canine corticotroph adenoma, and help elucidate the pathophysiology of dogs with Cushing's disease.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / veterinary. Adrenocorticotropic Hormone / biosynthesis. Dog Diseases / genetics. Glucocorticoids / physiology. Pituitary ACTH Hypersecretion / veterinary. Pituitary Neoplasms / veterinary
  • [MeSH-minor] 11-beta-Hydroxysteroid Dehydrogenases / genetics. Animals. Dogs. Feedback, Physiological. Female. Gene Expression / genetics. Male. Pro-Opiomelanocortin / genetics. RNA, Messenger / analysis. Receptors, Corticotropin-Releasing Hormone / genetics. Receptors, Glucocorticoid / genetics. Receptors, Mineralocorticoid / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 18818046.001).
  • [ISSN] 1879-0054
  • [Journal-full-title] Domestic animal endocrinology
  • [ISO-abbreviation] Domest. Anim. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glucocorticoids; 0 / RNA, Messenger; 0 / Receptors, Corticotropin-Releasing Hormone; 0 / Receptors, Glucocorticoid; 0 / Receptors, Mineralocorticoid; 66796-54-1 / Pro-Opiomelanocortin; 9002-60-2 / Adrenocorticotropic Hormone; EC 1.1.1.146 / 11-beta-Hydroxysteroid Dehydrogenases
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30. de Bruin C, Feelders RA, Waaijers AM, van Koetsveld PM, Sprij-Mooij DM, Lamberts SW, Hofland LJ: Differential regulation of human dopamine D2 and somatostatin receptor subtype expression by glucocorticoids in vitro. J Mol Endocrinol; 2009 Jan;42(1):47-56
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  • Dopamine agonists (DA) and somatostatin (SS) analogues have been proposed in the treatment of ACTH-producing neuro-endocrine tumours that cause Cushing's syndrome.
  • In this study, we investigated the effects of the GC dexamethasone (DEX) on D(2) and sst expression in three human neuro-endocrine cell lines: BON (carcinoid) and TT (medullary thyroid carcinoma) versus DMS (small cell lung cancer), which is severely GC resistant.
  • In DMS, DEX did not cause significant changes in the expression of these receptor subtypes.
  • In conclusion, we show that GCs selectively down-regulate sst(2), but not D(2) and only to a minor degree sst(5) in human neuro-endocrine BON and TT cells.
  • This mechanism may also be responsible for the low expression of sst(2) in corticotroph adenomas and underwrite the current interest in sst(5) and D(2) as possible therapeutic targets for a medical treatment of Cushing's disease.
  • [MeSH-minor] Animals. Antineoplastic Agents, Hormonal / metabolism. Cell Line. Cell Proliferation. DNA Fragmentation. Dexamethasone / metabolism. Dopamine / metabolism. Hormone Antagonists / metabolism. Humans. Mifepristone / metabolism. Octreotide / metabolism. RNA, Messenger / metabolism. Radioligand Assay. Somatostatin / metabolism

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  • (PMID = 18852217.001).
  • [ISSN] 1479-6813
  • [Journal-full-title] Journal of molecular endocrinology
  • [ISO-abbreviation] J. Mol. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Glucocorticoids; 0 / Hormone Antagonists; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / Receptors, Dopamine D2; 0 / Receptors, Somatostatin; 320T6RNW1F / Mifepristone; 51110-01-1 / Somatostatin; 7S5I7G3JQL / Dexamethasone; RWM8CCW8GP / Octreotide; VTD58H1Z2X / Dopamine
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31. Occhi G, Albiger N, Berlucchi S, Gardiman M, Scanarini M, Scienza R, Fassina A, Mantero F, Scaroni C: Peroxisome proliferator-activated receptor gamma in the human pituitary gland: expression and splicing pattern in adenomas versus normal pituitary. J Neuroendocrinol; 2007 Jul;19(7):552-9
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  • [Title] Peroxisome proliferator-activated receptor gamma in the human pituitary gland: expression and splicing pattern in adenomas versus normal pituitary.
  • Pituitary adenomas are slow-growing tumours arising within the pituitary gland.
  • If secreting, they give rise to well-known syndromes such as Cushing's disease or acromegaly; when hormonally inactive, they come to clinical attention often with local mass effects or pituitary deficiency.
  • Peroxisome proliferator-activated receptor gamma (PPARgamma), a nuclear hormone receptor with a key role in fat and glucose metabolism, but also involved in several neoplasia, has recently been detected in pituitary adenomas.
  • In the present study, we evaluated the occurrence and splicing profile of PPARgamma in 43 cases of pituitary adenoma of different subtypes and compared it to 12 normal pituitary glands.
  • By real-time polymerase chain reaction, PPARgamma was expressed as much in adrenocorticotrophic hormone (ACTH)-secreting and ACTH-silent adenomas as in controls, with a moderate underexpression in somatotrophinomas and prolactinomas and overexpression in 54% of nonfunctioning pituitary adenomas (NFPA).
  • There was no apparent qualitative change in the splicing profile of pathological pituitary glands, nor was the presence of specific isoforms with dominant negative effects against PPARgamma detected.
  • Western blotting revealed similar expression levels in the different subgroups of pituitary adenomas and normal glands.
  • The intra- and intergroup differences observed in pituitary adenomas may represent new elements in the process of understanding the different clinical responses of Cushing's and Nelson patients to PPARgamma-ligand treatment.
  • Moreover, the higher level of PPARgamma expression detected in the NFPA subgroup may suggest its possible role as a molecular target in these pituitary adenomas, paving the way for investigations on the effectiveness of treatment with thiazolidinediones in such patients.
  • [MeSH-major] Adenoma / metabolism. PPAR gamma / metabolism. Pituitary Gland / metabolism. Pituitary Neoplasms / metabolism. RNA Splicing

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  • (PMID = 17561883.001).
  • [ISSN] 0953-8194
  • [Journal-full-title] Journal of neuroendocrinology
  • [ISO-abbreviation] J. Neuroendocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / PPAR gamma; 0 / RNA, Messenger
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32. Giacomini D, Haedo M, Gerez J, Druker J, Páez-Pereda M, Labeur M, Stalla GK, Arzt E: Differential gene expression in models of pituitary prolactin-producing tumoral cells. Horm Res; 2009 Apr;71 Suppl 2:88-94
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  • [Title] Differential gene expression in models of pituitary prolactin-producing tumoral cells.
  • Although several genes and signalling pathways have been identified as important effectors in the development of pituitary tumours, our understanding of pituitary tumorigenesis remains incomplete and is the focus of much current research.
  • Use of the mRNA differential display technique in prolactinomas from D2-receptor knockout mice and in stable GH3 cell line clones with enhanced tumorigenicity in vivo has led to the identification of two genes that are involved in the pathogenic process--BMP-4 and RSUME.
  • In contrast, BMP-4 has an inhibitory role in corticotrophinomas.
  • RSUME (RWD-containing sumoylation enhancer) was identified from a transformed lactosomatotrophic cell line that had increased tumorigenic and angiogenic potential.
  • The differential expression and action of BMP-4 in prolactinomas and corticotrophinomas highlights the importance of studying a gene with contrasting actions in two cell lineages of the same organ in order to understand the pituitary transformation process.
  • Both BMP-4 and RSUME may be interesting targets for inhibiting steps involved in pituitary tumorigenesis.
  • [MeSH-major] Bone Morphogenetic Protein 4 / biosynthesis. Gene Expression Regulation, Neoplastic. Models, Biological. Neoplasm Proteins / biosynthesis. Prolactinoma / metabolism. Transcription Factors / biosynthesis
  • [MeSH-minor] Animals. Cell Hypoxia / genetics. Cell Line, Tumor. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / metabolism. Gene Expression Profiling. Humans. Mice. Mice, Knockout. Receptors, Dopamine D2 / genetics. Receptors, Dopamine D2 / metabolism. Signal Transduction / genetics

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  • [Copyright] Copyright 2009 S. Karger AG, Basel.
  • (PMID = 19407504.001).
  • [ISSN] 1423-0046
  • [Journal-full-title] Hormone research
  • [ISO-abbreviation] 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 / Neoplasm Proteins; 0 / RSUME protein, human; 0 / Receptors, Dopamine D2; 0 / Transcription Factors
  • [Number-of-references] 56
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33. Winczyk K, Pawlikowski M: Immunohistochemical detection of PPARgamma receptors in the human pituitary adenomas: correlation with PCNA. Folia Histochem Cytobiol; 2005;43(3):137-41
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  • [Title] Immunohistochemical detection of PPARgamma receptors in the human pituitary adenomas: correlation with PCNA.
  • The occurrence of peroxisome proliferator-activated receptors gamma (PPARgamma) was investigated in 51 human pituitary adenomas and in 6 non-tumoral human pituitary tissue samples.
  • The mean percentage of cells with positive nuclear reaction was 3-fold higher in pituitary adenomas in comparison with non-tumoral pituitary tissues.
  • It was clearly stronger in pituitary adenomas than in non-tumoral pituitary tissues.
  • A slight, statistically insignificant tendency towards negative correlation between PPARgamma and PCNA was found in somatotropinomas, prolactinomas, corticotropinomas and gonadotropinomas.
  • On the other hand, in null cell adenomas and "silent" corticotropinomas, a strong positve correlation between the expression of PPARgamma and PCNA was observed.
  • The strong expression of PPARgamma in human pituitary adenomas and its possible involvement in control of cell proliferation in these tumors give a good reason for the attempts of their treatment with PPARgamma ligands.

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  • (PMID = 16201313.001).
  • [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 / PPAR gamma; 0 / Proliferating Cell Nuclear Antigen
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34. 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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35. Giorgi RR, Chile T, Bello AR, Reyes R, Fortes MA, Machado MC, Cescato VA, Musolino NR, Bronstein MD, Giannella-Neto D, Corrêa-Giannella ML: Expression of neurotensin and its receptors in pituitary adenomas. J Neuroendocrinol; 2008 Sep;20(9):1052-7
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  • [Title] Expression of neurotensin and its receptors in pituitary adenomas.
  • The neurotensin (NT) produced in the hypothalamus and in pituitary gonadotrophs and thyrotrophs participates in neuroendocrine regulation.
  • Recently, the involvement of this peptide in normal and neoplastic cell proliferation has been postulated.
  • In the present study, we evaluated the expression of NT and its receptors (NTR1, 2 and 3) in a series of 50 pituitary adenomas [11 growth hormone (GH)-, eight prolactin (PRL)-, four adrenocorticotrophic hormone (ACTH)- and 27 nonfunctioning adenomas].
  • NT mRNA expression was significantly higher in functioning compared to nonfunctioning adenomas and with normal pituitary.
  • Nonfunctioning pituitary adenomas showed lower expression of NT mRNA than normal pituitary.
  • In the immunohistochemical study of functioning adenomas, NT was colocalised with GH, PRL and ACTH secreting cells.
  • In nonfunctioning adenomas, the NT immunoreactivity intensity was variable among the samples.
  • NTR3 mRNA expression was observed in all examined samples and was higher in the adenomas, both functioning and nonfunctioning, compared to normal pituitary.
  • By contrast, NTR1 and NTR2 mRNA were not detected in either pituitary adenomas or normal tissue.
  • The higher expression of NTR3, as well as the expression of NT by tumoural corticotrophs, lactotrophs and somatotrophs, which are cells types that do not express this peptide in the normal pituitary, suggests that NT autocrine and/or paracrine stimulation mediated by NTR3 may be a mechanism associated with the tumourigenesis of functioning adenomas.
  • [MeSH-major] Adenoma / genetics. Neurotensin / genetics. Pituitary Neoplasms / genetics. Receptors, Neurotensin / genetics
  • [MeSH-minor] Adult. Aged. Autocrine Communication / genetics. Autocrine Communication / physiology. Female. Gene Expression Regulation, Neoplastic. Humans. Male. Middle Aged. Paracrine Communication / genetics. Paracrine Communication / physiology. RNA, Messenger / metabolism. Tumor Cells, Cultured. Young Adult

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  • (PMID = 18624930.001).
  • [ISSN] 1365-2826
  • [Journal-full-title] Journal of neuroendocrinology
  • [ISO-abbreviation] J. Neuroendocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Receptors, Neurotensin; 39379-15-2 / Neurotensin
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36. Matsuno A: [Recent trends in the pathophysiology and treatment of pituitary adenomas]. Brain Nerve; 2009 Aug;61(8):957-62
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Recent trends in the pathophysiology and treatment of pituitary adenomas].
  • Recent molecular pathological investigations have elucidated the cytodifferentiation of pituitary cells and identified several transcriptional factors that regulate this cytodifferentiation of pituitary cells.
  • The patterns of cytodifferentiation are closely related to the pathogenesis of pituitary adenomas.
  • Meanwhile, the role of hypothalamic hormones in the development of pituitary adenomas has recently attracted the attention of investigators.
  • The expression of growth hormone-releasing hormone and corticotrophin releasing hormone in corticotroph adenomas have been demonstrated in somatotroph adenomas and corticotropin adenomas, respectively.
  • This finding indicates that the endogenous expression of hypothalamic hormones and their receptors in human pituitary adenoma cells has ample significance in the autocrine or paracrine regulation of pituitary hormone production and tumor extension induced by hypothalamic hormones produced by adenoma cells.
  • The recent progress in surgical techniques for treatment of pituitary adenomas has provided several alternatives: transsphenoidal surgery vs. transcranial surgery, sublabial approach vs. endonasal approach, and microsurgery vs. endoscopic surgery.
  • There have also been developments in the medical treatment of pituitary adenomas.
  • The frequently used dopamine agonist, cabergoline, is very effective for treating prolactin-producing adenoma.
  • Long-acting octreotide and pegvisomant are now available for the treatment of growth hormone producing adenoma.
  • Cabergoline is also used for growth hormone producing adenoma.
  • Temozolomide has recently been used for atypical adenomas or pituitary carcinomas.
  • Adult growth hormone deficiency sometimes occurs in postoperative patients with pituitary adenomas.
  • [MeSH-major] Adenoma / etiology. Adenoma / therapy. Pituitary Neoplasms / etiology. Pituitary Neoplasms / therapy
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Corticotropin-Releasing Hormone. Dacarbazine / analogs & derivatives. Dacarbazine / therapeutic use. Ergolines / therapeutic use. Growth Hormone-Releasing Hormone. Human Growth Hormone / analogs & derivatives. Human Growth Hormone / therapeutic use. Humans. Hypothalamic Hormones. Incidental Findings. Neurosurgical Procedures / methods. Neurosurgical Procedures / trends. Octreotide / therapeutic use. Prolactinoma. Receptors, Neuropeptide. Receptors, Pituitary Hormone-Regulating Hormone

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  • (PMID = 19697885.001).
  • [ISSN] 1881-6096
  • [Journal-full-title] Brain and nerve = Shinkei kenkyū no shinpo
  • [ISO-abbreviation] Brain Nerve
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Ergolines; 0 / Hypothalamic Hormones; 0 / Receptors, Neuropeptide; 0 / Receptors, Pituitary Hormone-Regulating Hormone; 0 / pegvisomant; 0 / somatotropin releasing hormone receptor; 12629-01-5 / Human Growth Hormone; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; 9015-71-8 / Corticotropin-Releasing Hormone; 9034-39-3 / Growth Hormone-Releasing Hormone; LL60K9J05T / cabergoline; RWM8CCW8GP / Octreotide
  • [Number-of-references] 32
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37. Lee EJ, Ahn JY, Noh T, Kim SH, Kim TS, Kim SH: Tumor tissue identification in the pseudocapsule of pituitary adenoma: should the pseudocapsule be removed for total resection of pituitary adenoma? Neurosurgery; 2009 Mar;64(3 Suppl):ons62-9; discussion ons69-70
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  • [Title] Tumor tissue identification in the pseudocapsule of pituitary adenoma: should the pseudocapsule be removed for total resection of pituitary adenoma?
  • OBJECTIVE: The microsurgical pseudocapsule can be found in the transition zone between an adenoma and the surrounding normal pituitary tissue.
  • Furthermore, we evaluated the remission rate, the changes in pituitary function, and the recurrence rate after intensive resection of the pseudocapsule.
  • METHODS: In 616 patients with pituitary adenomas (Hardy Types I-III) over a period of 14 years, we introduced intensive resection of the microsurgical pseudocapsule to achieve complete tumor removal.
  • A combined pituitary function test and radiological study were performed on the patients before surgery, 1 year after surgery, and at subsequent 1.5-year intervals 2 to 13 years postoperatively.
  • Tumor cluster infiltration was present in the pseudocapsule in 71 (43.6%) of these patients.
  • The presence of a pseudocapsule was slightly more frequent in prolactin-secreting tumors (70.9%) than in growth hormone-secreting (55.0%) and adrenocorticotropic hormone-secreting (40.0%) tumors.
  • In the 243 patients of the total resection group who underwent combined pituitary function tests more than 2 times after surgery, the surgical remission rate was 99.1% in clinically nonfunctional tumors, 88% in growth hormone-secreting, 70.6% in prolactin-secreting, and 100% in adrenocorticotropic hormone-secreting tumors.
  • There was no statistical difference in improvement or deterioration of pituitary function according to the existence or absence of the pseudocapsule.
  • The tumor recurrence rate was 0.8% in the total resection group and was 42.1% in the subtotal resection group.
  • CONCLUSION: We have shown that tumor tissue is frequently present within the pseudocapsule, suggesting that any tumor remnant in the pseudocapsule could be a source of recurrence and an obstacle to achieving complete remission.
  • These results indicate that intensive resection of the pseudocapsule could result in a higher remission rate without deteriorating pituitary function.
  • [MeSH-major] Neurosurgical Procedures / methods. Pituitary Gland / pathology. Pituitary Gland / surgery. Pituitary Neoplasms / pathology. Pituitary Neoplasms / surgery
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / surgery. Follow-Up Studies. Growth Hormone-Secreting Pituitary Adenoma / surgery. Humans. Magnetic Resonance Imaging. Microsurgery. Neoplasm Recurrence, Local / epidemiology. Pituitary Function Tests. Postoperative Period. Prolactinoma / surgery. Prospective Studies. Treatment Outcome

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  • (PMID = 19240574.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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38. 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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39. Ruebel KH, Leontovich AA, Jin L, Stilling GA, Zhang H, Qian X, Nakamura N, Scheithauer BW, Kovacs K, Lloyd RV: Patterns of gene expression in pituitary carcinomas and adenomas analyzed by high-density oligonucleotide arrays, reverse transcriptase-quantitative PCR, and protein expression. Endocrine; 2006 Jun;29(3):435-44
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  • [Title] Patterns of gene expression in pituitary carcinomas and adenomas analyzed by high-density oligonucleotide arrays, reverse transcriptase-quantitative PCR, and protein expression.
  • Very few of the genes that are important in pituitary tumor initiation, progression, and metastasis have been identified to date.
  • To identify potential genes that may be important in pituitary tumor progression and carcinoma development, we used Affymetrix GeneChip HGU-133A-oligonucleotide arrays, which contain more than 15,000 characterized genes from the human genome to study gene expression in an ACTH pituitary carcinoma metastatic to the liver and four pituitary adenomas.
  • Reverse-transcriptase real-time quantitative- PCR (RT-qPCR) was then used to analyze 4 nonneoplastic pituitaries, 19 adenomas, and the ACTH carcinoma.
  • A larger series of pituitary adenomas and carcinomas were also analyzed for protein expression using tissue microarrays (TMA) (n = 233) and by Western blotting (n = 18).
  • There were 4298 genes that were differentially expressed among the adenomas compared to the carcinoma, with 2057 genes overexpressed and 2241 genes underexpressed in the adenomas.
  • The beta-galactoside binding protein galactin-3 was underexpressed in some adenomas compared to the carcinomas.
  • Prolactin (PRL) and ACTH tumors had the highest levels of expression of galectin-3.
  • The human achaetescute homolog-1 ASCL1 (hASH-1) gene was also underexpressed in some adenomas compared to the carcinoma.
  • Prolactin and ACTH tumors had the highest levels of expression of hASH-1.
  • ID2, which has an important role in cell development and tumorigenesis, was underexpressed in some adenomas compared to the carcinomas.
  • Transducin-like enhancer of split four/ Groucho (TLE-4) was over-expressed in adenomas compared to the ACTH carcinoma.
  • These results indicate that the LGALS3, hASH1, ID2, and TLE-4 genes may have important roles in the development of pituitary carcinomas.
  • [MeSH-major] Adenoma / genetics. Carcinoma / genetics. Gene Expression Profiling / methods. Oligonucleotide Array Sequence Analysis / methods. Pituitary Neoplasms / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / metabolism. Blotting, Western. DNA-Binding Proteins / metabolism. Follicle Stimulating Hormone / secretion. GRB2 Adaptor Protein / metabolism. Growth Hormone-Secreting Pituitary Adenoma / metabolism. Humans. Immunohistochemistry. Inhibitor of Differentiation Protein 2 / metabolism. Luteinizing Hormone / secretion. Nuclear Proteins / metabolism. Prolactinoma / metabolism. Repressor Proteins / metabolism

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  • (PMID = 16943582.001).
  • [ISSN] 1355-008X
  • [Journal-full-title] Endocrine
  • [ISO-abbreviation] Endocrine
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 90249
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Validation Studies
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / GRB2 Adaptor Protein; 0 / GRB2 protein, human; 0 / ID2 protein, human; 0 / Inhibitor of Differentiation Protein 2; 0 / Nuclear Proteins; 0 / Repressor Proteins; 0 / TLE4 protein, human; 9002-67-9 / Luteinizing Hormone; 9002-68-0 / Follicle Stimulating Hormone
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40. Rocha Filho PA, Galvão AC, Teixeira MJ, Rabello GD, Fortini I, Calderaro M, Carrocini D: SUNCT syndrome associated with pituitary tumor: case report. Arq Neuropsiquiatr; 2006 Jun;64(2B):507-10
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  • [Title] SUNCT syndrome associated with pituitary tumor: case report.
  • MRI revealed a pituitary tumor with little suprasellar extent.
  • The subjects serial assays of prolactin, GH, TSH and ACTH were within normal levels.
  • Following transsphenoidal hypophysectomy, with complete removal of the tumor, the subject no more presented pain.
  • The pathological diagnosis was non-secreting adenoma.
  • [MeSH-major] Adenoma / complications. Pituitary Neoplasms / complications. SUNCT Syndrome / etiology

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  • (PMID = 16917628.001).
  • [ISSN] 0004-282X
  • [Journal-full-title] Arquivos de neuro-psiquiatria
  • [ISO-abbreviation] Arq Neuropsiquiatr
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Brazil
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41. 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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42. Prevedello DM, Pouratian N, Sherman J, Jane JA Jr, Vance ML, Lopes MB, Laws ER Jr: Management of Cushing's disease: outcome in patients with microadenoma detected on pituitary magnetic resonance imaging. J Neurosurg; 2008 Oct;109(4):751-9
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  • [Title] Management of Cushing's disease: outcome in patients with microadenoma detected on pituitary magnetic resonance imaging.
  • OBJECT: Outcomes of therapy for Cushing's disease (CD) vary depending on different aspects of presentation and diagnostic studies.
  • The patients included in the study were considered to be optimal surgical candidates, defined as an adult (>18 years of age) with classic clinical features of CD, laboratory studies confirming a central (pituitary/hypothalamic) adrenocorticotropic hormone-dependent source of disease, and an MR imaging study revealing a microadenoma in the sella turcica.
  • Surgical remission was achieved in 148 patients (88.6%), which was correlated with the surgeon's intraoperative identification of an adenoma (p=0.03).
  • Histopathological confirmation of an adrenocorticotropic hormone-secreting adenoma strongly correlated with remission (p=0.0001).
  • Gamma Knife surgery was the most common modality of radiotherapy used to treat 31 patients (18.5%) who did not achieve remission or later presented with recurrent disease.
  • CONCLUSIONS: Even in patients with ideal diagnostic criteria of CD, there remain a significant number of cases in which TSS alone is not adequate to assure long-lasting remission.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / pathology. ACTH-Secreting Pituitary Adenoma / surgery. Adenoma / pathology. Adenoma / surgery. Pituitary ACTH Hypersecretion / pathology. Pituitary ACTH Hypersecretion / surgery

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  • [CommentIn] J Neurosurg. 2012 Feb;116(2):269-71; discussion 270-1 [21923245.001]
  • (PMID = 18826366.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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43. Cho HY, Cho SW, Kim SW, Shin CS, Park KS, Kim SY: Silent corticotroph adenomas have unique recurrence characteristics compared with other nonfunctioning pituitary adenomas. Clin Endocrinol (Oxf); 2010 May;72(5):648-53
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  • [Title] Silent corticotroph adenomas have unique recurrence characteristics compared with other nonfunctioning pituitary adenomas.
  • OBJECTIVE: The prevalence of silent corticotroph adenomas (SCAs) is not rare among nonfunctioning pituitary adenomas (NFPAs); however, it is unknown whether the clinical significance of SCAs differs from that of NFPAs without ACTH immunoreactivity (non-SCAs).
  • MEASUREMENTS: We analysed whether clinical manifestations at diagnosis, postoperative recurrence rate and recurrence characteristics differed between SCA and non-SCA patients.
  • The mean age at the time of diagnosis was 44 years (range, 13-67 years) in the SCA group and 50 years (18-79 years) in the non-SCA group (P = 0.026), with respective follow-up periods of 5.2 (range, 1.0-16.0 years) and 4.2 years (0.5-16.1 years) (P = 0.255).
  • [MeSH-major] Adenoma / pathology. Adrenocorticotropic Hormone / analysis. Neoplasm Recurrence, Local. Pituitary Neoplasms / pathology

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  • (PMID = 19650787.001).
  • [ISSN] 1365-2265
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone
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44. Pouratian N, Prevedello DM, Jagannathan J, Lopes MB, Vance ML, Laws ER Jr: Outcomes and management of patients with Cushing's disease without pathological confirmation of tumor resection after transsphenoidal surgery. J Clin Endocrinol Metab; 2007 Sep;92(9):3383-8
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  • [Title] Outcomes and management of patients with Cushing's disease without pathological confirmation of tumor resection after transsphenoidal surgery.
  • CONTEXT: Despite the success of transsphenoidal surgery (TSS) for the treatment of Cushing's disease, in a number of cases, an ACTH-staining pituitary adenoma is not identified histologically.
  • PATIENTS: Of 490 TSS procedures for Cushing's disease between 1993 and 2004, we identified 111 cases without histological adenoma confirmation.
  • MAIN OUTCOME MEASURE: Remission and recurrence of Cushing's disease were measured.
  • RESULTS: Overall, 50% of these patients achieved remission, a figure lower than for our entire series (79%) and for patients with histological confirmation of an ACTH-staining adenoma (88%) (P < 0.001).
  • Although the overall recurrence rate (21%, seven of 33 evaluated) was not different from previously published long-term studies, in three of seven cases of recurrence, early recurrences were noted between 2 and 4 months after remission.
  • In patients who did not achieve remission, the most common and effective treatment options were repeat TSS, gamma-knife radiosurgery, and bilateral adrenalectomy.
  • CONCLUSION: The lower remission rate in patients without histological evidence of an adenoma is most likely a result of a decreased rate of adenoma extirpation.
  • The incidence of early recurrence may be a unique feature of this patient population; patients without histological confirmation of tumor resection therefore require close and consistent monitoring postoperatively.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / surgery. Pituitary ACTH Hypersecretion / diagnosis. Pituitary ACTH Hypersecretion / surgery
  • [MeSH-minor] Adenoma / diagnosis. Adenoma / pathology. Adenoma / surgery. Adolescent. Adult. Aged. Child. Female. Humans. Male. Middle Aged. Neoplasm Recurrence, Local / diagnosis. Neoplasm Recurrence, Local / pathology. Neoplasm, Residual. Prognosis. Remission Induction. Retrospective Studies. Treatment Failure. Treatment Outcome

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  • [CommentIn] Nat Clin Pract Endocrinol Metab. 2008 Jan;4(1):14-5 [17940518.001]
  • (PMID = 17595252.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] United States
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45. Hofland LJ: Somatostatin and somatostatin receptors in Cushing's disease. Mol Cell Endocrinol; 2008 May 14;286(1-2):199-205
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Somatostatin and somatostatin receptors in Cushing's disease.
  • Cushing's disease is caused by an ACTH secreting pituitary adenoma.
  • Somatostatin (SS) receptors (sst) are expressed on normal and tumoral corticotroph cells.
  • However, the role of somatostatin and in particular the current clinically available sst(2)-preferring SS analogs in the regulation of normal ACTH secretion, as well as in lowering ACTH and cortisol hypersecretion in patients with Cushing's disease, has been shown to be limited.
  • Recent studies have provided renewed insights into the expression of sst subtypes, as well as into the functional role of SS-analogs in the regulation of ACTH secretion by corticotroph tumors.
  • Sst(2) and sst(5) seem the predominantly expressed sst in corticotroph adenoma cells and targeting both these receptors with a new generation of multiligand SS analogs showed promising effects in terms of lowering ACTH release and urinary free cortisol (UFC) levels in patients with Cushing's disease.
  • In this review an overview of the current insights into the role of SS and sst in the regulation of normal and pathological ACTH secretion is provided.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / drug therapy. Adenoma / drug therapy. Pituitary ACTH Hypersecretion / drug therapy. Pituitary Neoplasms / drug therapy. Receptors, Somatostatin / metabolism. Somatostatin / analogs & derivatives. Somatostatin / metabolism

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  • (PMID = 18221833.001).
  • [ISSN] 1872-8057
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Hormone Antagonists; 0 / Receptors, Somatostatin; 51110-01-1 / Somatostatin; 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
  • [Number-of-references] 69
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46. 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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47. Labeur M, Paez-Pereda M, Arzt E, Stalla GK: Potential of retinoic acid derivatives for the treatment of corticotroph pituitary adenomas. Rev Endocr Metab Disord; 2009 Jun;10(2):103-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Potential of retinoic acid derivatives for the treatment of corticotroph pituitary adenomas.
  • Cushing's disease is a severe clinical condition caused by hypersecretion of corticosteroids due to excessive ACTH secretion from a pituitary adenoma.
  • This complex endocrine disorder still represents a major challenge for the physician in terms of efficient treatment.
  • In the last years there was only little progress in elucidating the molecular mechanisms responsible for the constitutive and autonomous ACTH secretion of pituitary corticotrophinomas.
  • As a consequence, no effective drug therapy is currently available, particularly if surgical excision is not successful.
  • In the present article we examine recent studies that have investigated the therapeutic potential of retinoic acid receptors as nuclear receptor targets for the treatment of Cushing's disease.
  • Retinoic acid is an efficient drug used for the treatment of different types of cancers and it proved to act in animal models of Cushing's disease.
  • The efficiency of this treatment in patients with this disorder still needs to be tested in clinical trials.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / drug therapy. Antineoplastic Agents / therapeutic use. Pituitary Neoplasms / drug therapy. Tretinoin / therapeutic use
  • [MeSH-minor] Animals. Humans. Pituitary ACTH Hypersecretion / drug therapy. Pituitary ACTH Hypersecretion / metabolism

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  • (PMID = 18604646.001).
  • [ISSN] 1573-2606
  • [Journal-full-title] Reviews in endocrine & metabolic disorders
  • [ISO-abbreviation] Rev Endocr Metab Disord
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 5688UTC01R / Tretinoin
  • [Number-of-references] 62
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48. 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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49. Bangaru ML, Woodliff J, Raff H, Kansra S: Growth suppression of mouse pituitary corticotroph tumor AtT20 cells by curcumin: a model for treating Cushing's disease. PLoS One; 2010;5(4):e9893
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Growth suppression of mouse pituitary corticotroph tumor AtT20 cells by curcumin: a model for treating Cushing's disease.
  • BACKGROUND: Pituitary corticotroph tumors secrete excess adrenocorticotrophic hormone (ACTH) resulting in Cushing's disease (CD).
  • Standard treatment includes surgery and, if not successful, radiotherapy, both of which have undesirable side effects and frequent recurrence of the tumor.
  • Curcumin, a commonly used food additive in South Asian cooking, has potent growth inhibitory effects on cell proliferation.
  • Our laboratory recently demonstrated that curcumin inhibited growth and induced apoptosis in prolactin- and growth hormone-producing tumor cells.
  • Subsequently, Schaaf et.al. confirmed our findings and also showed the in vivo effectiveness of curcumin to suppress pituitary tumorigenesis.
  • PRINCIPAL FINDINGS: Using the mouse corticotroph tumor cells, AtT20 cells, we report that curcumin had a robust, irreversible inhibitory effect on cell proliferation and clonogenic property.
  • Further, curcumin down-regulated the pro-survival protein Bcl-xL, depolarized the mitochondrial membrane, increased PARP cleavage, which led to apoptotic cell death.
  • Finally, curcumin had a concentration-dependent suppressive effect on ACTH secretion from AtT20 cells.
  • CONCLUSION: The ability of curcumin to inhibit NFkappaB and induce apoptosis in pituitary corticotroph tumor cells leads us to propose developing it as a novel therapeutic agent for the treatment of CD.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / drug therapy. Cell Proliferation / drug effects. Curcumin / pharmacology. Pituitary ACTH Hypersecretion / drug therapy
  • [MeSH-minor] Adrenocorticotropic Hormone / secretion. Animals. Antineoplastic Agents. Apoptosis / drug effects. Cell Line, Tumor. Dose-Response Relationship, Drug. Mice. NF-kappa B / antagonists & inhibitors

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  • (PMID = 20405005.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / NF-kappa B; 9002-60-2 / Adrenocorticotropic Hormone; IT942ZTH98 / Curcumin
  • [Other-IDs] NLM/ PMC2854133
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50. Stilling G, Sun Z, Zhang S, Jin L, Righi A, Kovācs G, Korbonits M, Scheithauer BW, Kovacs K, Lloyd RV: MicroRNA expression in ACTH-producing pituitary tumors: up-regulation of microRNA-122 and -493 in pituitary carcinomas. Endocrine; 2010 Aug;38(1):67-75
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MicroRNA expression in ACTH-producing pituitary tumors: up-regulation of microRNA-122 and -493 in pituitary carcinomas.
  • MicroRNAs (miRNAs) are involved in cell proliferation, differentiation, and apoptosis, and can function as tumor suppressor genes or oncogenes.
  • The expression of miRNAs in pituitary carcinomas has not been previously examined.
  • We used miRNA profiling with 1,145 probes to study miRNA expression in normal anterior pituitary (6 cases), adrenocorticotropin (ACTH)-producing adenomas (8 cases), and ACTH-producing pituitary carcinomas (two cases).
  • Real-time RT-PCR and in situ hybridization were used to confirm and independently validate miRNAs that were significantly up-regulated or down-regulated between the pituitary tissues.
  • There were more miRNAs up- (188) or down-regulated (160) between adenomas and normal pituitaries compared to carcinomas and normal pituitaries (92 up- and 91 down-regulated) or between carcinomas and adenomas (46 up- and 52 down-regulated).
  • Both real-time RT-PCR and in situ hybridization showed significant up-regulation of miRNA-122 between pituitary carcinomas and adenomas.
  • MiRNA-493 was also up-regulated in carcinomas compared to ACTH adenomas.
  • Analysis of genes that miRNA-493 interacts with included LGALS3 and RUNX2 ( http://microrna.sanger.ac.uk ) both of which have been shown to have roles in pituitary tumor cell growth.
  • These results provide information about marker miRNAs that may lead to further insights into the regulation of pituitary tumor growth and development.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / genetics. Adenoma / genetics. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. MicroRNAs / genetics
  • [MeSH-minor] Adult. Aged. Female. Humans. In Situ Hybridization. Oligonucleotide Array Sequence Analysis. Pituitary Gland, Anterior / pathology. Pituitary Gland, Anterior / physiology. Reverse Transcriptase Polymerase Chain Reaction. Up-Regulation / genetics

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  • (PMID = 20960104.001).
  • [ISSN] 1559-0100
  • [Journal-full-title] Endocrine
  • [ISO-abbreviation] Endocrine
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MIRN122 microRNA, human; 0 / MIRN493 microRNA, human; 0 / MicroRNAs
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51. Assimakopoulou M, Zolota V, Chondrogianni C, Gatzounis G, Varakis J: p75 and TrkC neurotrophin receptors demonstrate a different immunoreactivity profile in comparison to TrkA and TrkB receptors in human normal pituitary gland and adenomas. Neuroendocrinology; 2008;88(2):127-34
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  • [Title] p75 and TrkC neurotrophin receptors demonstrate a different immunoreactivity profile in comparison to TrkA and TrkB receptors in human normal pituitary gland and adenomas.
  • TrkA and TrkB receptors have been previously detected in numerous endocrine cells in human anterior pituitary and adenomas.
  • METHODS: Semi-serial paraffin-embedded sections of 5 human normal pituitaries and 30 adenomas were immunostained using specific antibodies.
  • RESULTS: Expression of p75(NTR) receptor was demonstrated in the intricate capillary and reticulin network in the anterior pituitary and in the pericapillary tissue and pituicytes in the posterior lobe. p75(NTR) immunoreactivity was absent from all adenomas.
  • In normal anterior pituitary, a few scattered cells showed weak TrkC immunoreactivity in contrast to a high percentage of endocrine cells distributed throughout the pars distalis and pars intermedia which exhibited strong TrkA and/or intermediate TrkB immunoreactivity.
  • Double immunohistochemistry demonstrated TrkA immunoreactivity in more than 80% of lactotropes and 70% of corticotropes and to a lesser extent in other cell types.
  • Furthermore, in the majority of adenomas, independently of type, sex and age, a high percentage of TrkA- and/or TrkB-positive cells was detected.
  • Interestingly, TrkC expression appeared to be increased in some adenomas compared to normal pituitary.
  • CONCLUSION: The above findings support a potential role of all neurotrophins, through their different receptors, in pituitary functions.
  • [MeSH-major] Adenoma / metabolism. Pituitary Gland / metabolism. Pituitary Neoplasms / metabolism. Receptor, Nerve Growth Factor / metabolism. Receptor, trkA / metabolism. Receptor, trkB / metabolism. Receptor, trkC / metabolism
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / metabolism. ACTH-Secreting Pituitary Adenoma / pathology. Adult. Aged. Female. Growth Hormone-Secreting Pituitary Adenoma / metabolism. Growth Hormone-Secreting Pituitary Adenoma / pathology. Humans. Immunohistochemistry. Male. Middle Aged. Prolactinoma / metabolism. Prolactinoma / pathology

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  • [Copyright] (c) 2008 S. Karger AG, Basel.
  • (PMID = 18319596.001).
  • [ISSN] 1423-0194
  • [Journal-full-title] Neuroendocrinology
  • [ISO-abbreviation] Neuroendocrinology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Receptor, Nerve Growth Factor; EC 2.7.10.1 / Receptor, trkA; EC 2.7.10.1 / Receptor, trkB; EC 2.7.10.1 / Receptor, trkC
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52. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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53. Marek J: [Pituitary adenomas--where is the treatment heading at the beginning of the 21st century?]. Vnitr Lek; 2010 Jul;56(7):690-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Pituitary adenomas--where is the treatment heading at the beginning of the 21st century?].
  • To treat pituitary adenomas, three modes of treatment are usually combined: neurosurgery, radiation and pharmacological.
  • Patients with acromegaly are usually diagnosed late and thus many neurosurgeries fail to completely remove the adenoma.
  • The same surgical and Gamma Knife procedures are used in patients with the Cushing's disease and TSH-secreting adenomas.
  • Ketoconazole, metyrapone and cabergoline are used until the radiation effect in the Cushing's disease is complete, similarly, somatostatine analogues are used in TSH-secreting adenomas.
  • Nonfunctional adenomas are less responsive to pharmacological treatment.
  • Proautophagic cytostatic temozolamide has been used in aggressive pituitary adenomas and carcinomas.
  • [MeSH-major] Adenoma / therapy. Pituitary Neoplasms / therapy
  • [MeSH-minor] Acromegaly / etiology. Humans. Pituitary ACTH Hypersecretion / etiology. Prolactinoma / therapy

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  • (PMID = 20842914.001).
  • [ISSN] 0042-773X
  • [Journal-full-title] Vnitr̆ní lékar̆ství
  • [ISO-abbreviation] Vnitr Lek
  • [Language] cze
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Czech Republic
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54. 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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55. 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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56. Mounier C, Pasquet F, Trouillas J, Perrin G, Jouanneau E, Borson-Chazot F, Colle B: [Nelson's syndrome: course of aggressive pituitary corticotroph adenoma]. Ann Endocrinol (Paris); 2007 Feb;68(1):28-33
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  • [Title] [Nelson's syndrome: course of aggressive pituitary corticotroph adenoma].
  • [Transliterated title] Syndrome de Nelson: évolution d'un adénome hypophysaire corticotrope agressif.
  • Nelson's syndrome was defined in 1958 as the association of an expanding pituitary tumor with high ACTH secretion after bilateral adrenalectomy for Cushing's disease.
  • Pituitary MRI and ACTH measurements led to the definition of Nelson's syndrome as the proliferation of a corticotrophic microadenoma or an aggressive and highly proliferative tumor residue induced by the decreased glucocorticoid inhibition after bilateral adrenalectomy.
  • Now, the problem is not the definition of Nelson's syndrome but rather the identification of markers predictive of tumor growth.
  • Based on a typical case and a review of the literature, we point out some predictive markers of tumor growth after bilateral adrenalectomy: young age at diagnosis, presence of tumor residue on pituitary MRI before adrenalectomy, markers of tumor aggressiveness (Ki-67>3%, mitoses, nuclear PTTG) and increase of ACTH levels during the first months following adrenalectomy.
  • [MeSH-major] Adenoma / physiopathology. Nelson Syndrome / physiopathology. Pituitary Neoplasms / physiopathology
  • [MeSH-minor] Adrenocorticotropic Hormone / analysis. Adrenocorticotropic Hormone / secretion. Adult. Female. Humans. Magnetic Resonance Imaging. Pituitary Gland / pathology

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  • (PMID = 17306208.001).
  • [ISSN] 0003-4266
  • [Journal-full-title] Annales d'endocrinologie
  • [ISO-abbreviation] Ann. Endocrinol. (Paris)
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone
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57. Santos AR, Fonseca Neto RM, Veiga JC, Viana Jr J, Scaliassi NM, Lancellotti CL, Lazarini PR: Endoscopic endonasal transsphenoidal approach for pituitary adenomas: technical aspects and report of casuistic. Arq Neuropsiquiatr; 2010 Aug;68(4):608-12
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  • [Title] Endoscopic endonasal transsphenoidal approach for pituitary adenomas: technical aspects and report of casuistic.
  • OBJECTIVE: Analyse technical aspects, effectiveness and morbidity of the endoscopic endonasal transphenoidal approach for pituitary adenomas.
  • METHOD: From January 2005 to September 2008, 30 consecutive patients underwent endoscopic endonasal resection of pituitary adenomas with a follow up from 3 to 36 months.
  • Twelve patients had non-functioning tumors, 9 had ACTH-secreting tumors, 8 had GH-secreting tumors and 1 prolactinoma.
  • CONCLUSION: The endonasal endoscopic approach for pituitary tumors is effective and has low morbidity.
  • [MeSH-major] Adenoma / surgery. Neuroendoscopy / methods. Pituitary Neoplasms / surgery

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  • (PMID = 20730318.001).
  • [ISSN] 1678-4227
  • [Journal-full-title] Arquivos de neuro-psiquiatria
  • [ISO-abbreviation] Arq Neuropsiquiatr
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Brazil
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58. Walsh MT, Couldwell WT: Symptomatic cystic degeneration of a clinically silent corticotroph tumor of the pituitary gland. Skull Base; 2010 Sep;20(5):367-70
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  • [Title] Symptomatic cystic degeneration of a clinically silent corticotroph tumor of the pituitary gland.
  • Clinically silent corticotroph tumors of the pituitary gland are those tumors that stain for adrenocorticotropic hormone (ACTH) but do not manifest with clinical or laboratory features of Cushing disease.
  • These tumors have been described as exhibiting more aggressive behavior than other nonfunctional pituitary tumors.
  • We present an unusual case of a clinically silent corticotropic adenoma of the pituitary gland that underwent cystic degeneration following recurrence after transsphenoidal surgery and radiation therapy.
  • Patients with clinically silent ACTH-secreting tumors should be monitored for aggressive tumor behavior and may require closer follow-up than those patients harboring other nonfunctional tumors.

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  • [Cites] Nucleic Acids Res. 1983 Oct 25;11(20):7191-203 [6634412.001]
  • (PMID = 21359002.001).
  • [ISSN] 1532-0065
  • [Journal-full-title] Skull base : official journal of North American Skull Base Society ... [et al.]
  • [ISO-abbreviation] Skull Base
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC3023327
  • [Keywords] NOTNLM ; Cortisol / Cushing disease / adrenocorticotropic hormone / corticotroph cells / cystic degeneration / nonfunctional pituitary adenoma
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59. Raica M, Coculescu M, Cimpean AM, Ribatti D: Endocrine gland derived-VEGF is down-regulated in human pituitary adenoma. Anticancer Res; 2010 Oct;30(10):3981-6
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  • [Title] Endocrine gland derived-VEGF is down-regulated in human pituitary adenoma.
  • BACKGROUND: Endocrine gland-derived vascular endothelial growth factor (EG-VEGF) is an angiogenic molecule restricted to endocrine glands and, particularly, to steroid-secreting cells.
  • MATERIALS AND METHODS: In this study, we investigated by immunohistochemistry the expression of EG-VEGF in 2 samples of normal adenohypophysis and 43 bioptic samples of pituitary adenoma.
  • Moreover, the expression of growth hormone (GH), prolactin (PRL), follicle-stimulating hormone (FSH), luteinizing hormone (LH), thyroid-stimulating hormone (TSH) and adrenocorticoprophic hormone (ACTH) were also estimated.
  • RESULTS: The results of this study for the first time demonstrate a down-regulation of EG-VEGF expression in human pituitary adenoma as compared to normal adenohypophysis, suggesting an impaired function of the neoplastic cells in terms of hormone release in the blood stream, as a consequence of impaired tumor angiogenesis in the tumor.
  • CONCLUSION: On the basis of our data showing a marked decrease in the expression of EG-VEGF in pituitary adenoma, with the exception of LH-secreting adenomas, we suggest that LH might be involved in the induction of EG-VEGF secretion.
  • [MeSH-major] Adenoma / metabolism. Pituitary Neoplasms / metabolism. Vascular Endothelial Growth Factor, Endocrine-Gland-Derived / biosynthesis
  • [MeSH-minor] Adrenocorticotropic Hormone / biosynthesis. Down-Regulation. Follicle Stimulating Hormone / biosynthesis. Human Growth Hormone / biosynthesis. Humans. Immunohistochemistry. Luteinizing Hormone / biosynthesis. Pituitary Gland, Anterior / metabolism. Prolactin / biosynthesis. Thyrotropin / biosynthesis

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  • (PMID = 21036711.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Vascular Endothelial Growth Factor, Endocrine-Gland-Derived; 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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60. Horiguchi K, Yamada M, Umezawa R, Satoh T, Hashimoto K, Tosaka M, Yamada S, Mori M: Somatostatin receptor subtypes mRNA in TSH-secreting pituitary adenomas: a case showing a dramatic reduction in tumor size during short octreotide treatment. Endocr J; 2007 Jun;54(3):371-8
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  • [Title] Somatostatin receptor subtypes mRNA in TSH-secreting pituitary adenomas: a case showing a dramatic reduction in tumor size during short octreotide treatment.
  • TSH-secreting adenoma is a rare pituitary adenoma, and the expression levels of the specific subtypes of somatostatin receptors (sstr) mRNAs have remained obscure.
  • To determine the quantitative expression of the sstr1-5 mRNAs in TSH-secreting adenomas that may be related to the efficacy of treatment with a somatostatin analogue, expression of the sstr1-5 mRNAs was examined and compared in TSH-secreting adenomas and other pituitary adenomas.
  • The pituitary adenomas were obtained at transsphenoidal surgery from 4 cases of TSH-secreting adenoma, including 1 patient showing a significant shrinkage of the tumor size after only 10 days of octreotide treatment, 2 patients without tumor size reduction and 1 patient without treatment, and 5 GH-secreting adenomas, 6 prolactinomas, 5 nonfunctioning adenomas, 4 ACTH-secreting adenomas and normal pituitaries at autopsy from 4 normal subjects.
  • In comparison to the normal pituitary, sstr2A>sstr1>sstr5>sstr3 mRNAs were expressed in the TSH-secreting adenomas examined.
  • The expression level of sstr2 mRNA was significantly higher than those in normal pituitary, prolactinomas, ACTH-secreting and nonfunctioning pituitary adenomas.
  • The patient with marked shrinkage of the tumor showed the highest expression of both sstr2 and sstr5 mRNAs among all the cases of pituitary adenoma.
  • A TSH-secreting tumor without shrinkage showed a similar expression level of sstr2 mRNA.
  • These findings demonstrated that TSH-secreting adenomas express sstr1, 2A, 3 and 5 mRNAs, predominantly sstr2A, and in addition to the expression of sstr2 mRNA, the expression level of sstr5 mRNA may be a factor affecting the tumor shrinkage by somatostatin analogues against TSH-secreting adenomas.
  • [MeSH-major] Adenoma / drug therapy. Adenoma / genetics. Octreotide / therapeutic use. Pituitary Neoplasms / drug therapy. Pituitary Neoplasms / genetics. Receptors, Somatostatin / genetics. Thyrotrophs / pathology. Tumor Burden / drug effects

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  • (PMID = 17420609.001).
  • [ISSN] 0918-8959
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Case Reports; Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / Receptors, Somatostatin; RWM8CCW8GP / Octreotide
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61. Liu JK, Fleseriu M, Delashaw JB Jr, Ciric IS, Couldwell WT: Treatment options for Cushing disease after unsuccessful transsphenoidal surgery. Neurosurg Focus; 2007;23(3):E8
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  • [Title] Treatment options for Cushing disease after unsuccessful transsphenoidal surgery.
  • Cushing disease is considered an aggressive pituitary endocrinopathy because of the devastating effects from untreated hypercortisolemia.
  • Although they are histologically benign, these adrenocorticotropic hormone (ACTH)-secreting pituitary tumors are associated with significant morbidity and premature death.
  • Currently, transsphenoidal surgery is the primary treatment of Cushing disease associated with an ACTH-secreting pituitary tumor, resulting in remission rates ranging from about 50 to 90%.
  • Some patients, however, will not achieve sustained remission after transsphenoidal surgery and can exhibit persistent or recurrent Cushing disease that requires multimodal treatment to achieve remission.
  • Despite undergoing multiple treatment modalities, some patients may ultimately require bilateral adrenalectomy for definitive treatment to eliminate hypercortisolemia associated with Cushing disease.
  • In this article, the authors review the treatment options for patients who have persistent or recurrent Cushing disease after unsuccessful transsphenoidal surgery.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / surgery. Adenoma / surgery. Pituitary ACTH Hypersecretion / therapy

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  • (PMID = 17961031.001).
  • [ISSN] 1092-0684
  • [Journal-full-title] Neurosurgical focus
  • [ISO-abbreviation] Neurosurg Focus
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 67
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62. Bocca G, Voorhoeve PG, de Delemarre-van Wall HA: [Cushing's syndrome in children]. Ned Tijdschr Geneeskd; 2006 Oct 28;150(43):2345-9
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  • [Title] [Cushing's syndrome in children].
  • In two girls, aged 13 and 16 years, Cushing's syndrome was diagnosed.
  • In addition, the first showed a decrease in linear growth and weight gain; a pituitary adenoma was found, which was surgically excised.
  • She had an adrenal adenoma, visible on MRI, which was excised during laparoscopy.
  • Cushing's syndrome is a rare disease in childhood.
  • Arriving at an aetiological diagnosis may be difficult and is based on the performance and interpretation of endocrinologic function and laboratory tests such as determination of the cortisol level in blood, saliva and urine, a dexamethasone-suppression test, and a corticotropin assay in blood drawn from the cerebral cavernous sinuses.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / diagnosis. Adenoma / diagnosis. Cushing Syndrome / diagnosis. Hydrocortisone / blood
  • [MeSH-minor] Adolescent. Dexamethasone. Diagnosis, Differential. Female. Growth. Humans. Magnetic Resonance Imaging. Treatment Outcome. Weight Gain

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  • [CommentIn] Ned Tijdschr Geneeskd. 2007 Mar 3;151(9):560; author reply 560-1 [17375397.001]
  • [CommentOn] Ned Tijdschr Geneeskd. 2006 Oct 28;150(43):2365-9 [17100127.001]
  • [CommentOn] Ned Tijdschr Geneeskd. 2006 Oct 28;150(43):2390-3 [17100132.001]
  • [CommentOn] Ned Tijdschr Geneeskd. 2006 Oct 28;150(43):2359-64 [17100126.001]
  • (PMID = 17100122.001).
  • [ISSN] 0028-2162
  • [Journal-full-title] Nederlands tijdschrift voor geneeskunde
  • [ISO-abbreviation] Ned Tijdschr Geneeskd
  • [Language] dut
  • [Publication-type] Case Reports; Comment; English Abstract; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 7S5I7G3JQL / Dexamethasone; WI4X0X7BPJ / Hydrocortisone
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63. Manetti L, Bogazzi F, Giovannetti C, Raffaelli V, Genovesi M, Pellegrini G, Ruocco L, Iannelli A, Martino E: Changes in coagulation indexes and occurrence of venous thromboembolism in patients with Cushing's syndrome: results from a prospective study before and after surgery. Eur J Endocrinol; 2010 Nov;163(5):783-91
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  • [Title] Changes in coagulation indexes and occurrence of venous thromboembolism in patients with Cushing's syndrome: results from a prospective study before and after surgery.
  • OBJECTIVES: To evaluate whether patients with Cushing's syndrome (CS) had i) changes in coagulative and fibrinolytic parameters associated with CS activity and ii) higher prevalence of venous thromboembolic events (VTE).
  • DESIGN: Prospective study conducted on patients with CS evaluated at diagnosis and 12 months after surgery.
  • PATIENTS AND METHODS: Forty patients with active CS (36 with Cushing's disease (CD) and 4 with an adrenal adenoma) were evaluated.
  • Forty normal subjects and 70 patients with non-ACTH-secreting pituitary adenomas served as controls.
  • Patients with still active disease after surgery had higher coagulative parameters than those in remission (VWF (P<0.0001), PAI-1 (P=0.004), TAT (P=0.0001), ATIII (P=0.0002) and α(2) antiplasmin (or SERPINF2; P=0.006)), whereas aPTT levels (P=0.007) were significantly reduced.
  • VTE occurred in three patients with CD (7.5%): one had a pulmonary embolism and two patients had a deep venous thrombosis; no patients submitted to transsphenoidal surgery for non-Cushing's pituitary adenoma had VTE (P=0.04).
  • Thromboprophylaxis seems to be appropriated in patients with active disease, particularly in the postoperative period.


64. 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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65. 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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66. 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.


67. Martínez-Fuentes AJ, Moreno-Fernández J, Vázquez-Martínez R, Durán-Prado M, de la Riva A, Tena-Sempere M, Diéguez C, Jiménez-Reina L, Webb SM, Pumar A, Leal-Cerro A, Benito-López P, Malagón MM, Castaño JP: Ghrelin is produced by and directly activates corticotrope cells from adrenocorticotropin-secreting adenomas. J Clin Endocrinol Metab; 2006 Jun;91(6):2225-31
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  • [Title] Ghrelin is produced by and directly activates corticotrope cells from adrenocorticotropin-secreting adenomas.
  • CONTEXT: In Cushing's disease, ACTH hypersecretion by pituitary corticotrope adenoma cells and resulting hypercortisolism is accompanied by a severely blunted GH secretory response.
  • Interestingly, in Cushing's disease, ghrelin markedly increases plasma ACTH, whereas its stimulatory action on GH secretion is reduced.
  • Although the reported expression of ghrelin receptors (GHS-R) in corticotrope tumors offers a potential mechanism for ghrelin-induced ACTH hypersecretion, studies on the direct effects of synthetic GH secretagogues on corticotropinoma cells offered contradictory results.
  • OBJECTIVE AND DESIGN: To evaluate the direct action of ghrelin on corticotropinoma cells from two patients with Cushing's disease, we measured its effect on free cytosolic calcium concentration ([Ca(2+)](i)).
  • Additionally, expression of GHS-R and its ligand ghrelin was examined in these cells and in five additional corticotropinomas.
  • RESULTS: Ghrelin (10(-6) m) induced a marked [Ca(2+)](i) increase in 89.5% (case 1; n = 19 cells) and 85% (case 2; n = 13 cells) of corticotropinoma cells.
  • Moreover, RT-PCR showed that expression of GHS-R isoforms is accompanied by that of ghrelin in all seven corticotrope adenomas examined.
  • Importantly, double immunogold electron microscopy revealed that ghrelin is costored within ACTH secretory vesicles in densely granulated adenomatous corticotropes.
  • CONCLUSIONS: These results constitute the first demonstration that ghrelin acts directly on corticotrope tumor cells derived from patients with Cushing's disease.
  • The presence of ghrelin and GHS-R suggests that pituitary ghrelin may play an autocrine/paracrine role in regulating ACTH release in Cushing's disease.
  • Our findings provide a plausible cellular basis for the exaggerated ACTH response to ghrelin in Cushing's disease and suggest novel research strategies to develop medical treatments for this disease.
  • [MeSH-major] Adenoma / secretion. Adrenocorticotropic Hormone / secretion. Peptide Hormones / physiology. Pituitary Neoplasms / secretion

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  • (PMID = 16551736.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ghrelin; 0 / Peptide Hormones; 0 / RNA, Messenger; 0 / Receptors, G-Protein-Coupled; 0 / Receptors, Ghrelin; 66796-54-1 / Pro-Opiomelanocortin; 9002-60-2 / Adrenocorticotropic Hormone; SY7Q814VUP / Calcium
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68. Kamenicky P, Houdoin L, Ferlicot S, Salenave S, Brailly S, Droupy S, Meduri G, Sasano H, Suzuki T, Young J, Chanson P: Benign cortisol-secreting adrenocortical adenomas produce small amounts of androgens. Clin Endocrinol (Oxf); 2007 Jun;66(6):778-88
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  • [Title] Benign cortisol-secreting adrenocortical adenomas produce small amounts of androgens.
  • BACKGROUND: Serum androgen levels are below normal in patients with benign cortisol-secreting adrenocortical adenomas, owing to ACTH suppression.
  • The objective of the study was to analyse the androgen-producing ability of cortisol-secreting adrenocortical adenomas.
  • METHODS: Dehydroepiandrosterone sulfate (DHEAS), Delta4androstenedione and testosterone concentrations were measured before and after adrenalectomy and then at 6-month intervals in 20 women (eight cortisol-secreting adrenocortical adenomas, six subclinical cortisol-secreting adrenocortical adenomas, and six nonfunctional adenomas).
  • RESULTS: Before adrenalectomy, serum androgen concentrations were measurable in all women with clinically apparent and subclinical cortisol-secreting adrenocortical adenomas.
  • Postoperatively, during adrenocortical insufficiency, DHEAS, Delta4androstenedione and testosterone concentrations fell to near the detection limit in all patients with cortisol-secreting adrenocortical adenomas (P = 0.008 for each marker) and showed a similar tendency to fall in all patients with subclinical cortisol-secreting adrenocortical adenomas.
  • Pre- and post-treatment androgen concentrations did not differ in patients with nonfunctional adenomas.
  • Immunohistochemical analysis confirmed CYP17, HSD3B2, SULT2A1 and CYB5 expression by all cortisol-producing tumours.
  • The intensity of CYP17 and SULT2A1 expression was stronger in cortisol-secreting adenomas than in their adjacent normal adrenal tissue.
  • CONCLUSION: Both clinically apparent and subclinical cortisol-secreting adrenocortical adenomas appear to show moderate autonomous androgen production.
  • Thus, weak androgen secretion in patients with adrenocortical tumours should not necessarily be considered as a sign of malignancy.
  • [MeSH-major] Adenoma / secretion. Adrenal Cortex Neoplasms / secretion. Androgens / secretion. Hydrocortisone / secretion
  • [MeSH-minor] Adolescent. Adrenalectomy. Adrenocorticotropic Hormone / blood. Adult. Aged. Aged, 80 and over. Androstenedione / blood. Dehydroepiandrosterone Sulfate / blood. Estrogens / blood. Female. Follow-Up Studies. Gonadotropins, Pituitary / blood. Humans. Immunohistochemistry. Menstrual Cycle. Middle Aged. Postoperative Period. Retrospective Studies. Statistics, Nonparametric. Testosterone / blood

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  • (PMID = 17408424.001).
  • [ISSN] 0300-0664
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgens; 0 / Estrogens; 0 / Gonadotropins, Pituitary; 3XMK78S47O / Testosterone; 409J2J96VR / Androstenedione; 57B09Q7FJR / Dehydroepiandrosterone Sulfate; 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
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69. Lodish MB, Sinaii N, Patronas N, Batista DL, Keil M, Samuel J, Moran J, Verma S, Popovic J, Stratakis CA: Blood pressure in pediatric patients with Cushing syndrome. J Clin Endocrinol Metab; 2009 Jun;94(6):2002-8
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  • CONTEXT: Hypertension (HTN) has been reported in up to 60% of children with Cushing syndrome (CS), but its course, side effects, and potential differences among various causes of CS have not been adequately studied.
  • DESIGN: Data from 86 children with corticotropinomas [Cushing disease (CD)] and 27 children with ACTH-independent CS (AICS) were analyzed.

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  • (PMID = 19293264.001).
  • [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 / Intramural NIH HHS / /
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone
  • [Other-IDs] NLM/ PMC2690429
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70. Barahona MJ, Sojo L, Wägner AM, Bartumeus F, Oliver B, Cano P, Webb SM: Determinants of neurosurgical outcome in pituitary tumors. J Endocrinol Invest; 2005 Oct;28(9):787-94
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  • [Title] Determinants of neurosurgical outcome in pituitary tumors.
  • OBJECTIVE: Neurosurgery is one of the main therapies for pituitary tumors; optimising outcome is highly desirable for the patient and the health system.
  • We have analysed predictors of outcome in surgically treated pituitary adenomas operated in this centre.
  • DESIGN AND PATIENTS: A total of 289 patients underwent neurosurgery for a pituitary tumor, by the same two neurosurgeons, between 1982 and 2001.
  • Most tumors (70.2%) were macroadenomas; 28.4% were non-functioning, 27.3% secreted PRL, 26.3% GH of which 14 (4.8%) also secreted PRL, 17.3% ACTH, 0.3% FSH and 0.3% TSH.
  • RESULTS: A stepwise, forward logistic regression analysis revealed tumor size as the only significant predictor of radiological cure [odds ratio (OR) for macroadenoma 0.16 vs microadenoma, p=0.0005].
  • Hormonally, PRL-secretion by the tumor was a predictor of poor prognosis (OR 3.29 for cure of non-PRL-secreting tumors, p=0.005), as was tumor size (OR 0.45 for cure of macroadenomas, p=0.005).
  • Considering simultaneous radiological and hormonal remission, tumor size (OR 0.35 for macroadenoma, p=0.0002), and operation date (OR 0.40 for up to 1991, p=0.0002) were the only significant predictors.
  • CONCLUSIONS: PRL secretion, tumor size and operation date are the main predictors of neurosurgical outcome in pituitary tumors, the latter suggesting that neurosurgical experience plays an important role.
  • [MeSH-major] Adenoma / surgery. Neurosurgical Procedures / methods. Pituitary Neoplasms / surgery

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  • (PMID = 16370556.001).
  • [ISSN] 0391-4097
  • [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] 12629-01-5 / Human Growth Hormone; 9002-60-2 / Adrenocorticotropic Hormone
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71. Rollin G, Ferreira NP, Czepielewski MA: Prospective evaluation of transsphenoidal pituitary surgery in 108 patients with Cushing's disease. Arq Bras Endocrinol Metabol; 2007 Nov;51(8):1355-61
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  • [Title] Prospective evaluation of transsphenoidal pituitary surgery in 108 patients with Cushing's disease.
  • Transsphenoidal pituitary surgery (TSS) remains the treatment of choice for Cushing's disease (CD).
  • Despite the widespread acceptance of this procedure as the first line treatment in CD, the indication of a second TSS in not cured or relapsed DC patients is not consensus.
  • Fourteen patients underwent second TSS (5 had already been operated in others centers; in 5 patients the first surgery was not curative; in 4 patients CD relapsed).
  • In patients with negative pituitary imaging remission rates were 71.4% (p = 0.003; vs. microadenomas).
  • The low remission rates after a second TSS suggest that this approach could not be a good therapeutic choice when the first one was not curative.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / surgery. Adenoma / surgery. Hypophysectomy / standards. Pituitary ACTH Hypersecretion / surgery. Pituitary Neoplasms / surgery. Sphenoid Sinus / surgery
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Female. Follow-Up Studies. Humans. Male. Middle Aged. Postoperative Complications / diagnosis. Recurrence. Remission Induction. Reoperation. Treatment Outcome

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  • (PMID = 18209874.001).
  • [ISSN] 0004-2730
  • [Journal-full-title] Arquivos brasileiros de endocrinologia e metabologia
  • [ISO-abbreviation] Arq Bras Endocrinol Metabol
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] Brazil
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72. Giacomini D, Páez-Pereda M, Theodoropoulou M, Gerez J, Nagashima AC, Chervin A, Berner S, Labeur M, Refojo D, Renner U, Stalla GK, Arzt E: Bone morphogenetic protein-4 control of pituitary pathophysiology. Front Horm Res; 2006;35:22-31
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  • [Title] Bone morphogenetic protein-4 control of pituitary pathophysiology.
  • Bone morphogenetic protein-4 (BMP-4), a member of the transforming growth factor-Beta(TGF-Beta) family, is overexpressed in different prolactinoma models and induces the development of these lineage adenomas.
  • SMAD proteins activated by growth factors of the TGF-Beta and BMP family interact with estrogen receptors to stimulate the proliferation of prolactin and growth hormone-secreting cells.
  • Furthermore, BMP-4 presents differential expression in normal and adenomatous corticotropes and inhibitory action on corticotropinoma cell proliferation.
  • The present review highlights not only the crucial and opposite role of BMP-4 in the progression of pituitary adenomas but also that BMP-4 and retinoic acid interaction might serve as a potential new mechanism target for therapeutic approaches for Cushing disease.
  • [MeSH-major] Bone Morphogenetic Proteins / physiology. Pituitary Diseases / etiology
  • [MeSH-minor] Adrenocorticotropic Hormone / secretion. Animals. Bone Morphogenetic Protein 4. Gene Expression. Humans. Models, Biological. Neurons / secretion. Pituitary Gland / cytology. Pituitary Gland / growth & development. Pituitary Gland / metabolism. Pituitary Gland / secretion. Receptors, Transforming Growth Factor beta / metabolism. Transforming Growth Factor beta / physiology. Tretinoin / pharmacology

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  • (PMID = 16809920.001).
  • [ISSN] 0301-3073
  • [Journal-full-title] Frontiers of hormone research
  • [ISO-abbreviation] Front Horm Res
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / BMP4 protein, human; 0 / Bone Morphogenetic Protein 4; 0 / Bone Morphogenetic Proteins; 0 / Receptors, Transforming Growth Factor beta; 0 / Transforming Growth Factor beta; 5688UTC01R / Tretinoin; 9002-60-2 / Adrenocorticotropic Hormone
  • [Number-of-references] 42
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73. 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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74. Tinnel BA, Henderson MA, Witt TC, Fakiris AJ, Worth RM, Des Rosiers PM, Edmondson JW, Timmerman RD, Lo SS: Endocrine response after gamma knife-based stereotactic radiosurgery for secretory pituitary adenoma. Stereotact Funct Neurosurg; 2008;86(5):292-6
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  • [Title] Endocrine response after gamma knife-based stereotactic radiosurgery for secretory pituitary adenoma.
  • PURPOSE: To examine treatment outcomes of Gamma Knife-based stereotactic radiosurgery (GK-based SRS) for secretory pituitary adenomas.
  • MATERIALS AND METHODS: 25 patients were treated with GK-based SRS for secretory pituitary adenomas with >or=12 months of follow-up.
  • For adrenocorticotrophic hormone-secreting tumors, 6 of 12 patients (50%) showed normalization of their endocrine levels at a median of 10 months.
  • For growth hormone-secreting tumors, 4 of 9 patients (44%) showed normalization of endocrine levels at a median time of 30 months.
  • CONCLUSION: GK-based SRS provides a reasonable rate of endocrine normalization of secretory pituitary adenoma.
  • [MeSH-major] Pituitary Neoplasms / surgery. Prolactin / blood. Prolactin / secretion. Prolactinoma / surgery. Radiosurgery
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / secretion. ACTH-Secreting Pituitary Adenoma / surgery. Adenoma / secretion. Adenoma / surgery. Adrenocorticotropic Hormone / secretion. Adult. Aged. Aged, 80 and over. Female. Follow-Up Studies. Growth Hormone-Secreting Pituitary Adenoma / secretion. Growth Hormone-Secreting Pituitary Adenoma / surgery. Human Growth Hormone / secretion. Humans. Hydrocortisone / blood. Insulin-Like Growth Factor I / metabolism. Male. Middle Aged. Retrospective Studies. Treatment Outcome

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  • [Copyright] Copyright 2008 S. Karger AG, Basel.
  • (PMID = 18758206.001).
  • [ISSN] 1423-0372
  • [Journal-full-title] Stereotactic and functional neurosurgery
  • [ISO-abbreviation] Stereotact Funct Neurosurg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I; 9002-60-2 / Adrenocorticotropic Hormone; 9002-62-4 / Prolactin; WI4X0X7BPJ / Hydrocortisone
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75. Bronstein MD, Melmed S: [Pituitary tumorigenesis]. Arq Bras Endocrinol Metabol; 2005 Oct;49(5):615-25
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  • [Title] [Pituitary tumorigenesis].
  • Pituitary adenomas, almost invariably adenomas, account for 10% to 15% of all intracranial neoplasms and are incidentally detected in up to 27% of non selected autopsies.
  • Functionally, they are classified as secreting adenomas (PRL, GH, ACTH, TSH, LH, and FSH, and those co-secreting two or more hormones), and clinically non secreting or "non functioning" tumors.
  • Diagnosis is based on the hypersecretion phenotype (acromegaly, Cushing, etc), and on mass effect of macroadenomas leading to neurological disturbances, mainly visual complaints and headache.
  • Pituitary tumorigenesis mechanisms include those of primary hypothalamic versus pituitary origin, the latter is supported by evidence of pituitary adenoma monoclonality, as well as the absence of hyperplastic tissue surrounding the surgically removed tumor, and the relative independence of tumor hypothalamic control.
  • Nevertheless, a permissive role of the hypothalamus on tumor progression is also postulated.
  • Several molecular mechanisms involved in pituitary tumorigenesis have been unraveled including oncogenes, tumor suppressor genes and growth factors involved in neoplastic development, and will be described in this review.
  • [MeSH-major] Adenoma. Pituitary Neoplasms

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  • (PMID = 16444345.001).
  • [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
  • [Number-of-references] 68
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76. Ren SG, Melmed S: Pyridoxal phosphate inhibits pituitary cell proliferation and hormone secretion. Endocrinology; 2006 Aug;147(8):3936-42
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  • [Title] Pyridoxal phosphate inhibits pituitary cell proliferation and hormone secretion.
  • Pyridoxal phosphate (PLP), a bioactive form of pyridoxine, dose-dependently (10-1000 microm) inhibited cell proliferation in rat pituitary MMQ and GH3 cells and in mouse AtT-20 cells.
  • After 4 d, MMQ cell numbers were reduced by up to 81%, GH3 cell numbers were reduced by up to 64% (P < 0.05), and AtT-20 cell numbers were reduced by up to 90%.
  • Cell proliferation rates recovered and dose-dependently reverted to control levels after PLP withdrawal.
  • PLP (400-1000 microm) reduced GH3 cell GH and prolactin secretion and AtT-20 cell ACTH secretion (adjusted for cell number) by approximately 70% after 2 d.
  • The 100 microm PLP also inhibited prolactin secretion (65%, P < 0.05) in primary rat pituitary cells treated for 2 d.
  • Furthermore, PLP induced AtT-20 and GH3 cell apoptosis (28 vs. 6, P < 0.05; 26 vs. 3, P < 0.05, respectively) and dose-dependently reduced content of the antiapoptosis gene Bcl-2.
  • These results indicate that pharmacological doses of PLP inhibit pituitary cell proliferation and hormone secretion, in part mediated through PLP-induced cell-cycle arrest and apoptosis.
  • Pyridoxine may therefore be appropriate for testing as a relatively safe drug for adjuvant treatment of hormone-secreting pituitary adenomas.

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  • (PMID = 16690808.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA075979; United States / NCI NIH HHS / CA / CA 75979
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-bcl-2; 12001-76-2 / Vitamin B Complex; 5V5IOJ8338 / Pyridoxal Phosphate; 9002-62-4 / Prolactin; 9002-72-6 / Growth Hormone
  • [Other-IDs] NLM/ NIHMS10630; NLM/ PMC1513048
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77. Goh KP, Lee HY, Rajasoorya RC: Triple jeopardy in the pituitary. Pituitary; 2008;11(3):331-6
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  • [Title] Triple jeopardy in the pituitary.
  • Aggressive pituitary tumors are rare the pathogenesis is not well established.
  • The development of pituitary tumor after apoplexy has also been rarely reported.
  • We describe the sequential development of Cushing's disease, apoplexy and aggressive pituitary tumor in the same patient.
  • A 31-year old male presented with eutopic ACTH dependent Cushing's syndrome which failed initial pituitary surgery.
  • An episode of pituitary apoplexy then occurred which was followed by the development of a null-cell pituitary tumor.
  • This second tumor exhibited an aggressive behavior with invasion into the surrounding structures and systemic spread clinically.
  • This case provides important evidence for the hypotheses of the pathogenesis of aggressive pituitary tumors which could have arisen from surviving adenoma cells following apoplexy or as a de novo development of pituitary carcinoma from cells which were not part of the original adenoma.
  • This is the first report of a transformation of Cushing's disease to an aggressive and invasive null cell tumor after pituitary irradiation, apoplexy and surgery.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / complications. Adenoma / complications. Carcinoma / etiology. Neoplasms, Second Primary. Pituitary ACTH Hypersecretion / complications. Pituitary Apoplexy / complications. Pituitary Gland / pathology. Pituitary Neoplasms / etiology
  • [MeSH-minor] Adrenalectomy. Adult. Fatal Outcome. Humans. Magnetic Resonance Imaging. Male. Neoplasm Invasiveness. Radiotherapy, Adjuvant

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  • (PMID = 18058238.001).
  • [ISSN] 1386-341X
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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78. Colao A, Filippella M, Pivonello R, Di Somma C, Faggiano A, Lombardi G: Combined therapy of somatostatin analogues and dopamine agonists in the treatment of pituitary tumours. Eur J Endocrinol; 2007 Apr;156 Suppl 1:S57-63
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Combined therapy of somatostatin analogues and dopamine agonists in the treatment of pituitary tumours.
  • Pituitary tumours express both somatostatin and dopamine receptors.
  • Medical treatment with somatostatin analogues is a cornerstone of GH- and TSH-secreting tumours, while treatment with dopamine agonists is a cornerstone of prolactin-secreting tumours.
  • Dopamine agonists have also demonstrated some efficacy in patients with GH- and TSH-secreting adenomas.
  • Neither ACTH-secreting nor clinically non-functioning tumours have a well-established medical treatment.
  • Nevertheless, some recent results have indicated a potential usefulness of the dopamine agonist cabergoline in patients with pituitary-dependent Cushing's disease.
  • Some studies conducted in small series have documented an additive effect of both drugs in patients with GH-secreting adenomas.
  • No data are available in other pituitary tumour histotypes.
  • Preliminary observations in patients with clinically non-functioning adenomas are very promising.

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  • [ErratumIn] Eur J Endocrinol. 2007 Oct;157(4):543
  • (PMID = 17413190.001).
  • [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] 0 / Dopamine Agonists; 0 / Receptors, Dopamine; 0 / Receptors, Somatostatin; 51110-01-1 / Somatostatin
  • [Number-of-references] 59
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79. 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.


80. Kurowska M, Tarach JS, Zgliczyński W, Malicka J, Zieliński G, Janczarek M: Acromegaly in a patient with normal pituitary gland and somatotropic adenoma located in the sphenoid sinus. Endokrynol Pol; 2008 Jul-Aug;59(4):348-51
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  • [Title] Acromegaly in a patient with normal pituitary gland and somatotropic adenoma located in the sphenoid sinus.
  • In most cases it is caused by GHRH or rarely GH-secreting neoplasms.
  • Even rarer are ectopic pituitary adenomas located in the sphenoid sinus or nasopharynx that originate from pituitary remnants in the craniopharyngeal duct.
  • This dissertation presents the difficulties in visualizing GH-secreting adenoma located in the sphenoid sinus.
  • MRI imaging revealed a slightly asymmetric pituitary gland (14 yen 4 mm) without focal lesions.
  • After preliminary treatment with a long-acting somatostatin analogue, transsphenoidal pituitary tumour removal was performed.
  • Histopathological, electron microscopical and immunohistochemical analysis revealed densely granulated somatotropic pituitary adenoma: GH(+), PRL(-), ACTH(-), TSH(-), FSH(-), LH(-), MIB1 < 1%, SSTR3(+) and SSTR5(+).
  • Post-surgical evaluation showed normal pituitary MRI scans, GH and IGF-1 levels 0.18 mug/l and 140 mg/l, respectively, as well as normal GH suppression with oral glucose.
  • The careful analysis of possible pituitary embryonic malformations points out their significance for proper localization of extrapituitary adenomas.
  • [MeSH-major] Acromegaly / etiology. Adenoma / complications. Choristoma / complications. Paranasal Sinus Neoplasms / complications. Pituitary Gland. Pituitary Neoplasms / complications. Sphenoid Sinus
  • [MeSH-minor] Diagnosis, Differential. Humans. Magnetic Resonance Imaging. Male. Middle Aged

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  • (PMID = 18777506.001).
  • [ISSN] 0423-104X
  • [Journal-full-title] Endokrynologia Polska
  • [ISO-abbreviation] Endokrynol Pol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Poland
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81. 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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82. Roelfsema F, Kok S, Kok P, Pereira AM, Biermasz NR, Smit JW, Frolich M, Keenan DM, Veldhuis JD, Romijn JA: Pituitary-hormone secretion by thyrotropinomas. Pituitary; 2009;12(3):200-10
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  • [Title] Pituitary-hormone secretion by thyrotropinomas.
  • Hormone secretion by somatotropinomas, corticotropinomas and prolactinomas exhibits increased pulse frequency, basal and pulsatile secretion, accompanied by greater disorderliness.
  • Regulation of non-TSH pituitary hormones in this context is not well understood.
  • Cross-ApEn synchrony between TSH and GH did not differ between patients and controls, but TSH and PRL synchrony was reduced in patients.
  • We conclude that TSH secretion by thyrotropinomas shares many characteristics of other pituitary hormone-secreting adenomas.
  • In addition, abnormalities in GH and PRL secretion exist ranging from decreased (joint) regularity to overt hypersecretion, although not always clinically obvious, suggesting tumoral transformation of thyrotrope lineage cells.
  • [MeSH-major] Adenoma / physiopathology. Pituitary Hormones / blood. Pituitary Hormones / secretion. Pituitary Neoplasms / blood

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  • (PMID = 19051037.001).
  • [ISSN] 1573-7403
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / M01 RR000585
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Pituitary Hormones; 67763-96-6 / Insulin-Like Growth Factor I; 9002-62-4 / Prolactin; 9002-71-5 / Thyrotropin; 9002-72-6 / Growth Hormone
  • [Other-IDs] NLM/ PMC2712623
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83. 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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84. Young WF Jr, du Plessis H, Thompson GB, Grant CS, Farley DR, Richards ML, Erickson D, Vella A, Stanson AW, Carney JA, Abboud CF, Carpenter PC: The clinical conundrum of corticotropin-independent autonomous cortisol secretion in patients with bilateral adrenal masses. World J Surg; 2008 May;32(5):856-62
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  • [Title] The clinical conundrum of corticotropin-independent autonomous cortisol secretion in patients with bilateral adrenal masses.
  • BACKGROUND: Management of patients with bilateral adrenal masses and corticotropin (ACTH)-independent Cushing syndrome (CS) or subclinical CS is problematic.
  • We report our experience with adrenal venous sampling (AVS) in the evaluation of 10 patients with bilateral masses who had ACTH-independent CS or subclinical CS.
  • PATIENTS AND METHODS: Ten patients (9 women, 1 man, mean age 56.4 years) with bilateral adrenal masses and ACTH-independent CS (n=3) or subclinical CS (n=7) underwent Avs. Autonomous cortisol secretion was documented in all cases with suppressed serum ACTH concentrations and lack of cortisol suppression with dexamethasone administration.
  • Cortisol and epinephrine levels were measured from each adrenal vein (AV) and from a peripheral vein (PV).
  • Successful catheterization was confirmed with AV:PV epinephrine gradients.
  • A cortisol AV:PV gradient>6.5 was consistent with a cortisol-secreting adenoma in 11 adrenal glands; 5 patients had clinically important bilateral autonomous cortisol hypersecretion, 3 had bilateral cortisol-secreting adenomas, and 2 had ACTH-independent macronodular adrenal hyperplasia.
  • During a mean follow-up of 36.1 months (range: 0.7-123 months), CS or clinically important cortisol secretory autonomy did not recur.
  • CONCLUSIONS: Adrenal venous sampling contributed to the localization of autonomous hypercortisolism in the setting of ACTH-independent CS or subclinical CS in patients with bilateral adrenal masses.
  • [MeSH-major] Adrenal Cortex Neoplasms / blood. Adrenocortical Adenoma / blood. Cushing Syndrome / diagnosis. Cushing Syndrome / surgery. Hydrocortisone / blood

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  • (PMID = 18074172.001).
  • [ISSN] 0364-2313
  • [Journal-full-title] World journal of surgery
  • [ISO-abbreviation] World J Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
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85. Izumoto S, Arita N: [Treatment of pituitary adenomas: recent topics]. No Shinkei Geka; 2010 Jan;38(1):79-89
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  • [Title] [Treatment of pituitary adenomas: recent topics].
  • [MeSH-major] Pituitary Neoplasms / therapy
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / therapy. Female. Humans. Male. Prolactinoma / therapy

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  • (PMID = 20085107.001).
  • [ISSN] 0301-2603
  • [Journal-full-title] No shinkei geka. Neurological surgery
  • [ISO-abbreviation] No Shinkei Geka
  • [Language] jpn
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
  • [Number-of-references] 52
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86. 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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87. Castillo V, Giacomini D, Páez-Pereda M, Stalla J, Labeur M, Theodoropoulou M, Holsboer F, Grossman AB, Stalla GK, Arzt E: Retinoic acid as a novel medical therapy for Cushing's disease in dogs. Endocrinology; 2006 Sep;147(9):4438-44
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  • [Title] Retinoic acid as a novel medical therapy for Cushing's disease in dogs.
  • Cushing's disease is almost always caused by an ACTH-secreting pituitary tumor, but effective medical therapy is currently limited.
  • Because retinoic acid has been shown to be potentially useful in decreasing corticotroph secretion and proliferation in rodent models, we have studied its action in dogs with Cushing's disease.
  • A randomized treatment with retinoic acid (n = 22) vs. ketoconazole (n = 20) in dogs with Cushing's disease was assigned for a period of 180 d.
  • Clinical signs, plasma ACTH and alpha-MSH, the cortisol/creatinine urine ratio, and pituitary magnetic resonance imaging were assessed and compared at different time points.
  • We recorded a significant reduction in plasma ACTH and alpha-MSH, and also in the cortisol/creatinine urine ratio, of the dogs treated with retinoic acid.
  • Pituitary adenoma size was also significantly reduced at the end of retinoic acid treatment.
  • No adverse events or signs of hepatotoxicity were observed, suggesting that the drug is not only effective but also safe.
  • Retinoic acid treatment controls ACTH and cortisol hyperactivity and tumor size in dogs with ACTH-secreting tumors, leading to resolution of the clinical phenotype.
  • This study highlights the possibility of using retinoic acid as a novel therapy in the treatment of ACTH-secreting tumors in humans with Cushing's disease.
  • [MeSH-major] Dog Diseases / drug therapy. Pituitary ACTH Hypersecretion / veterinary. Tretinoin / therapeutic use
  • [MeSH-minor] Adenoma / pathology. Adrenocorticotropic Hormone / blood. Animals. Body Weight. Creatinine / urine. Dogs. Female. Hydrocortisone / urine. Ketoconazole / therapeutic use. Magnetic Resonance Imaging / veterinary. Male. Pituitary Gland / pathology. Pituitary Neoplasms / pathology. Survival Rate. alpha-MSH / blood

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  • (PMID = 16740975.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 5688UTC01R / Tretinoin; 581-05-5 / alpha-MSH; 9002-60-2 / Adrenocorticotropic Hormone; AYI8EX34EU / Creatinine; R9400W927I / Ketoconazole; WI4X0X7BPJ / Hydrocortisone
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88. 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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89. Kristof RA, Klingmüller D, Schramm J: Delayed postoperative hyponatremia followed by acute renal failure in a patient with an ACTH-secreting microadenoma of the pituitary. Zentralbl Neurochir; 2007 Aug;68(3):142-4
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  • [Title] Delayed postoperative hyponatremia followed by acute renal failure in a patient with an ACTH-secreting microadenoma of the pituitary.
  • The selective transsphenoidal adenomectomy of an ACTH-secreting microadenoma was followed by clinically symptomatic delayed hyponatremia in an otherwise healthy patient.
  • Until now, acute renal failure has not been reported under these circumstances.
  • This unique case demonstrates the need of close monitoring of patients with delayed hyponatremia following pituitary surgery.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / surgery. Acute Kidney Injury / etiology. Adenoma / surgery. Hyponatremia / etiology. Postoperative Complications / metabolism

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  • (PMID = 17665343.001).
  • [ISSN] 0044-4251
  • [Journal-full-title] Zentralblatt für Neurochirurgie
  • [ISO-abbreviation] Zentralbl. Neurochir.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
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90. Cristina C, Perez-Millan MI, Luque G, Dulce RA, Sevlever G, Berner SI, Becu-Villalobos D: VEGF and CD31 association in pituitary adenomas. Endocr Pathol; 2010 Sep;21(3):154-60
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  • [Title] VEGF and CD31 association in pituitary adenomas.
  • Pituitary tumors are usually less vascularized than the normal pituitary, and the role of angiogenesis in these adenomas is contentious.
  • We determined the protein expression of VEGF and CD31, an endothelial marker, in a series of 56 surgically removed pituitary adenomas using Western blot assay.
  • Prolactinomas had higher VEGF protein expression compared to nonfunctioning or ACTH- and GH-secreting adenomas, while CD31 was similar in the different adenoma histotypes.
  • VEGF and CD31 were not affected by sex, age, years of adenoma evolution, or proliferation rate (Ki67 and PCNA) for all adenoma types.
  • Only in nonfunctioning adenomas CD31 concentration increased significantly with age.
  • There was a positive correlation between CD31 and VEGF expression when all adenoma histotypes were considered, or when prolactinomas and nonfunctioning adenomas were evaluated separately.
  • The positive association of VEGF and CD31 expression suggests the participation of angiogenesis in adenoma development, while epithelial cell proliferation in pituitary tumors is not directly related to VEGF or CD31 expression, and other factors, such as primary genetic alterations may be involved.
  • [MeSH-major] Adenoma / metabolism. Antigens, CD31 / biosynthesis. Biomarkers, Tumor / analysis. Pituitary Neoplasms / metabolism. Vascular Endothelial Growth Factor A / biosynthesis

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  • (PMID = 20473646.001).
  • [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 / Antigens, CD31; 0 / Biomarkers, Tumor; 0 / Vascular Endothelial Growth Factor A
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91. 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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92. van der Hoek J, Waaijers M, van Koetsveld PM, Sprij-Mooij D, Feelders RA, Schmid HA, Schoeffter P, Hoyer D, Cervia D, Taylor JE, Culler MD, Lamberts SW, Hofland LJ: Distinct functional properties of native somatostatin receptor subtype 5 compared with subtype 2 in the regulation of ACTH release by corticotroph tumor cells. Am J Physiol Endocrinol Metab; 2005 Aug;289(2):E278-87
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  • [Title] Distinct functional properties of native somatostatin receptor subtype 5 compared with subtype 2 in the regulation of ACTH release by corticotroph tumor cells.
  • In a series of human corticotroph adenomas, we recently found predominant mRNA expression of somatostatin (SS) receptor subtype 5 (sst5).
  • After 72 h, the multiligand SS analog SOM230, which has a very high sst5 binding affinity, but not Octreotide (OCT), significantly inhibited basal ACTH release.
  • To further explore the role of sst5 in the regulation of ACTH release, we conducted additional studies with mouse AtT-20 cells.
  • SOM230 showed a 7-fold higher ligand binding affinity and a 19-fold higher potency in stimulating guanosine 5'-O-(3-thiotriphosphate) binding in AtT-20 cell membranes compared with OCT.
  • SOM230 potently suppressed CRH-induced ACTH release, which was not affected by 48-h dexamethasone (DEX) pretreatment.
  • However, DEX attenuated the inhibitory effects of OCT on ACTH release, whereas it increased the inhibitory potency of BIM-23268, an sst5-specific analog, on ACTH release.
  • Quantitative PCR analysis showed that DEX lowered sst(2A+2B) mRNA expression significantly after 24 and 48 h, whereas sst5 mRNA levels were not significantly affected by DEX treatment.
  • Finally, after SS analog preincubation, compared with OCT both SOM230 and BIM-23268 showed a significantly higher inhibitory effect on CRH-induced ACTH release.
  • In conclusion, our data support the concept that the sst5 receptor might be a target for new therapeutic agents to treat Cushing's disease.
  • [MeSH-major] Adrenocorticotropic Hormone / secretion. Corticotropin-Releasing Hormone / physiology. Pituitary Gland / secretion. Receptors, Somatostatin / physiology
  • [MeSH-minor] Animals. Dose-Response Relationship, Drug. Down-Regulation. Glucocorticoids / physiology. Mice. Octreotide / pharmacology. Pituitary Neoplasms. RNA, Messenger / analysis. Somatostatin / analogs & derivatives. Somatostatin / pharmacology. Stimulation, Chemical. Tumor Cells, Cultured

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  • (PMID = 15769796.001).
  • [ISSN] 0193-1849
  • [Journal-full-title] American journal of physiology. Endocrinology and metabolism
  • [ISO-abbreviation] Am. J. Physiol. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BIM 23268; 0 / Glucocorticoids; 0 / RNA, Messenger; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 0 / somatostatin receptor 5; 51110-01-1 / Somatostatin; 9002-60-2 / Adrenocorticotropic Hormone; 9015-71-8 / Corticotropin-Releasing Hormone; 98H1T17066 / pasireotide; RWM8CCW8GP / Octreotide
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93. Santoro A, Minniti G, Ruggeri A, Esposito V, Jaffrain-Rea ML, Delfini R: Biochemical remission and recurrence rate of secreting pituitary adenomas after transsphenoidal adenomectomy: long-term endocrinologic follow-up results. Surg Neurol; 2007 Nov;68(5):513-8; discussion 518
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  • [Title] Biochemical remission and recurrence rate of secreting pituitary adenomas after transsphenoidal adenomectomy: long-term endocrinologic follow-up results.
  • BACKGROUND: Transsphenoidal surgery is safe and effective in patients with secreting pituitary adenomas; however, variable outcomes have been reported according to the different criteria used to define the biochemical remission of hormone hypersecretion.
  • We report the long-term endocrinologic follow-up results of a large cohort of patients who underwent TSS for secreting pituitary adenomas according to the most recent stringent criteria of cure.
  • METHODS: Two hundred ten consecutive patients were operated on by TSS between 1995 and 2004 for a secreting pituitary adenoma (65 PRL-, 109 GH-, and 36 ACTH-secreting adenomas) and were considered for the study.
  • RESULTS: The overall remission rate was 65% for the whole series, being 64%, 61%, and 75% for PRL-, GH-, and ACTH-secreting adenomas, respectively.
  • Remission rates were significantly higher in GH- and ACTH-secreting pituitary macroadenomas than in macroprolactinomas.
  • At a median follow-up of 56 months, tumor recurrence was 0%, 11%, and 14% for GH-, ACTH-, and PRL-secreting tumors.
  • Tumor size, cavernous sinus invasion, and high hormone levels were negatively correlated to the outcome.
  • CONCLUSION: Transsphenoidal surgery remains an effective treatment for secreting pituitary tumors according to the most recent criteria of cure.
  • Patients with PRL- or ACTH-secreting adenomas may recur after apparently successful surgery, thereby justifying long-term careful endocrinologic follow-up.
  • [MeSH-major] Adenoma / surgery. Hyperpituitarism / prevention & control. Pituitary Neoplasms / surgery
  • [MeSH-minor] Adolescent. Adult. Aged. Female. Follow-Up Studies. Humans. Male. Middle Aged. Pituitary Hormones, Anterior / blood. Pituitary Hormones, Anterior / secretion. Recurrence. Remission Induction. Retrospective Studies. Time Factors. Treatment Outcome

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  • (PMID = 17961741.001).
  • [ISSN] 0090-3019
  • [Journal-full-title] Surgical neurology
  • [ISO-abbreviation] Surg Neurol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Pituitary Hormones, Anterior
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94. Fomekong E, Maiter D, Grandin C, Raftopoulos C: Outcome of transsphenoidal surgery for Cushing's disease: a high remission rate in ACTH-secreting macroadenomas. Clin Neurol Neurosurg; 2009 Jun;111(5):442-9
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  • [Title] Outcome of transsphenoidal surgery for Cushing's disease: a high remission rate in ACTH-secreting macroadenomas.
  • OBJECTIVE: Although numerous studies have shown that transsphenoidal surgery is the best initial treatment for Cushing disease offering 59-95% of success, fewer information is available on the long-term outcome in the subgroup of patients harboring ACTH-secreting macroadenomas.
  • The aims of this study were to analyze our 10-year experience with transsphenoidal surgery in Cushing's disease and to examine whether remission rates were different between micro- and macroadenomas.
  • PATIENTS AND METHODS: Forty consecutive patients with proven Cushing's disease (28 microadenomas, 12 macroadenomas [diameter: 10-25 mm], 3 patients with no visible adenoma at MRI) underwent transsphenoidal surgery (TSS) assisted by neuronavigation in our center between 1996 and 2007.
  • The diagnosis was made using standard endocrinological criteria including bilateral inferior petrosal sinus sampling (BIPSS) with CRH stimulation in all patients with discordant or equivocal biochemical and radiological testing.
  • Interestingly, a very good remission rate (92%) was observed in the subset of macroadenomas, similar to that found in the group of microadenomas (84%, NS), while no post-surgical remission was observed in the 3 patients with no visible adenoma at MRI (p<0.01).
  • Of the 8 patients not in remission after repeated TSS surgery, 3 underwent radiation therapy and three had bilateral adrenalectomy, allowing remission of their hypercortisolism.
  • CONCLUSION: While our overall results are in accordance with other published series, we show here that ACTH-secreting pituitary macroadenomas are usually not associated with a bad outcome, in contrast with patients with no visible adenoma at preoperative MRI.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / surgery. Cushing Syndrome / surgery. Neurosurgical Procedures. Sphenoid Bone / surgery
  • [MeSH-minor] Adolescent. Adult. Aged. Female. Follow-Up Studies. Humans. Hydrocortisone / blood. Magnetic Resonance Imaging. Male. Middle Aged. Pituitary Hormones / blood. Treatment Outcome. Young Adult

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  • (PMID = 19200645.001).
  • [ISSN] 1872-6968
  • [Journal-full-title] Clinical neurology and neurosurgery
  • [ISO-abbreviation] Clin Neurol Neurosurg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Pituitary Hormones; WI4X0X7BPJ / Hydrocortisone
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95. Kobayashi T: Long-term results of stereotactic gamma knife radiosurgery for pituitary adenomas. Specific strategies for different types of adenoma. Prog Neurol Surg; 2009;22:77-95
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  • [Title] Long-term results of stereotactic gamma knife radiosurgery for pituitary adenomas. Specific strategies for different types of adenoma.
  • Long-term results of gamma knife radiosurgery for pituitary adenomas are presented and treatment strategies for different adenoma types are discussed.
  • Two hundred and sixty-seven patients with pituitary adenoma have been treated by gamma knife radiosurgery during the past 12 years.
  • There were 131 cases of nonfunctioning and 136 cases of functioning adenomas, in which 71 GH-producing, 33 PRL-producing and 32 ACTH-producing adenomas were included.
  • Micro- and small adenomas could be cured by gamma knife radiosurgery alone.
  • Surgical or chemical debulking was necessary before radiosurgery for a large tumor with extrasellar extension.
  • Nonfunctioning adenomas showed higher control rates than functioning adenomas even with lower dose treatment.
  • Cushing disease showed the best response because of the smallest tumor size with the highest dose treatment.
  • The rate of hormone normalization was also high in Cushing disease but lower in prolactinoma and lowest in acromegaly.
  • High-dose treatment was necessary for functioning adenomas to control tumor growth and oversecretion of hormones.
  • In conclusion, gamma knife radiosurgery was effective and safe for the treatment of pituitary adenomas.
  • However, the treatment strategies should be specific to each adenoma type according to the radiosensitivity, chemosensitivity and biological nature of the tumor.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / surgery. Acromegaly / surgery. Adenoma / surgery. Radiosurgery
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Child. Female. Follow-Up Studies. Growth Hormone-Secreting Pituitary Adenoma / pathology. Growth Hormone-Secreting Pituitary Adenoma / surgery. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Patient Satisfaction. Pituitary ACTH Hypersecretion / pathology. Pituitary ACTH Hypersecretion / surgery. Prolactinoma / pathology. Prolactinoma / surgery. Treatment Outcome. Young Adult

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  • (PMID = 18948721.001).
  • [ISSN] 0079-6492
  • [Journal-full-title] Progress in neurological surgery
  • [ISO-abbreviation] Prog Neurol Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
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96. 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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97. Gruszka A, Kunert-Radek J, Pawlikowski M, Stepien H: Serum endostatin levels are elevated and correlate with serum vascular endothelial growth factor levels in patients with pituitary adenomas. Pituitary; 2005;8(2):163-8
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  • [Title] Serum endostatin levels are elevated and correlate with serum vascular endothelial growth factor levels in patients with pituitary adenomas.
  • The purpose of our study was to evaluate serum concentrations of endostatin in patients harbouring various pituitary adenoma types and to examine the relationship of serum endostatin levels to circulating vascular endothelial growth factor (VEGF) levels.
  • Preoperative serum endostatin and VEGF concentrations were measured using competitive enzyme immunoassays in 71 patients with pituitary adenomas (20 somatotropinomas, 3 corticotropinomas, 6 prolactinomas and 42 clinically nonfunctioning pituitary adenomas - CNFPAs) and compared with levels from age-matched controls.
  • Serum endostatin concentrations were significantly higher in all pituitary adenoma types, except for prolactinomas (somatotropinomas: 124 +/- 16; p < 0.02, corticotropinomas: 157 +/- 42; p < 0.02, prolactinomas: 141 +/- 37; p > 0.05, CNFPAs: 169 +/- 11 ng/ml; p < 0.000005 vs 73 +/- 10 ng/ml in controls).
  • There was a significant positive correlation between endostatin and VEGF serum levels in patients with pituitary adenomas (r = +0.322; p = 0.006).
  • The simultaneous elevation of endostatin and VEGF may attenuate the pro-angiogenic action of VEGF and be responsible for rather weak neovascularization of pituitary adenomas.
  • Prospective studies are required to assess the usefulness of circulating endostatin and VEGF as markers of progression or recurrence of pituitary tumors.
  • [MeSH-major] Adenoma / blood. Endostatins / blood. Pituitary Neoplasms / blood. Vascular Endothelial Growth Factor A / blood

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  • (PMID = 16379029.001).
  • [ISSN] 1386-341X
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Endostatins; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A
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98. Moore AF, Grinspoon SK: A dural tale. J Clin Endocrinol Metab; 2007 Sep;92(9):3367-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / diagnosis. Adenoma / diagnosis. Dura Mater / pathology
  • [MeSH-minor] Adult. Cushing Syndrome / diagnosis. Cushing Syndrome / etiology. Diagnosis, Differential. Humans. Magnetic Resonance Imaging. Male

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  • (PMID = 17823272.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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99. Pecori Giraldi F, Pesce S, Maroni P, Pagliardini L, Lasio G, Losa M, Cavagnini F: Inhibitory effect of prepro-thyrotrophin-releasing hormone (178-199) on adrenocorticotrophic hormone secretion by human corticotroph tumours. J Neuroendocrinol; 2010 Apr;22(4):294-300
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibitory effect of prepro-thyrotrophin-releasing hormone (178-199) on adrenocorticotrophic hormone secretion by human corticotroph tumours.
  • Prepro-thyrotrophin-releasing hormone (TRH) (178-199), a 22-amino acid cleavage product of the TRH prohormone, has been postulated to act as an adrenocorticotrophin hormone (ACTH)-release inhibitor.
  • Indeed, although in vitro evidence indicates that this peptide may inhibit basal and stimulated ACTH secretion in rodent anterior pituitary primary cultures and cell lines, not all studies concur and no study has as yet evaluated the effect of this peptide in Cushing's disease.
  • Twenty-four human ACTH-secreting pituitary tumours (13 macroadenomas, 11 microadenomas) were collected during surgery and incubated with 10 or 100 nm preproTRH(178-199).
  • ACTH secretion was assessed after 4 and 24 h of incubation by immunometric assay and expressed relative to levels observed in control, unchallenged wells (= 100%).
  • Parallel experiments were performed in rat anterior pituitary primary cultures.
  • A clear inhibition of ACTH secretion at 4 and 24 h was observed in 12 specimens (for 10 nm ppTRH: 70 +/- 4% control at 4 h and 83 +/- 5% control at 24 h; for 100 nm ppTRH: 70 +/- 4% control at 4 h and 85 +/- 5% control at 24 h), whereas a mild and short-lasting stimulatory effect was observed in three tumours and no changes in ACTH secretion in the remaining nine tumoural specimens.
  • Significant inhibition of ACTH secretion by preproTRH(178-199) in rat pituitary cultures was observed after 24 h of incubation.
  • The present study conducted in a large series of human corticotroph tumours shows that preproTRH(178-199) inhibits tumoural ACTH secretion in a sizable proportion of specimens, in close relation to the size of the tumour and its sensitivity to glucocorticoid negative feedback.
  • This appears a promising avenue of research and further studies are warranted to explore the full scope of preproTRH(178-199) as a regulator of ACTH secretion.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / secretion. Adenoma / secretion. Adrenocorticotropic Hormone / secretion. Peptide Fragments / pharmacology. Protein Precursors / pharmacology. Thyrotropin-Releasing Hormone / pharmacology
  • [MeSH-minor] Animals. Cell Culture Techniques. Cells, Cultured. Corticotropin-Releasing Hormone / pharmacology. Dexamethasone / pharmacology. Dose-Response Relationship, Drug. Down-Regulation / drug effects. Drug Evaluation, Preclinical. Female. Hormone Antagonists / pharmacology. Humans. Male. Pituitary Gland, Anterior / drug effects. Pituitary Gland, Anterior / metabolism. Rats

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  • (PMID = 20136686.001).
  • [ISSN] 1365-2826
  • [Journal-full-title] Journal of neuroendocrinology
  • [ISO-abbreviation] J. Neuroendocrinol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hormone Antagonists; 0 / Peptide Fragments; 0 / Protein Precursors; 122018-92-2 / prepro-thyrotropin-releasing hormone (178-199); 5Y5F15120W / Thyrotropin-Releasing Hormone; 7S5I7G3JQL / Dexamethasone; 9002-60-2 / Adrenocorticotropic Hormone; 9015-71-8 / Corticotropin-Releasing Hormone
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100. Rosales C, Fierrard H, Bertagna X, Raffin-Sanson ML: [Management of hypercortisolism]. Rev Med Interne; 2008 Apr;29(4):337-46
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • PURPOSE: Cushing's syndrome is a rare but frequently considered disease.
  • Its diagnosis can lead to some difficulties, including confirming the effective endogenous hypercortisolism and determining its cause.
  • The severity of this disease, the diversity of its complications and the multiple therapeutic options make its management challenging.
  • The aim of this review is to present the most recent data about management of Cushing's syndrome, especially diagnostic approaches and therapeutic options.
  • MAIN POINTS: We retained the following points: midnight salivary cortisol is a useful tool in the diagnosis of Cushing's syndrome; the desmopressin test can help to distinguish between Cushing's syndrome and "pseudoCushing's" due to alcohol consumption or psychiatric disorders; cavernous sinus and inferior petrosal sinus sampling is indicated in the evaluation of ACTH-dependent Cushing's syndromes when pituitary imaging is normal or equivocal or when dynamic tests are contradictory; multislice computed-tomography of the chest and the abdomen and somatostatin analogue scintigraphy, eventually combined, are the best imaging procedures in occult ectopic ACTH syndromes; patients with Cushing's disease should be referred to a neurosurgeon experienced in corticotroph adenomas surgery; metabolic consequences of Cushing's syndrome, such as cardiovascular risk factors and osteoporosis need an aggressive treatment.
  • PERSPECTIVES: The incidence of Cushing's syndrome is only 1/100000 per year.
  • Endocrinological management of the disease improves metabolic disorders in these patients.
  • If these results are confirmed, screening for Cushing's syndrome should be systematically performed in these populations.

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  • (PMID = 18226430.001).
  • [ISSN] 0248-8663
  • [Journal-full-title] La Revue de medecine interne
  • [ISO-abbreviation] Rev Med Interne
  • [Language] FRE
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Enzyme Inhibitors; 78E4J5IB5J / Mitotane; R9400W927I / Ketoconazole
  • [Number-of-references] 42
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