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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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[Title] Systematic analysis of G protein-coupled receptor gene expression in adrenocorticotropin-independent macronodular adrenocortical hyperplasia identifies novel targets for pharmacological control of adrenal Cushing's syndrome.

CONTEXT: Stimulation of cortisol secretion through abnormally expressed G protein-coupled receptors (GPCRs) is a frequent feature of ACTH-independent macronodular adrenal hyperplasia (AIMAH).

This has opened a pharmacological strategy that targets GPCRs for the treatment of Cushing's syndrome in AIMAH.

OBJECTIVE: The objective of the study was to identify new GPCR targets for the pharmacological treatment of adrenal Cushing's syndrome.

DESIGN AND PATIENTS: We designed a cDNA chip containing 865 nucleotidic sequences of GPCRs. mRNAs were extracted from three normal adrenals, 18 AIMAHs, four adrenals from Cushing's disease patients, and 13 cortisol-secreting adenomas.

RESULTS: The ACTH MC2 receptor showed a low expression in 15 of 18 AIMAHs samples, whereas several previously undescribed GPCR genes were found highly expressed in a subset of AIMAH, such as the receptors for motilin (MLNR; three of 18 AIMAHs) and γ-aminobutyric acid (GABBR1; five of 18 AIMAHs), and the α2A adrenergic receptor (ADRA2A; 13 of 18 AIMAHs), on which we focused our attention.

Western blot and immunochemistry analyses showed expression of ADRA2A protein in AIMAH but not in normal adrenal cortex.

CONCLUSION: ADRA2A is a potential target for pharmacological treatment of Cushing's syndrome linked to AIMAH.

[MeSH-minor] ACTH-Secreting Pituitary Adenoma / genetics. ACTH-Secreting Pituitary Adenoma / pathology. Adrenergic alpha-2 Receptor Agonists. Adrenocorticotropic Hormone / metabolism. Adrenocorticotropic Hormone / physiology. Antihypertensive Agents / administration & dosage. Antihypertensive Agents / pharmacology. Cells, Cultured. Clonidine / administration & dosage. Clonidine / pharmacology. Gene Expression. Gene Expression Profiling. Humans. Hyperplasia / genetics. Hyperplasia / metabolism. Oligonucleotide Array Sequence Analysis. Pituitary Neoplasms / genetics. Pituitary Neoplasms / pathology. Receptors, Adrenergic, alpha-2 / genetics. Receptors, Adrenergic, alpha-2 / metabolism. Receptors, Adrenergic, alpha-2 / physiology

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(PMID = 20660048.001).

[ISSN] 1945-7197

[Journal-full-title] The Journal of clinical endocrinology and metabolism

[ISO-abbreviation] J. Clin. Endocrinol. Metab.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / ADRA2A protein, human; 0 / Adrenergic alpha-2 Receptor Agonists; 0 / Antihypertensive Agents; 0 / Receptors, Adrenergic, alpha-2; 0 / Receptors, G-Protein-Coupled; 9002-60-2 / Adrenocorticotropic Hormone; MN3L5RMN02 / Clonidine

   

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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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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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[Title] Reduction of a pancreatic tumor after total removal of an ACTH secreting pituitary tumor: differential diagnosis of Cushing's syndrome.

Endocrinologic tests sometimes fail to distinguish adrenocorticotropic hormone (ACTH)-secreting pituitary adenoma from ectopic ACTH-secreting tumor.

The authors experienced a case of Cushing's disease associated with a pancreatic tumor.

Venous sampling contributed to the final diagnosis of Cushing's disease in this complex case, while endocrinologic tests showed paradoxical results.

A 54-year-old woman presented with Cushing's syndrome and pancreatic tumor.

Magnetic resonance imaging (MRI) failed to reveal a pituitary tumor, but a gadolinium-enhanced tumor with cystic components was seen in the pancreatic tail.

Results of conventional endocrinologic tests suggested ectopic ACTH syndrome, but venous sampling including cavernous sinus sampling indicated an ACTH-secreting pituitary adenoma.

Transsphenoidal surgery revealed a pituitary microadenoma, and total removal of the tumor was achieved.

Postoperative abdominal MRI revealed that the pancreatic tumor diminished gradually without treatment.

Selective cavernous sinus sampling was useful for distinguishing ACTH-secreting pituitary adenoma from ectopic ACTH syndrome in this complex case.

This was a rare case in which the pancreatic tumor diminished after total removal of the ACTH-secreting pituitary adenoma.

[MeSH-major] Adrenocorticotropic Hormone / secretion. Cushing Syndrome / diagnosis. Pancreatic Neoplasms / complications. Pituitary Neoplasms / secretion

[MeSH-minor] ACTH Syndrome, Ectopic / diagnosis. Adenoma / secretion. Adenoma / surgery. Diagnosis, Differential. Female. Follow-Up Studies. Humans. Magnetic Resonance Imaging. Middle Aged. Pituitary ACTH Hypersecretion / diagnosis. Positron-Emission Tomography

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(PMID = 16618978.001).

[ISSN] 0918-8959

[Journal-full-title] Endocrine journal

[ISO-abbreviation] Endocr. J.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Japan

[Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone

   

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[Title] Hypopituitarism in Cushing's disease.

Impaired GH secretion usually accompanies Cushing's syndrome and a variable proportion of patients reportedly fail to recover normal GH secretion after successful treatment.

We prospectively studied 34 patients (27 females and 7 males, age range 21- 68 yr) formerly affected by Cushing's disease.

All patients had undergone transsphenoidal surgery with the removal of an ACTH-secreting adenoma.

Our experience has demonstrated a GHD in a high percentage of patients with Cushing's disease even after long-term remission of hypercortisolism obtained by surgery alone.

This finding is significant as it highlights that even the most favorable therapeutical course, i.e. remission achieved by surgery, is often accompanied by impaired GH release.

Assessment of GH secretion is therefore recommended in all patients cured from Cushing's disease, even if not submitted to radiotherapy.

[MeSH-major] Hypopituitarism / complications. Pituitary ACTH Hypersecretion / complications

[MeSH-minor] ACTH-Secreting Pituitary Adenoma / complications. ACTH-Secreting Pituitary Adenoma / surgery. Adenoma / complications. Adenoma / surgery. Adult. Aged. Female. Follow-Up Studies. Growth Disorders / epidemiology. Growth Disorders / etiology. Human Growth Hormone / blood. Human Growth Hormone / secretion. Humans. Male. Middle Aged. Prevalence. Young Adult

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(PMID = 19020385.001).

[ISSN] 0391-4097

[Journal-full-title] Journal of endocrinological investigation

[ISO-abbreviation] J. Endocrinol. Invest.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Italy

[Chemical-registry-number] 12629-01-5 / Human Growth Hormone

   

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[Title] Prevalence of pituitary adenomas: a community-based, cross-sectional study in Banbury (Oxfordshire, UK).

BACKGROUND: Pituitary adenomas (PAs) are associated with increased morbidity and mortality.

All cases of PAs were found following an exhaustive computer database search of agreed terms by the staff of each Practice and data on age, gender, presenting manifestations and their duration, imaging features at diagnosis, history of multiple endocrine neoplasia type 1 and family history of PA were collected.

RESULTS: A total of 63 patients with PA were identified amongst the study population of 81,149, with a prevalence of 77.6 PA cases/100,000 inhabitants (prolactinomas; PRLoma: 44.4, nonfunctioning PAs: 22.2, acromegaly; ACRO: 8.6, corticotroph adenoma: 1.2 and unknown functional status; UFS: 1.2/100,000 inhabitants).

The distribution of each PA subtype was for PRLoma 57%, nonfunctioning PAs 28%, ACRO 11%, corticotroph adenoma 2% and UFS 2%.

The median age at diagnosis and the duration of symptoms until diagnosis (in years) were for PRLoma 32.0 and 1.5, nonfunctioning PAs 51.5 and 0.8, ACRO 47 and 4.5 and corticotroph adenoma 57 and 7, respectively.

Five patients (7.9%) presented with classical pituitary apoplexy, with a prevalence of 6.2 cases/100,000 inhabitants.

[MeSH-major] Adenoma / epidemiology. Pituitary Neoplasms / epidemiology

[MeSH-minor] Adolescent. Adult. Aged. Cross-Sectional Studies. Delayed Diagnosis. England / epidemiology. Female. Humans. Male. Middle Aged. Prevalence. Young Adult

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[CommentIn] Clin Endocrinol (Oxf). 2010 Mar;72(3):290-1 [19832856.001]

(PMID = 19650784.001).

[ISSN] 1365-2265

[Journal-full-title] Clinical endocrinology

[ISO-abbreviation] Clin. Endocrinol. (Oxf)

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

   

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[Title] Ghrelin stimulates adrenocorticotrophic hormone (ACTH) secretion by human ACTH-secreting pituitary adenomas in vitro.

Ghrelin is a brain-gut peptide with wide-ranging endocrine, metabolic, cardiovascular and neural effects.

Ghrelin, like its synthetic counterparts, the growth hormone (GH) secretagogues, has been shown to markedly stimulate adrenocorticotrophic hormone (ACTH) and cortisol secretion in humans and the ACTH-releasing effect of GH secretagogues is even greater in patients with pituitary ACTH-secreting tumours.

The aim of the present study was to evaluate the effect of ghrelin on ACTH secretion by human pituitary corticotroph tumours in vitro to test the functionality of this circuit.

Nine ACTH-secreting pituitary tumours (four microadenomas, five macroadenomas) were collected during surgery and incubated with 10-100 nM human ghrelin or with 10 nM human corticotrophin-releasing hormone (CRH).

Control experiments were performed in rat anterior pituitary primary cultures.

ACTH secretion was assessed after 4 h and 24 h incubation by immunometric assay.

After 4 h of incubation with ghrelin, medium ACTH concentrations were two- to ten-fold higher compared to ACTH concentrations in unstimulated wells.

The ACTH-releasing effect of ghrelin was significantly less than the response elicited by 10 nM CRH (up to 40-fold) Similar results were obtained after 24 h of incubation and a superimposable response pattern was observed in rat anterior pituitary primary cultures.

The present study demonstrates that the endogenous GH secretagogue, ghrelin, stimulates ACTH secretion directly from human tumoural corticotrophs, as well as from normal rat pituitary, and indicates that the marked ACTH release elicited by ghrelin in patients with Cushing's disease in vivo is due, at least in part, to its action on the pituitary tumour.

Moreover, these data uphold the concept of a functional intratumoural ghrelin paracrine circuit in human corticotroph adenomas.

[MeSH-major] ACTH-Secreting Pituitary Adenoma / secretion. Adenoma / secretion. Adrenocorticotropic Hormone / secretion. Corticotrophs / secretion. Peptide Hormones / physiology

[MeSH-minor] Adult. Animals. Corticotropin-Releasing Hormone / physiology. Female. Ghrelin. Humans. In Vitro Techniques. Male. Middle Aged. Pituitary ACTH Hypersecretion / metabolism. Pituitary Gland, Anterior / metabolism. Rats

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(PMID = 17280594.001).

[ISSN] 0953-8194

[Journal-full-title] Journal of neuroendocrinology

[ISO-abbreviation] J. Neuroendocrinol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Ghrelin; 0 / Peptide Hormones; 9002-60-2 / Adrenocorticotropic Hormone; 9015-71-8 / Corticotropin-Releasing Hormone

   

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[Title] Endoscopic transsphenoidal treatment in recurrent and residual pituitary adenomas--first experience.

AIM OF THE STUDY: The aim of the study has been the assessment of the endoscopic method in the surgical management of recurrent and residual pituitary adenomas, as concerns treatment efficiency, substantial complications, and its possible advantages for the operating surgeon and patient.

MATERIAL AND METHODS: In Department of Neurosurgery, Silesian University School of Medicine in Katowice, between October 2001 and June 2004, 125 patients underwent endoscopic surgery due to pituitary adenoma.

The analysis comprised 20 patients, who were operated on due to recurrent adenomas or residual tumour not completely removed during the first surgical procedure.

The analysed group had 14 non-functioning adenomas, 4 GH-secreting adenomas, 1 PRL-secreting adenoma and 1 ACTH-secreting adenoma.

11 of the 20 adenomas infiltrated the cavernous sinuses.

In the group of 11 patients with adenomas not infiltrating the cavernous sinuses, recovery was reported for 8 of them, that is 73%.

CONCLUSIONS: The endoscopic method is a safe, hardly invasive and efficient surgical technique in the treatment of recurrent and residual pituitary adenomas.

[MeSH-major] Adenoma / surgery. Neoplasm Recurrence, Local / surgery. Neuroendoscopy. Pituitary Neoplasms / surgery. Sphenoid Sinus / surgery

[MeSH-minor] Adult. Aged. Female. Follow-Up Studies. Humans. Male. Middle Aged. Neoplasm, Residual. Reoperation. Treatment Outcome

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(PMID = 16547875.001).

[ISSN] 0946-7211

[Journal-full-title] Minimally invasive neurosurgery : MIN

[ISO-abbreviation] Minim Invasive Neurosurg

[Language] eng

[Publication-type] Journal Article

[Publication-country] Germany

   

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[Title] Cushing's disease due to double pituitary ACTH-secreting adenomas: the first case report.

Double pituitary adenomas are rare occurrences in autoptical, surgical and neuroradiological series and are mostly due to non-functioning pituitary adenomas, GH-secreting and prolactin-secreting adenomas.

ACTH secreting tumours are more rare and, to our knowledge, two distinct ACTH-producing adenomas within the same pituitary have never been reported.

We herewith describe a 56 year old woman with Cushing' s disease due to two clearly distinct ACTH-secreting pituitary adenomas.

She presented with signs and symptoms of hypercortisolism and hormonal testing was indicative for pituitary-dependent Cushing' s syndrome.

Sellar MRI visualized an asymmetric pituitary gland with suspect lesions in both the right and the left pituitary lobes.

Pathology confirmed the existence of two distinct adenomas located in different sites in the gland.

Both presented ACTH immunoreactivity but displayed distinct morphological features.

Our case indicates that double ACTH-secreting pituitary adenomas may occur in patients with Cushing' s disease.

[MeSH-major] ACTH-Secreting Pituitary Adenoma / pathology. Adenoma / pathology. Neoplasms, Multiple Primary / pathology. Pituitary ACTH Hypersecretion / etiology

[MeSH-minor] Cushing Syndrome / etiology. Female. Humans. Middle Aged. Pituitary Neoplasms / pathology

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(PMID = 20595779.001).

[ISSN] 1348-4540

[Journal-full-title] Endocrine journal

[ISO-abbreviation] Endocr. J.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Japan

   

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[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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[Title] Fractionated stereotactic conformal radiotherapy for secreting and nonsecreting pituitary adenomas.

OBJECTIVE: To assess the medium-term outcome in a cohort of patients with residual or recurrent pituitary adenoma treated with fractionated stereotactic conformal radiotherapy (SCRT).

PATIENTS AND METHODS: Ninety-two patients (median age 50 years) with a residual or recurrent nonfunctioning (67) or a secreting (25) pituitary adenoma were treated between 1995 and 2003.

Eighteen patients had a GH-secreting, five PRL-secreting and two an ACTH-secreting pituitary adenoma.

In secreting adenomas, hormone levels declined progressively, becoming normal in more than a third of patients with GH-secreting and PRL-secreting pituitary tumours.

Hypopituitarism was the most common long-term effect; 22% of patients had worsening of pituitary function.

CONCLUSION: SCRT as a high-precision technique of localized irradiation achieves tumour and hormone control of pituitary adenomas comparable with previously published data on the efficacy of conventional radiotherapy.

Despite the potential advantage of reducing the volume of normal brain irradiated, the theoretical benefit over conventional radiotherapy in terms of the reduction in long-term morbidity has not yet been demonstrated and requires longer follow-up.

Potential effect on long-term cognitive function has not been tested.

[MeSH-major] Adenoma / radiotherapy. Pituitary Neoplasms / radiotherapy. Radiotherapy, Conformal / methods

[MeSH-minor] Adrenocorticotropic Hormone / secretion. Adult. Aged. Cohort Studies. Female. Growth Hormone / secretion. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Neoplasm Recurrence, Local / pathology. Neoplasm Recurrence, Local / radiotherapy. Neoplasm, Residual / pathology. Neoplasm, Residual / radiotherapy. Prolactinoma / radiotherapy. Prolactinoma / secretion. Radiotherapy Dosage. Statistics, Nonparametric. Treatment Outcome

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(PMID = 16649974.001).

[ISSN] 0300-0664

[Journal-full-title] Clinical endocrinology

[ISO-abbreviation] Clin. Endocrinol. (Oxf)

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone; 9002-72-6 / Growth Hormone

   

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[Title] No mutations in TPIT, a corticotroph-specific gene, in human tumoral pituitary ACTH-secreting cells.

BACKGROUND: TPIT is a recently identified transcription factor specific to proopiomelanocortin (POMC)-expressing cells within the pituitary and plays a pivotal role in the embryonal development of POMC lineage.

As with other transcription factors, TPIT could theoretically also be involved in corticotroph adenomatous transformation and ACTH hypersecretion and published data indicate that TPIT is present in normal and adenomatous human corticotrophs.

OBJECTIVE: The aim of the present study was to corroborate this finding and to seek evidence for mutations in the TPIT coding sequence in human tumoral corticotrophs.

DESIGN AND METHODS: Eight human ACTH-secreting pituitary adenomas were collected during surgery, mRNA extracted from primary cultures and reverse transcribed.

RESULTS: TPIT mRNA was detected in all 8 ACTH-secreting pituitary adenomas without apparent mRNA variants.

Lastly, sequencing did not reveal differences in the nucleotide arrangement compared with the published sequence.

CONCLUSIONS: Aberrant TPIT is unlikely to play a role in corticotroph tumoral trasformation, ie, Cushing's disease, as the entire coding sequence is expressed without any mutation by human pituitary ACTH-secreting adenomas.

Conversely, the significance of this transcription factor in tumoral ACTH hypersecretion remains to be clarified.

[MeSH-major] Adrenocorticotropic Hormone / secretion. Homeodomain Proteins / genetics. Mutation / genetics. Pituitary Neoplasms / genetics. Transcription Factors / genetics

[MeSH-minor] Humans. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism. Reverse Transcriptase Polymerase Chain Reaction. T-Box Domain Proteins. Tumor Cells, Cultured

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[Cites] J Clin Endocrinol Metab. 1999 Apr;84(4):1414-9 [10199788.001]

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(PMID = 16483181.001).

[ISSN] 0391-4097

[Journal-full-title] Journal of endocrinological investigation

[ISO-abbreviation] J. Endocrinol. Invest.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Italy

[Chemical-registry-number] 0 / Homeodomain Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / T-Box Domain Proteins; 0 / TBX19 protein, human; 0 / Transcription Factors; 9002-60-2 / Adrenocorticotropic Hormone

   

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[Title] Octreotide and the novel multireceptor ligand somatostatin receptor agonist pasireotide (SOM230) block the adrenalectomy-induced increase in mitotic activity in male rat anterior pituitary.

Acting principally through the latter, it inhibits basal and CRH-stimulated ACTH secretion from the AtT20 corticotroph cell line and ACTH release from a proportion of human corticotroph adenomas both in vitro and in vivo.

Data supporting an additional antiproliferative effect has led to pasireotide being explored as a potential therapy for patients with Cushing's disease.

We have compared the effects of pasireotide and octreotide on adrenalectomy-induced mitotic and apoptotic activity in the male rat anterior pituitary.

Pasireotide and octreotide had no effect on baseline pituitary cell turnover and no measurable effects on apoptosis.

However, the wave of increased mitotic activity normally seen in the pituitary after adrenalectomy was completely abolished.

Nevertheless, pasireotide and octreotide did not diminish the increase in ACTH-immunopositive cell index after adrenalectomy, indicating that cell division and differentiation of hormonally null cells in the pituitary are under independent control.

In conclusion, basal cell turnover in the pituitary is not inhibited by pasireotide or octreotide.

Bilateral adrenalectomy stimulates differentiation of preexisting null cells into ACTH-positive cells.

Cell division after bilateral adrenalectomy occurs in a specific subpopulation of hormonally null cells that are equally sensitive to the antiproliferative effects of pasireotide and octreotide, implicating SSTR2 receptors in this antimitotic response.

[MeSH-major] Adrenalectomy. Mitosis / drug effects. Octreotide / pharmacology. Pituitary Gland, Anterior / drug effects. Receptors, Somatostatin / agonists. Somatostatin / analogs & derivatives

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(PMID = 17347306.001).

[ISSN] 0013-7227

[Journal-full-title] Endocrinology

[ISO-abbreviation] Endocrinology

[Language] eng

[Grant] United Kingdom / Wellcome Trust / /

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Receptors, Somatostatin; 0 / Sstr2 protein, rat; 51110-01-1 / Somatostatin; 9002-60-2 / Adrenocorticotropic Hormone; 98H1T17066 / pasireotide; RWM8CCW8GP / Octreotide

   

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[Title] Effect of mitotane on pituitary corticotrophs in clinically normal dogs.

OBJECTIVE: To evaluate the effects of mitotane administration on the function and morphology of pituitary corticotrophs in clinically normal dogs.

In both groups, ACTH stimulation testing and corticotrophin-releasing hormone (CRH) stimulation testing were performed.

Magnetic resonance imaging (MRI) of the pituitary gland and brain was performed in mitotane treatment group dogs before and after administration of mitotane.

After CRH stimulation testing and MRI, dogs were euthanatized and the pituitary gland and adrenal glands were excised for gross and histologic examination.

RESULTS: ACTH concentrations in mitotane treatment group dogs were significantly higher than in the control group dogs following CRH stimulation.

Magnetic resonance imaging revealed that pituitary glands were significantly larger in treatment group dogs after administration of mitotane, compared with before administration.

Immunohistochemistry revealed hypertrophy of corticotrophs in pituitary glands of mitotane treatment group dogs.

In instances of corticotroph adenoma, hypertrophy of individual corticotrophs induced by mitotane may greatly facilitate enlargement of the pituitary gland and increases in ACTH secretion.

[MeSH-major] Adrenocorticotropic Hormone / metabolism. Corticotropin-Releasing Hormone / metabolism. Health. Mitotane / pharmacology. Pituitary Gland / drug effects. Pituitary Gland / metabolism

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(PMID = 16881851.001).

[ISSN] 0002-9645

[Journal-full-title] American journal of veterinary research

[ISO-abbreviation] Am. J. Vet. Res.

[Language] eng

[Publication-type] Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 78E4J5IB5J / Mitotane; 9002-60-2 / Adrenocorticotropic Hormone; 9015-71-8 / Corticotropin-Releasing Hormone

   

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[Title] ACTH-secreting pituitary adenoma within an ovarian teratoma.

The differential diagnosis of Cushing's syndrome is one of the most difficult tasks in medicine, and it is especially problematic in cases with "occult" ectopic ACTH syndrome.

We describe the case of a 26-year-old woman who was found to suffer from ectopic ACTH syndrome due to pituitary microadenoma, localized within a mature ovarian teratoma.

Cushing's syndrome caused by ovarian neoplasia is unusual, but when it occurs, it is most often due to excessive cortisol production by the ovary.

Only rarely has ectopic ACTH syndrome in association with an ovarian tumor been described.

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(PMID = 16137552.001).

[ISSN] 0953-6205

[Journal-full-title] European journal of internal medicine

[ISO-abbreviation] Eur. J. Intern. Med.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Netherlands

   

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[Title] MicroRNAs differentially expressed in ACTH-secreting pituitary tumors.

OBJECTIVE: The aim of the study was to analyze the differential expression of let-7a, miR-15a, miR-16, miR-21, miR-141, miR-143, miR-145, and miR-150 in corticotropinomas and normal pituitary tissue and verify whether their profile of expression correlates with tumor size or remission after treatment.

MATERIAL AND METHODS: ACTH-secreting pituitary tumor samples were obtained during transphenoidal surgery from patients with Cushing disease and normal pituitary tissues from autopsies.

RESULTS: We found underexpression of miR-145 (2.0-fold; P = 0.04), miR-21 (2.4-fold; P = 0.004), miR-141 (2.6-fold; P = 0.02), let-7a (3.3-fold; P = 0.003), miR-150 (3.8-fold; P = 0.04), miR-15a (4.5-fold; P = 0.03), miR-16 (5.0-fold; P = 0.004), and miR-143 (6.4-fold; P = 0.004) in ACTH-secreting pituitary tumors when compared to normal pituitary tissues.

There were no differences between miRNA expression and tumor size as well as miRNA expression and ratio of remission after surgery, except in patients presenting lower miR-141 expression who showed a better chance of remission.

However, the lack of knowledge about miRNA target genes postpones full understanding of the biological functions of down-regulated or up-regulated miRNAs in corticotropinomas.

[MeSH-major] ACTH-Secreting Pituitary Adenoma / genetics. Adenoma / genetics. MicroRNAs / analysis

[MeSH-minor] Adolescent. Adult. Female. Humans. Male. Middle Aged. Pituitary ACTH Hypersecretion / genetics. Young Adult

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(PMID = 18840638.001).

[ISSN] 0021-972X

[Journal-full-title] The Journal of clinical endocrinology and metabolism

[ISO-abbreviation] J. Clin. Endocrinol. Metab.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / MicroRNAs

   

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[Title] Pituitary tumor type affects the chance of biochemical remission after radiosurgery of hormone-secreting pituitary adenomas.

OBJECTIVE: Reported biochemical remission rates have ranged widely after stereotactic radiosurgery for patients with hormone-secreting pituitary adenomas.

Confounding variables include histology, radiation dose, use of pituitary-suppressive medications, and length of follow-up.

METHODS: A retrospective review of 46 patients with pituitary adenomas (growth hormone-secreting, n = 27; prolactin-secreting, n = 11; adrenocorticotropin-secreting, n = 8) undergoing radiosurgery between January 1990 and December 2003 was conducted.

All received a tumor margin dose of 18 Gy or more and were off pituitary-suppressive medications for at least 1 month before radiosurgery.

RESULTS: The 4-year remission rates were 87% for patients with Cushing's disease, 67% for patients with acromegaly, and 18% for patients with prolactinomas.

Patients with oversecretion of adrenocorticotropin or growth hormone were more likely to achieve remission after radiosurgery than patients with prolactinomas (hazard ratio, 4.4; 95% confidence interval, 1.1-18.2; P = 0.04).

Of 44 patients with normal or partial anterior pituitary function before radiosurgery, 16 (36%) developed one or more new anterior pituitary deficits.

The incidence of new anterior pituitary deficits was 26% at 4 years.

CONCLUSION: There seems to be a differential sensitivity after radiosurgery for hormone-secreting pituitary adenomas.

Remission rates are greater for patients with Cushing's disease and acromegaly, whereas radiosurgery is less effective in achieving biochemical remission for patients with prolactinomas.

[MeSH-major] Adenoma / metabolism. Adenoma / surgery. Pituitary Hormones / metabolism. Pituitary Neoplasms / metabolism. Pituitary Neoplasms / surgery. Radiosurgery

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[CommentIn] Neurosurgery. 2010 May;66(5):E1030; author reply E1030 [20404679.001]

(PMID = 18824993.001).

[ISSN] 1524-4040

[Journal-full-title] Neurosurgery

[ISO-abbreviation] Neurosurgery

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Pituitary Hormones

   

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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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[Title] Interferon-gamma inhibits cellular proliferation and ACTH production in corticotroph tumor cells through a novel janus kinases-signal transducer and activator of transcription 1/nuclear factor-kappa B inhibitory signaling pathway.

Moreover, IFNG modulates normal pituitary hormone secretion, and was shown to inhibit the expression of the ACTH precursor POMC in murine ACTH-secreting AtT-2010/21/2008 tumor cells.

We have studied the functional role of IFNG on pituitary tumor cells, focusing on the involvement of IFNG in the molecular events leading to the control of POMC transcriptional repression.

Herein, it is shown that IFNG inhibits AtT-20 tumor cell proliferation without inducing apoptosis.

In addition, 1 and 2 IFNG receptor immunoreactivity was detected in human corticotropinoma cells.

Interestingly, IFNG inhibits ACTH production from these cells in primary cell culture, without affecting basal ACTH biosynthesis in normal non-tumoral pituitary cells.

[MeSH-major] Adrenocorticotropic Hormone / biosynthesis. Cell Proliferation / drug effects. Interferon-gamma / pharmacology. Janus Kinases / metabolism. NF-kappa B / metabolism. Pituitary Neoplasms / metabolism. STAT1 Transcription Factor / metabolism

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(PMID = 18715881.001).

[ISSN] 1479-6805

[Journal-full-title] The Journal of endocrinology

[ISO-abbreviation] J. Endocrinol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / NF-kappa B; 0 / STAT1 Transcription Factor; 66796-54-1 / Pro-Opiomelanocortin; 82115-62-6 / Interferon-gamma; 9002-60-2 / Adrenocorticotropic Hormone; EC 2.7.10.2 / Janus Kinases

   

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[Title] Evaluation of proopiomelanocortin mRNA in the peripheral blood from patients with Cushing's syndrome of different origin.

ACTH-dependent Cushing's syndrome is due to ACTH overproduction originating from a pituitary corticotroph adenoma (Cushing's disease) or from ectopic tumors (ectopic ACTH syndrome).

Due to difficulties in the differential diagnosis between these two forms of hypercortisolism it would be important to have molecular tools able to discriminate the two conditions.

In order to analyse the presence of different POMC transcripts, we extracted total RNA from peripheral lymphocytes of 10 patients with Cushing's disease, 10 with ectopic Cushing syndrome, and 20 controls as well as from pituitary tissues (2 ACTH-omas and a normal pituitary polyA+ sample).

Northern blot analysis correctly revealed a 1072 nt mRNA molecule in pituitary ACTH-oma and in the normal pituitary polyA+ RNA samples, whereas neither this molecule nor other alternative transcripts were detected in blood samples from patients and controls.

This study further underlines the need for alternative approaches in the diagnosis of ACTH-dependent Cushing's syndrome.

[MeSH-major] ACTH Syndrome, Ectopic / diagnosis. ACTH-Secreting Pituitary Adenoma / diagnosis. Adenoma / diagnosis. Biomarkers, Tumor / genetics. Cushing Syndrome / diagnosis. Pro-Opiomelanocortin / genetics

[MeSH-minor] Blotting, Northern. Diagnosis, Differential. Humans. RNA, Messenger / blood. Reverse Transcriptase Polymerase Chain Reaction

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(PMID = 18075284.001).

[ISSN] 1720-8386

[Journal-full-title] Journal of endocrinological investigation

[ISO-abbreviation] J. Endocrinol. Invest.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Italy

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / RNA, Messenger; 66796-54-1 / Pro-Opiomelanocortin

   

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[Title] A Postnatal Pax7 Progenitor Gives Rise to Pituitary Adenomas.

Pituitary adenomas are classified into functioning and nonfunctioning (silent) tumors on the basis of hormone secretion.

However, the mechanism of tumorigenesis and the cell of origin for pituitary adenoma subtypes remain to be elucidated.

Employing a tamoxifen-inducible mouse model, we demonstrate that a novel postnatal Pax7(+) progenitor cell population in the pituitary gland gives rise to silent corticotroph macro-adenomas when the retinoblastoma tumor suppressor is conditionally deleted.

While Pax transcriptional factors are critical for embryonic patterning as well as postnatal stem cell renewal for many organs, we have discovered that Pax7 marks a restricted cell population in the postnatal pituitary intermediate lobe.

This Pax7(+) early progenitor cell population is overlapping but ontologically downstream of the Nestin(+) pituitary stem cell population, yet upstream of another newly discovered Myf6(+) late progenitor cell population.

Interestingly, the Pax7(+) progenitor cell population is evolutionarily conserved in primates and humans, and Pax7 expression is maintained not only in murine tumors but also in human functioning and silent corticotropinomas.

Taken together, our results strongly suggest that human silent corticotroph adenomas may in fact arise from a Pax7 lineage of the intermediate lobe, a region of the human pituitary bearing closer scientific interest as a reservoir of pituitary progenitor cells.

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(PMID = 20811506.001).

[ISSN] 1947-6019

[Journal-full-title] Genes & cancer

[ISO-abbreviation] Genes Cancer

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / CA133229-03; United States / NCRR NIH HHS / RR / P41 RR012553; United States / NCI NIH HHS / CA / R01 CA133229

[Publication-type] JOURNAL ARTICLE

[Publication-country] United States

   

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[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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[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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CONTEXT: Hormone secretion by somatotropinomas, corticotropinomas, and prolactinomas exhibits increased pulsatility and basal secretion, accompanied by greater disorderliness.

CONCLUSION: TSH secretion by thyrotropinomas shares many characteristics with other pituitary hormone-secreting adenomas.

[MeSH-major] Adenoma / physiopathology. Adenoma / secretion. Circadian Rhythm / physiology. Pituitary Neoplasms / physiopathology. Pituitary Neoplasms / secretion. Pulsatile Flow / physiology. Thyrotropin / secretion

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(PMID = 18682501.001).

[ISSN] 0021-972X

[Journal-full-title] The Journal of clinical endocrinology and metabolism

[ISO-abbreviation] J. Clin. Endocrinol. Metab.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 9002-71-5 / Thyrotropin

   

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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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[Title] Survivin products in pituitary tumors.

Still very little is known about survivin expression in pituitary tumors.

In spite of the fact that pituitary tumors in histological examination are usually benign, in the clinical process a certain number of pituitary adenomas is capable of aggressive growth, recurrence and invasion of the surrounding structures.

The aim of the present study was to assess the presence of survivin transcripts and protein in different types of pituitary tumors and to evaluate survivin expression levels in invasive and non-invasive pituitary tumors.

DESIGN AND METHODS: The analyzed material consisted of tumor tissue samples obtained during standard neurosurgical removal of the tumor from 23 patients in whom acromegaly (n=14), non-functioning pituitary tumor (n=6), prolactinoma (n=2) and corticotropinoma (n=1) were diagnosed.

As a control of the study normal pituitary tissue obtained at autopsy was used.

RESULTS: Our study demonstrated the presence of survivin mRNA in all 23 analyzed pituitary tumors.

Survivin expression was also observed in normal pituitary, but the level of its expression was 6-fold lower than in tumors tissue when studied by real time RT-PCR.

The difference between the levels of survivin expression in invasive and non-invasive tumors was not statistically significant.

Immunohistochemical analyses revealed the presence of the protein in both normal and tumor tissue of pituitary.

Immunostaining of tumor tissue was not uniform.

The presence of the protein in normal pituitary was restricted to small population of cells.

CONCLUSIONS: The present study showed that overexpression of survivin is characteristic for pituitary tumors.

Further analysis of this protein expression profile should demonstrate whether survivin might be use as a prognostic marker in diagnosis and therapy of pituitary adenomas.

[MeSH-major] Adenoma / metabolism. Apoptosis Regulatory Proteins / metabolism. Microtubule-Associated Proteins / metabolism. Neoplasm Proteins / metabolism. Pituitary Gland / metabolism. Pituitary Neoplasms / metabolism

[MeSH-minor] ACTH-Secreting Pituitary Adenoma / metabolism. Adult. Female. Growth Hormone-Secreting Pituitary Adenoma / metabolism. Humans. Inhibitor of Apoptosis Proteins. Male. Middle Aged. Prolactinoma / metabolism. RNA, Messenger / analysis

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(PMID = 19112393.001).

[ISSN] 0172-780X

[Journal-full-title] Neuro endocrinology letters

[ISO-abbreviation] Neuro Endocrinol. Lett.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Sweden

[Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / RNA, Messenger

   

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[Title] Cyclic Cushing's syndrome: a clinical challenge.

Cyclic Cushing's syndrome (CS) is a rare disorder, characterized by repeated episodes of cortisol excess interspersed by periods of normal cortisol secretion.

Our review of 65 reported cases demonstrates that cyclic CS originates in 54% of cases from a pituitary corticotroph adenoma, in 26% from an ectopic ACTH-producing tumour and in about 11% from an adrenal tumour, the remainder being unclassified.

When cyclic CS is biochemically confirmed, further imaging and laboratory studies are guided by the presence or absence of ACTH dependency.

In cases of suspected ectopic ACTH production, specific biochemical testing for carcinoids or neuroendocrine tumours is required, including measurements of serotonin in platelets and/or urine, chromogranin A and calcitonin.

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(PMID = 17766705.001).

[ISSN] 0804-4643

[Journal-full-title] European journal of endocrinology

[ISO-abbreviation] Eur. J. Endocrinol.

[Language] ENG

[Publication-type] Journal Article; Review

[Publication-country] England

[Chemical-registry-number] WI4X0X7BPJ / Hydrocortisone

[Number-of-references] 108

   

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[Title] Results of transsphenoidal surgery in a large series of patients with pituitary adenoma.

OBJECTIVE: To report the efficacy and safety of microsurgical transsphenoidal surgery in a series of previously untreated patients with pituitary adenoma.

METHODS: One thousand one hundred forty consecutive patients undergoing transsphenoidal resection of a pituitary adenoma at our department from January 1990 through December 2002 were included in our study.

Patients were considered in remission of disease when strict hormonal and radiological criteria of cure were met.

RESULTS: The most frequent tumor type was clinically nonfunctioning adenoma (NFPA) (33.2%), followed by growth hormone-secreting adenoma (28.1%), adrenocorticotropin-secreting adenoma (23.0%), prolactin-secreting adenoma (13.2%), and last, thyrotropin-secreting adenoma (2.5%).

There were 788 macroadenomas (69.1%), and in 233 patients (20.4%), the tumor invaded one or both cavernous sinuses.

The overall rate of early surgical success was achieved in 504 (66.1%) of the 762 patients with a hormone-active adenoma.

In patients with NFPA, no residual adenoma was present in 234 patients (64.8%).

CONCLUSION: Transsphenoidal surgery is an effective and safe treatment for most patients with pituitary adenoma and could be considered the first-choice therapy in all cases except for prolactinomas responsive to dopamine agonists.

Other treatment methods, such as radiotherapy, stereotactic radiosurgery, and medical therapy, play an important role in patients not cured by surgery.

[MeSH-major] Adenoma / surgery. Hypophysectomy / methods. Pituitary Neoplasms / surgery. Sphenoid Sinus / surgery

[MeSH-minor] Adult. Female. Humans. Male. Middle Aged. Pituitary Hormones / metabolism. Postoperative Complications. Retrospective Studies. Treatment Outcome. Vision Disorders / etiology

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(PMID = 15918938.001).

[ISSN] 1524-4040

[Journal-full-title] Neurosurgery

[ISO-abbreviation] Neurosurgery

[Language] eng

[Publication-type] Clinical Trial; Comparative Study; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Pituitary Hormones

   

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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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[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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[Title] Current state of the art in the diagnosis and surgical treatment of Cushing disease: early experience with a purely endoscopic endonasal technique.

OBJECT: Transsphenoidal pituitary surgery is the primary therapy for Cushing disease because of its potential to produce lasting remission without the need for long-term drug or hormone replacement therapy.

The authors evaluated the current role of pure endoscopic endonasal pituitary surgery in the treatment of Cushing disease.

METHODS: Twenty-five patients underwent pure endoscopic surgery for confirmed Cushing disease.

Final histological results were consistent with adrenocorticotropin hormone (ACTH)-secreting adenoma in 20 patients.

Three patients presented with new anterior pituitary deficiency, but no one had permanent diabetes insipidus.

Treatment failure was attributable to involvement of the cavernous sinus in two patients, incomplete tumor removal in one, negative exploration in one, and nodular corticotroph hyperplasia of the pituitary gland in one.

CONCLUSIONS: Early results indicated that endoscopic endonasal surgery is a safe and effective treatment for ACTH-producing adenomas.

Further studies with a larger number of patients and longer follow-ups are required to determine whether this more minimally invasive pure endoscopic approach should become the standard of care for the surgical treatment of Cushing disease.

[MeSH-major] ACTH-Secreting Pituitary Adenoma / surgery. Adenoma / surgery. Endoscopy. Paranasal Sinuses / surgery. Pituitary ACTH Hypersecretion / diagnosis. Pituitary ACTH Hypersecretion / surgery

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(PMID = 17961027.001).

[ISSN] 1092-0684

[Journal-full-title] Neurosurgical focus

[ISO-abbreviation] Neurosurg Focus

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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[Title] Metallothionein isoform 3 gene is differentially expressed in corticotropin-producing pituitary adenomas.

In order to search for candidate genes related to pituitary adenoma aggressiveness, the present investigation was intended to compare the mRNA expression profile from a pool of four nonfunctional pituitary adenomas (NFPA) with a spinal cord metastasis of a nonfunctional pituitary carcinoma (MNFPC).

The metallothionein isoform 3 (MT3) gene was differentially expressed in nonfunctional adenomas in comparison to the metastasis of nonfunctional carcinoma.

A microarray dataset comprising 19,881 probes was employed for comparing expression profiles of a spinal cord metastasis of a nonfunctional pituitary carcinoma with a pool of four nonfunctional pituitary adenomas.

RT-qPCR confirmed the microarray findings and was used to investigate MT3 mRNA gene expression in tumor samples of a series of 52 different pituitary adenoma subtypes comprising 10 corticotropin (ACTH)-producing, 18 growth hormone (GH)-producing, 8 prolactin (PRL)-producing, and 16 nonfunctional adenomas.

MT3 mRNA expression was statistically significantly higher in ACTH-producing pituitary adenomas and in nonfunctional pituitary adenomas in comparison to the other pituitary adenoma subtypes.

The more abundant expression of this gene in ACTH-producing pituitary adenomas suggests that MT3 could be related to distinct pituitary cell lineage regulating the activity of some transcription factor of importance in hormone production and/or secretion.

[MeSH-major] Adenoma / metabolism. Adrenocorticotropic Hormone / metabolism. Nerve Tissue Proteins / biosynthesis. Pituitary Neoplasms / metabolism

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(PMID = 16601360.001).

[ISSN] 0028-3835

[Journal-full-title] Neuroendocrinology

[ISO-abbreviation] Neuroendocrinology

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] Switzerland

[Chemical-registry-number] 0 / Nerve Tissue Proteins; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / growth inhibitory factor; 12629-01-5 / Human Growth Hormone; 9002-60-2 / Adrenocorticotropic Hormone; 9002-62-4 / Prolactin

   

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[Title] Modification of hormonal secretion in clinically silent pituitary adenomas.

BACKGROUND: Silent pituitary adenomas are a subtype of adenomas characterized by positive immunoreactivity for one or more hormones classically secreted by normal pituitary cells but without clinical expression, although in some occasions enhanced or changed secretory activity can develop over time.

Silent corticotroph adenomas are the classical example of this phenomenon.

PATIENTS AND METHODS: A series of about 500 pituitary adenomas seen over a period of 20 years were screened for modification in hormonal secretion.

RESULTS: Two cases were retrieved, one silent somatotroph adenoma and one thyrotroph adenoma, both without specific clinical features or biochemical abnormalities, which presented 20 years after initial surgery with evidence of acromegaly and hyperthyroidism, respectively.

While the acromegaly was controlled by a combination of somatostatin analogs and growth hormone (GH) receptor antagonist therapy, neurosurgery was necessary to manage the thyrotroph adenoma.

Apparently, the mechanisms responsible for the secretory modifications are different, being a change in secretory capacity in the silent somatotroph adenoma and a quantitative change in the silent thyrotroph adenoma.

CONCLUSIONS: These two cases, one somatotroph and one thyrotroph adenoma, are an illustration that clinically silent pituitary adenomas may in rare circumstances evolve over time and become active, as previously demonstrated in silent corticotroph adenomas.

[MeSH-major] Pituitary Neoplasms / metabolism

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(PMID = 18350381.001).

[ISSN] 1573-7403

[Journal-full-title] Pituitary

[ISO-abbreviation] Pituitary

[Language] eng

[Publication-type] Case Reports; Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I; 9002-71-5 / Thyrotropin

[Number-of-references] 30

   

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[Title] The multi-ligand somatostatin analogue SOM230 inhibits ACTH secretion by cultured human corticotroph adenomas via somatostatin receptor type 5.

OBJECTIVE: Currently, there is no effective medical treatment for patients with pituitary-dependent Cushing's disease.

We compared the in vitro effects of the sst(2)-preferring SS analogue octreotide (OCT) and the multi-ligand SOM230 on ACTH release by human and mouse corticotroph tumour cells.

METHODS: By quantitative RT-PCR the sst subtype expression level was determined in human corticotroph adenomas.

In vitro, the inhibitory effect of OCT and SOM230 on ACTH release by dispersed human corticotroph adenoma cells and mouse AtT20 corticotroph adenoma cells was determined.

RESULTS: Corticotroph adenomas expressed predominantly sst(5) mRNA (six out of six adenomas), whereas sst(2) mRNA expression was detected at significantly lower levels.

In a 72 h incubation with 10 nmol/l SOM230, ACTH release was inhibited in three out of five cultures (range -30 to -40%).

Ten nmol/l OCT slightly inhibited ACTH release in only one of five cultures (- 28%).

In AtT20 cells, expressing sst(2), sst(3) and sst(5), SOM230 inhibited ACTH secretion with high potency (IC(50) 0.2 nmol/l).

Dexamethasone (10 nmol/l) pre-treatment did not influence the sensitivity of the cells to the inhibitory effect of SOM230, suggesting that sst(5) is relatively resistant to negative control by glucocorticoids.

CONCLUSIONS: The selective expression of sst(5) receptors in corticotroph adenomas and the preferential inhibition of ACTH release by human corticotroph adenoma cells by SOM230 in vitro, suggest that SOM230 may have potential in the treatment of patients with pituitary-dependent Cushing's disease.

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(PMID = 15817922.001).

[ISSN] 0804-4643

[Journal-full-title] European journal of endocrinology

[ISO-abbreviation] Eur. J. Endocrinol.

[Language] ENG

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Glucocorticoids; 0 / RNA, Messenger; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 5; 51110-01-1 / Somatostatin; 9002-60-2 / Adrenocorticotropic Hormone; 98H1T17066 / pasireotide; RWM8CCW8GP / Octreotide

   

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[Title] Differential gene expression by fiber-optic beadarray and pathway in adrenocorticotrophin-secreting pituitary adenomas.

BACKGROUND: Adrenocorticotrophin (ACTH)-secreting pituitary adenomas account for approximately 7% - 14% of all pituitary adenomas, but its pathogenesis is still enigmatic.

This study aimed to explore mechanisms underlying the pathogenesis of ACTH-secreting pituitary adenomas.

METHODS: We used fiber-optic beadarray to examine gene expression in three ACTH-secreting adenomas compared with three normal pituitaries.

Four differentially expressed genes from the three ACTH-secreting adenomas and three normal pituitaries were chosen randomly for validation by reverse transcriptase-real time quantitative polymerase chain reaction (RT-qPCR).

Bioinformatic and pathway analysis showed that the genes HIGD1B, EPS8, HPGD, DAPK2, and IGFBP3 and the transforming growth factor (TGF)-β signaling pathway and extracellular matrix (ECM)-receptor interaction pathway may play important roles in tumorigenesis and progression of ACTH-secreting pituitary adenomas.

CONCLUSIONS: Our data suggest that numerous aberrantly expressed genes and several pathways are involved in the pathogenesis of ACTH-secreting pituitary adenomas.

[MeSH-major] ACTH-Secreting Pituitary Adenoma / etiology. Adenoma / etiology. Gene Expression Profiling. Oligonucleotide Array Sequence Analysis / methods. Signal Transduction / physiology

[MeSH-minor] Adult. Disease Progression. Expressed Sequence Tags. Extracellular Matrix Proteins / physiology. Female. Fiber Optic Technology. Humans. Male. Middle Aged. Real-Time Polymerase Chain Reaction. Reverse Transcriptase Polymerase Chain Reaction. Transforming Growth Factor alpha / physiology

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(PMID = 22166531.001).

[ISSN] 0366-6999

[Journal-full-title] Chinese medical journal

[ISO-abbreviation] Chin. Med. J.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] China

[Chemical-registry-number] 0 / Extracellular Matrix Proteins; 0 / Transforming Growth Factor alpha

   

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Many oncogenic mutations promote tumor growth by inducing autonomous activity of proteins that normally transmit proliferative signal initiated by extracellular factors.

The G proteins couple an array of seven transmembrane receptors at the cell surface with a variety of intracellular effectors, which produce second messenger molecules.

A subset of endocrine tumors, such as GH- or ACTH-secreting pituitary adenomas, functioning thyroid adenomas, adrenocortical and gonadal tumors were associated with somatic activating mutations in the highly conserved codons of the Gs (Arg201 and Gln227) and Gi (Arg179 and Gln205) proteins.

[MeSH-major] Endocrine Gland Neoplasms / genetics. GTP-Binding Protein alpha Subunits, Gi-Go / genetics. GTP-Binding Protein alpha Subunits, Gs / genetics. Mutation / genetics. Oncogenes / genetics

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(PMID = 16444361.001).

[ISSN] 0004-2730

[Journal-full-title] Arquivos brasileiros de endocrinologia e metabologia

[ISO-abbreviation] Arq Bras Endocrinol Metabol

[Language] por

[Publication-type] English Abstract; Journal Article; Review

[Publication-country] Brazil

[Chemical-registry-number] EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gi-Go; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs

[Number-of-references] 64

   

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[Title] Identification and characterization of two novel truncated but functional isoforms of the somatostatin receptor subtype 5 differentially present in pituitary tumors.

DESIGN AND RESULTS: A rapid amplification of cDNA ends PCR approach on samples from a human pituitary tumor and a cell line enabled identification of two novel alternatively spliced sst5 receptor variants.

Both novel receptors show a differential expression pattern in normal tissues and are also present in pituitary tumors of diverse etiology including nonfunctioning adenomas, corticotropinomas, somatotropinomas, and a prolactinoma.

Specifically, whereas sst5TMD5 is selectivity activated by somatostatin compared with cortistatin, cells transfected with sst5TMD4 almost exclusively respond to cortistatin and not to somatostatin.

CONCLUSIONS: Our results demonstrate the existence of two previously unidentified sst5 spliced variants with distinct distribution in normal tissues and pituitary tumors, unique ligand-selective signaling properties, and subcellular distribution, which could contribute to somatostatin and cortistatin signaling in normal and tumoral cells.

[MeSH-major] Adenoma / genetics. Pituitary Neoplasms / genetics. Receptors, Somatostatin / genetics

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(PMID = 19401364.001).

[ISSN] 1945-7197

[Journal-full-title] The Journal of clinical endocrinology and metabolism

[ISO-abbreviation] J. Clin. Endocrinol. Metab.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Protein Isoforms; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 5

   

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[Title] A spectrum of behaviour in silent corticotroph pituitary adenomas.

Silent corticotroph adenomas (SCA) are pituitary tumours positive on immunohistochemical staining for ACTH but without clinical evidence of Cushing's disease in the patient.

Previous reports suggest that these tumours may behave in a more aggressive way then other pituitary adenomas.

We identified 22 patients in whom trans-sphenoidal surgery was performed for a non-functioning adenoma (NFA) with positive immunostaining for ACTH between 1990 and 2000 and examined the history of their disease.

In four cases hypercortisolaemia was observed later in the course of the disease.

Pathological indices (increased mitotic range and Ki-67) did not predict recurrence or malignant transformation.

We suggest that certain 'silent' corticotroph tumours may have the potential for ACTH secretion leading to hypercortisolaemia at a later stage in the disease.

[MeSH-major] Adenoma / physiopathology. Pituitary Neoplasms / physiopathology

[MeSH-minor] Adrenocorticotropic Hormone / analysis. Adult. Aged. Anti-Inflammatory Agents / analysis. Female. Humans. Hydrocortisone / analysis. Immunohistochemistry / methods. Magnetic Resonance Imaging / methods. Male. Middle Aged. Neoplasm Recurrence, Local / surgery. Reoperation. Treatment Outcome. Vision Disorders / etiology

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(PMID = 16147581.001).

[ISSN] 0268-8697

[Journal-full-title] British journal of neurosurgery

[ISO-abbreviation] Br J Neurosurg

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Anti-Inflammatory Agents; 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone

   

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[Title] Long-term follow-up results of postoperative radiation therapy for Cushing's disease.

OBJECTIVES: Radiotherapy is currently used in patients with residual or recurrent pituitary adenomas after surgery.

However, there is little information of long-term outcome of patients with Cushing's disease following radiotherapy.

We assessed the long-term efficacy and toxicity of conventional radiotherapy in the control of Cushing's disease after unsuccessful transsphenoidal surgery.

PATIENTS AND METHODS: Forty patients with Cushing's disease were treated with conventional external beam radiotherapy at our Institution between 1988 and 2002.

The persistence of active disease after surgery was diagnosed by the increased high plasma cortisol levels, high 24 h urinary cortisol levels and absence of cortisol suppression after administration of dexamethasone.

CONCLUSION: Radiotherapy is effective in the long-term tumour- and hormone hypersecretion control of ACTH-secreting pituitary adenomas, however with a high prevalence of hypopituitarism.

[MeSH-major] ACTH-Secreting Pituitary Adenoma / radiotherapy. Adenoma / radiotherapy. Neoplasm Recurrence, Local / radiotherapy. Neoplasm, Residual / radiotherapy. Pituitary ACTH Hypersecretion / radiotherapy

[MeSH-minor] Adult. Disease-Free Survival. Female. Follow-Up Studies. Humans. Hydrocortisone / blood. Male. Middle Aged

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[Cites] Clin Endocrinol (Oxf). 2005 Feb;62(2):210-6 [15670198.001]

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(PMID = 17356896.001).

[ISSN] 0167-594X

[Journal-full-title] Journal of neuro-oncology

[ISO-abbreviation] J. Neurooncol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] WI4X0X7BPJ / Hydrocortisone

   

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[Title] [Immunohistochemistry for pituitary hormones and Ki-67 in growth hormone producing pituitary adenomas].

[Transliterated title] Evaluación por inmunohistoquímica de la expresión de hormonas hipofisiarias y del marcador de proliferación celular Ki-67 en tejido de adenomas causantes de acromegalia.

BACKGROUND: Growth hormone (GH) producing adenomas, frequently express several hormones.

AIM: To measure the immunohistochemical hormone expression in pituitary adenomas, excised from patients with acromegaly.

To determine if the plurihormonal condition of these adenomas is associated with a higher proliferative capacity, assessed through the expression of Ki-67.

MATERIAL AND METHODS: Forty one paraffin embedded surgical samples of pituitary adenomas from patients with acromegalia were studied.

Immunohistochemistry for GH, prolactin (PRL), follicle stimulating hormone (FSH), luteinizing hormone (LH), thyroid stimulating hormone (TSH), adrenocorticotropin (ACTH) and for the expression of Ki-67 was carried out.

CONCLUSIONS: Half of GH producing pituitary adenomas are plurihormonal.

There are no differences in the expression of Ki-67 between mono and plurihormonal adenomas.

[MeSH-major] Adenoma / metabolism. Growth Hormone-Secreting Pituitary Adenoma / metabolism. Human Growth Hormone / metabolism. Ki-67 Antigen / metabolism. Neoplasm Proteins / metabolism. Pituitary Neoplasms / metabolism

[MeSH-minor] Acromegaly / physiopathology. Acromegaly / surgery. Adrenocorticotropic Hormone / analysis. Adult. Aged. Female. Follicle Stimulating Hormone / analysis. Humans. Immunohistochemistry. Male. Middle Aged. Prolactin / analysis. Proliferating Cell Nuclear Antigen / analysis. Statistics, Nonparametric. Thyrotropin / analysis

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(PMID = 18949157.001).

[ISSN] 0034-9887

[Journal-full-title] Revista médica de Chile

[ISO-abbreviation] Rev Med Chil

[Language] spa

[Publication-type] English Abstract; Journal Article

[Publication-country] Chile

[Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Neoplasm Proteins; 0 / Proliferating Cell Nuclear Antigen; 12629-01-5 / Human Growth Hormone; 9002-60-2 / Adrenocorticotropic Hormone; 9002-62-4 / Prolactin; 9002-68-0 / Follicle Stimulating Hormone; 9002-71-5 / Thyrotropin

   

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[Title] Coexistence of corticotroph adenoma and thyrotroph hyperplasia in a dog.

Pituitary thyrotroph hyperplasia results from prolonged primary hypothyroidism in humans, mice and rats.

In dogs with Cushing's disease, many cases have low serum thyroid hormones concentrations due to euthyroid sick syndrome.

A 6-year-old castrated male Beagle diagnosed with Cushing's disease had a high serum thyroid stimulating hormone (TSH) concentration that was treated by hypophysectomy.

On histological examination, the resected pituitary gland contained both a corticotroph adenoma and thyrotroph hyperplasia.

The TSH-positive cell ratio in this case was greater than that of healthy Beagles.

In the present case, the pituitary thyrotroph hyperplasia was probably caused by primary hypothyroidism.

In conclusion, this Beagle is the first histological confirmation of the coexistence of a corticotroph adenoma and thyrotroph hyperplasia.

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(PMID = 19194082.001).

[ISSN] 0916-7250

[Journal-full-title] The Journal of veterinary medical science

[ISO-abbreviation] J. Vet. Med. Sci.

[Language] ENG

[Publication-type] Case Reports; Journal Article

[Publication-country] Japan

   

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[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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[Title] Sonic hedgehog regulates CRH signal transduction in the adult pituitary.

It is known to be involved in pituitary development, but its role in the adult pituitary has not been investigated.

Here, we show Shh and Gli1 immunoreactivity in adult human corticotroph cells.

Administration of Shh (5 microg/ml) alone and in combination with corticotrophin-releasing hormone (CRH; 100 nM) in dispersed rat anterior pituitary and AtT-20 mouse corticotrophinoma cells increased corticotrophin (ACTH) secretion and pro-opiomelanocortin (POMC) promoter activity.

Shh and CRH act additively in increasing CRH receptor 1 (CRH-R1).

Taken together, our results demonstrate a new role for Shh and Gli1 in corticotroph function and provide a new link between Shh and CRH signaling pathways.

[MeSH-major] Corticotropin-Releasing Hormone / physiology. Pituitary Gland / chemistry. Pituitary Gland / metabolism. Signal Transduction / physiology. Trans-Activators / physiology

[MeSH-minor] Adrenocorticotropic Hormone / secretion. Adult. Animals. Cell Line, Tumor. Cells, Cultured. Hedgehog Proteins. Humans. Kruppel-Like Transcription Factors. Male. Mice. Pro-Opiomelanocortin / genetics. Rats. Rats, Sprague-Dawley. Transcription Factors / antagonists & inhibitors. Transcription Factors / metabolism. Transcription, Genetic / physiology

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(PMID = 15572433.001).

[ISSN] 1530-6860

[Journal-full-title] FASEB journal : official publication of the Federation of American Societies for Experimental Biology

[ISO-abbreviation] FASEB J.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / GLI1 protein, human; 0 / Gli protein, mouse; 0 / Gli protein, rat; 0 / Hedgehog Proteins; 0 / Kruppel-Like Transcription Factors; 0 / SHH protein, human; 0 / Trans-Activators; 0 / Transcription Factors; 66796-54-1 / Pro-Opiomelanocortin; 9002-60-2 / Adrenocorticotropic Hormone; 9015-71-8 / Corticotropin-Releasing Hormone

   

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[Title] Pituitary corticotroph hyperplasia preceding adenoma in a patient with Nelson's syndrome.

We report the case of a 42-year-old woman with Cushing's disease and Nelson's syndrome.

A detailed morphologic study demonstrated nodular hyperplasia of corticotroph cells but no adenoma.

Following a long-lasting remission (14 years), Cushing's disease recurred.

After an unsuccessful second transsphenoidal surgery, Cushing's disease persisted and both adrenals were removed (at the age of 34).

The pituitary tumor proved to be a corticotroph adenoma; it was removed by the transsphenoidal approach (at the age of 42).

Although in most patients Cushing's disease is due to an ACTH-secreting pituitary corticotroph adenoma which precedes the manifestation of Nelson's syndrome, our case indicates not only that corticotroph hyperplasia may cause Cushing's disease but that it may exist before the development of Nelson's syndrome after the removal of both adrenals.

Our study supports the view that protracted stimulation of corticotrophs resulting from the elimination of the negative inhibitory feedback effect by corticosteroids plays a role in adenoma initiation.

[MeSH-major] ACTH-Secreting Pituitary Adenoma / etiology. Adenoma / etiology. Hyperplasia / complications. Nelson Syndrome / etiology. Pituitary ACTH Hypersecretion / complications

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(PMID = 16550740.001).

[ISSN] 0722-5091

[Journal-full-title] Clinical neuropathology

[ISO-abbreviation] Clin. Neuropathol.

[Language] eng

[Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Germany

   

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[Title] Silent subtype 3 pituitary adenoma: a clinicopathologic analysis of the Mayo Clinic experience.

BACKGROUND: Macroadenomas represent 50% of pituitary tumours and are often (30%) nonfunctioning.

Their immunophenotype suggests differentiation toward a specific pituitary cell line.

A substantial proportion of tumours with particularly aggressive behaviour are so called 'silent subtype 3 adenoma'.

Its diagnosis requires ultrastructural confirmation.

Although once included among silent corticotroph adenomas, this aggressive, morphologically distinctive tumour is now recognized as a major form of plurihormonal adenoma and, in fact, some patients might present with clinical hormonal excess.

The cytogenesis and pathobiology of silent subtype 3 adenomas is unsettled.

DESIGN: This retrospective, single institution study found 27 confirmed examples of silent subtype 3 adenoma, a frequency of 0.9% of adenomas.

RESULTS: The study group was comprised of 16 men (59%) and 11 women (41%); two patients (7%) had definitive diagnosis of multiple endocrine neoplasia type 1 (MEN1).

Most tumours were plurihormonal, featuring immunoreactivity for PRL (17), GH (15), TSH (16) or ACTH (3); only one lesion was immunonegative.

CONCLUSION: Silent subtype 3 adenoma, a plurihormonal tumour, is rare and aggressive in nature.

This adenoma must be considered in the differential of often clinically nonfunctioning but plurihormonal adenomas featuring variable cytologic atypia.

Electron microscopy is required for confirmation of the diagnosis.

The cytogenesis of silent subtype 3 adenoma remains unsettled.

[MeSH-major] Pituitary Neoplasms / pathology

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(PMID = 19170710.001).

[ISSN] 1365-2265

[Journal-full-title] Clinical endocrinology

[ISO-abbreviation] Clin. Endocrinol. (Oxf)

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Hormones

   

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[Title] Immunohistochemical properties of silent corticotroph adenoma and Cushing's disease.

Proopiomelanocortin processing in corticotroph cells is known to be operated by prohormone convertase (PC) 1/3 which is activating several pro-proteins and prohormones by intracellular limited proteolysis processing.

In this study, we hypothesized that PC1/3 expression differs between Cushing's disease (CD) and silent corticotroph adenoma (SCA), and investigated whether PC1/3 expression is involved in the adrenocorticotropin (ACTH) silence of SCA.

We performed immunohistochemical analysis of pituitary adenoma specimens for six adenohypophysial hormones, PC1/3 and chromogranin A (CgA).

Subjects for this study consisted of 12 anterior pituitary adenomas of CD (1 male, 11 female; 14-70 years old) and 31 non-functioning adenomas (23 male, 8 female; 32-71 years old).ACTH immunoreactivity was observed in all of CD and three of 31 non-functioning adenomas.

Cushing's adenomas and SCAs were all positive for PC1/3.

PC1/3-positive cells did not always colocalize with ACTH but some of them colocalized with CgA in SCAs.

Even if PC1/3 is not present in corticotroph cells, PC1/3 immunoreactivity in SCA may originate from CgA-positive cells.

We conclude that immunohistochemistry for PC1/3 is not helpful for differential diagnosis between CD and SCA in clinical practice, though the regulation of PC1/3 expression is likely to be an important etiological factor in ACTH silence of SCA.

The diversity of immunohistochemical properties of SCA leads us to speculate that it is not a single entity and may be a general diagnostic term for adenomas of varying etiology.

[MeSH-major] Adenoma / metabolism. Pituitary ACTH Hypersecretion / metabolism. Pituitary Neoplasms / metabolism

[MeSH-minor] Adolescent. Adrenocorticotropic Hormone / metabolism. Adult. Aged. Chromogranin A / blood. Corticotropin-Releasing Hormone. Female. Follicle Stimulating Hormone / metabolism. Gonadotropin-Releasing Hormone. Growth Hormone-Releasing Hormone. Human Growth Hormone / metabolism. Humans. Immunohistochemistry. Male. Middle Aged. Proprotein Convertases / blood. Thyrotropin

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(PMID = 17410413.001).

[ISSN] 1386-341X

[Journal-full-title] Pituitary

[ISO-abbreviation] Pituitary

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Chromogranin A; 12629-01-5 / Human Growth Hormone; 33515-09-2 / Gonadotropin-Releasing Hormone; 9002-60-2 / Adrenocorticotropic Hormone; 9002-68-0 / Follicle Stimulating Hormone; 9002-71-5 / Thyrotropin; 9015-71-8 / Corticotropin-Releasing Hormone; 9034-39-3 / Growth Hormone-Releasing Hormone; EC 3.4.21.- / Proprotein Convertases

   

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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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A 64-year-old woman was previously treated for Cushing's disease with trans-sphenoidal surgery, external beam radiotherapy and bilateral adrenalectomy.

Progression of an aggressive corticotroph adenoma was evident 3 years post-adrenalectomy; involvement of the clivus was treated with surgery and gamma knife radiosurgery.

ACTH levels peaked at 2472 and 2265 pmol/l pre- and post-hydrocortisone respectively.

Treatment with temozolomide resulted in a significant improvement in symptoms, a reduction of plasma ACTH to 389 pmol/l and regression of tumour on magnetic resonance imaging scan after four cycles of treatment.

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(PMID = 18984772.001).

[ISSN] 1479-683X

[Journal-full-title] European journal of endocrinology

[ISO-abbreviation] Eur. J. Endocrinol.

[Language] ENG

[Publication-type] Case Reports; Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; 9002-60-2 / Adrenocorticotropic Hormone

   

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[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