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[Title] Facial metrics in children with corticotrophin-producing pituitary adenomas suggest abnormalities in midface development.

BACKGROUND: Tumors of the hypothalamic-pituitary unit have been linked to genetic syndromes that are associated with midfacial abnormalities.

AIM: We hypothesized that mutations of genes that affect the development of the face (and consequently of the anterior pituitary) may be present in children with ACTH-producing pituitary adenomas, and if this is true then facial measurements would be different from those predicted by parental features.

METHODS: We studied 20 children with corticotropinomas and a control group and their parents.

RESULTS: Significant differences were seen between the children with pituitary adenomas and their parents for vertical facial height measures: nasal length (p < 0.001), lower facial height (p < 0.03) and overall facial height (p < 0.01).

CONCLUSION: We conclude that some of the indices of midline craniofacial development, in particular those affecting the vertical axis, are different in children with corticotroph adenomas producing ACTH.

[MeSH-major] ACTH-Secreting Pituitary Adenoma / pathology. Adenoma / pathology. Face / pathology. Maxillofacial Abnormalities / etiology. Maxillofacial Development / physiology

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(PMID = 19344074.001).

[ISSN] 0334-018X

[Journal-full-title] Journal of pediatric endocrinology & metabolism : JPEM

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

[Language] eng

[Databank-accession-numbers] ClinicalTrials.gov/ NCT00001595

[Grant] United States / NICHD NIH HHS / HD / Z01 HD000642; United States / Intramural NIH HHS / / ZIA HD000642-13; United States / NICHD NIH HHS / HD / Z01-HD-000642-04

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural

[Publication-country] Germany

[Other-IDs] NLM/ NIHMS310299; NLM/ PMC3143028

   

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[Title] The role of inferior petrosal sinus sampling in the diagnostic localization of Cushing's disease.

Cushing's syndrome can present a complex problem of differential diagnosis.

Of cases in which hypercortisolemia results from an adrenocorticotropic hormone (ACTH)-dependent process, approximately 80% are due to a pituitary adenoma (Cushing's disease [CD]), 10% are due to adrenal lesions, and the remaining 10% are secondary to ectopic ACTH secretion.

For patients with CD, surgical removal of the pituitary adenoma is the treatment of choice.

Thus, localization of the source of ACTH secretion is critical in guiding timely treatment decisions.

Inferior petrosal sinus sampling (IPSS) is considered to be the gold standard for confirming the origin of ACTH secretion in patients with Cushing's syndrome.

A number of other techniques are discussed including sampling from the cavernous sinus, the jugular vein, and multiple sites to aid the diagnosis and lateralization of ACTH-producing pituitary adenomas.

[MeSH-major] Petrosal Sinus Sampling / methods. Pituitary ACTH Hypersecretion / diagnosis

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(PMID = 17961020.001).

[ISSN] 1092-0684

[Journal-full-title] Neurosurgical focus

[ISO-abbreviation] Neurosurg Focus

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

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

[Number-of-references] 46

   

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[Title] Bone morphogenetic protein-4 inhibits corticotroph tumor cells: involvement in the retinoic acid inhibitory action.

The molecular mechanisms governing the pathogenesis of ACTH-secreting pituitary adenomas are still obscure.

In this study, we report that bone morphogenetic protein-4 (BMP-4) is expressed in the corticotrophs of human normal adenohypophysis and its expression is reduced in corticotrophinomas obtained from Cushing's patients compared with the normal pituitary.

BMP-4 treatment of AtT-20 mouse corticotrophinoma cells has an inhibitory effect on ACTH secretion and cell proliferation.

AtT-20 cells stably transfected with a dominant-negative form of the BMP-4 signal cotransducer Smad-4 or the BMP-4 inhibitor noggin have increased tumorigenicity in nude mice, showing that BMP-4 has an inhibitory role on corticotroph tumorigenesis in vivo.

Because the activation of the retinoic acid receptor has an inhibitory action on Cushing's disease progression, we analyzed the putative interaction of these two pathways.

Indeed, retinoic acid induces both BMP-4 transcription and expression and its antiproliferative action is blocked in Smad-4dn- and noggin-transfected Att-20 cells that do not respond to BMP-4.

This new mechanism is a potential target for therapeutic approaches for Cushing's disease.

[MeSH-major] Adenoma / pathology. Bone Morphogenetic Proteins / pharmacology. Bone Morphogenetic Proteins / physiology. Cushing Syndrome / pathology. Pituitary Neoplasms / pathology. Tretinoin / pharmacology

[MeSH-minor] Animals. Bone Morphogenetic Protein 4. Cell Division / drug effects. Cell Line, Tumor. Humans. Immunohistochemistry. Mice. Pituitary Gland / pathology. Pituitary Gland / physiology. Reference Values

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(PMID = 16195406.001).

[ISSN] 0013-7227

[Journal-full-title] Endocrinology

[ISO-abbreviation] Endocrinology

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / BMP4 protein, human; 0 / Bmp4 protein, mouse; 0 / Bone Morphogenetic Protein 4; 0 / Bone Morphogenetic Proteins; 5688UTC01R / Tretinoin

   

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[Title] Expression of somatostatin receptor subtypes in human pituitary adenomas -- immunohistochemical studies.

BACKGROUND: The highly variable expression of SSTR subtypes in pituitary adenomas (PA) may partially explain why the subgroup of somatotropinomas or other adenomas do not respond to the therapeutic action of currently used long-acting somatostatin analogues like octreotide or lanreotide.

RESULTS: The pattern of SSTR immunostaining (estimated according to the percentage frequency of appearance) was in acromegaly: SSTR 5 > SSTR 1 > SSTR 2A = SSTR 3 > SSTR 2B, in prolactinomas: SSTR 2B = SSTR 3 = SSTR 5 > SSTR 1 = SSTR 2A, in gonadotropinomas: SSTR 3 > SSTR 2B > SSTR 1 = SSTR 2A > SSTR 5, in corticotropinomas: SSTR 2A > SSTR 1 = SSTR 3 > SSTR 5 > SSTR 2B.

In PA immunonegative for pituitary hormones, we noticed only a weak staining of all receptor subtypes including SSTR 4.

In plurihormonal adenomas with positive GH phenotype the staining pattern was: SSTR 5 > SSTR 1 = SSTR 2B and in plurihormonal PA with negative GH phenotype: SSTR 1 = SSTR 5 > SSTR 2A = SSTR 2B = SSTR 3.

In plurihormonal adenoma with ACTH immunopositivity, the staining pattern was: SSTR = SSTR 2A = SSTR 3 = SSTR 5.

SSTR 1 and SSTR 5 were the most frequent subtypes of somatostatin receptor in plurihormonal adenomas without ACTH expression.

Apart from applying SSTR 2 and SSTR 5-preferring octreotide and lanreotide - newly synthesized multiligand analogues, such as SOM 230, KE 108, or other SST selective analogues, may represent a further useful approach for the treatment, especially in cases other than somatotropinoma or thyrotropinoma.

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

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(PMID = 19753537.001).

[ISSN] 0423-104X

[Journal-full-title] Endokrynologia Polska

[ISO-abbreviation] Endokrynol Pol

[Language] eng

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

[Publication-country] Poland

[Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Peptides, Cyclic; 0 / Protein Isoforms; 0 / Receptors, Somatostatin; 0G3DE8943Y / lanreotide; 51110-01-1 / Somatostatin; RWM8CCW8GP / Octreotide

   

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[Title] The diagnostic value of fused positron emission tomography/computed tomography in the localization of adrenocorticotropin-secreting pituitary adenoma in Cushing's disease.

Despite the high resolution of magnetic resonance imaging (MRI) of the pituitary gland, up to 40% of cases of Cushing's disease (CD) have normal MRI.

Objective of this study is to explore the diagnostic potential of PET-CT for localization of adrenocorticotropin-secreting pituitary adenomas in CD.

PET-CT was performed in 12 cases with de novo (7 cases) or persistent CD (5 cases) that were proven to have CD on biochemical, radiological and/or histopathological findings.

PET-CT was positive in 7 of the 12 cases of CD (58%) showing a focal area of uptake in the pituitary gland.

If these findings are confirmed in larger studies, PET-CT might become an important diagnostic technique, especially when the more invasive and technically demanding procedure of IPSS is not available or inconclusive.

[MeSH-major] ACTH-Secreting Pituitary Adenoma / diagnosis. Pituitary ACTH Hypersecretion / pathology. Positron-Emission Tomography / methods. Tomography, X-Ray Computed / methods

[MeSH-minor] Adult. Female. Humans. Magnetic Resonance Imaging / methods. Male. Middle Aged. Pituitary Gland / metabolism. Pituitary Gland / pathology

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(PMID = 19387839.001).

[ISSN] 1573-7403

[Journal-full-title] Pituitary

[ISO-abbreviation] Pituitary

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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[Title] Endocrine outcome of endoscopic endonasal transsphenoidal surgery in functioning pituitary adenomas.

OBJECTIVE: Microscopic and endoscopic transsphenoidal approach (TSA) are major surgical techniques in the treatment of pituitary adenoma.

Endoscopic endonasal transsphenoidal approach (EETSA) has been increasingly used for pituitary adenomas, however, its surgical outcome particularly in functioning pituitary adenoma has been debated.

Here, we investigated the endocrine outcome of the patients with growth hormone (GH) and adrenocorticotropic hormone (ACTH) secreting pituitary adenoma treated by EETSA.

METHODS: We treated 80 patients with pituitary adenoma by EETSA since 2004, of which 12 patients were affected by functioning pituitary adenomas (9 GH, 3 ACTH, 0 PRL; 9 macro, 3 micro).

Surgical outcome of those patients treated by EETSA was compared with that of the 11 functioning pituitary adenoma patients (8 GH, 3 ACTH; 8 macro, 3 micro) who underwent sublabial microscopic TSA between 1997 and 2003.

CONCLUSION: EETSA appears to be an effective and safe method for the treatment of functioning pituitary adenomas.

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(PMID = 19096666.001).

[ISSN] 2005-3711

[Journal-full-title] Journal of Korean Neurosurgical Society

[ISO-abbreviation] J Korean Neurosurg Soc

[Language] eng

[Publication-type] Journal Article

[Publication-country] Korea (South)

[Other-IDs] NLM/ PMC2588303

[Keywords] NOTNLM ; ACTH-secreting pituitary adenoma / Endoscopy / GH-secreting pituitary adenoma / Transsphenoidal approach

   

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Dopamine agonists (DA) and somatostatin (SS) analogues have been proposed in the treatment of ACTH-producing neuro-endocrine tumours that cause Cushing's syndrome.

In this study, we investigated the effects of the GC dexamethasone (DEX) on D(2) and sst expression in three human neuro-endocrine cell lines: BON (carcinoid) and TT (medullary thyroid carcinoma) versus DMS (small cell lung cancer), which is severely GC resistant.

In DMS, DEX did not cause significant changes in the expression of these receptor subtypes.

In conclusion, we show that GCs selectively down-regulate sst(2), but not D(2) and only to a minor degree sst(5) in human neuro-endocrine BON and TT cells.

This mechanism may also be responsible for the low expression of sst(2) in corticotroph adenomas and underwrite the current interest in sst(5) and D(2) as possible therapeutic targets for a medical treatment of Cushing's disease.

[MeSH-minor] Animals. Antineoplastic Agents, Hormonal / metabolism. Cell Line. Cell Proliferation. DNA Fragmentation. Dexamethasone / metabolism. Dopamine / metabolism. Hormone Antagonists / metabolism. Humans. Mifepristone / metabolism. Octreotide / metabolism. RNA, Messenger / metabolism. Radioligand Assay. Somatostatin / metabolism

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(PMID = 18852217.001).

[ISSN] 1479-6813

[Journal-full-title] Journal of molecular endocrinology

[ISO-abbreviation] J. Mol. Endocrinol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Glucocorticoids; 0 / Hormone Antagonists; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / Receptors, Dopamine D2; 0 / Receptors, Somatostatin; 320T6RNW1F / Mifepristone; 51110-01-1 / Somatostatin; 7S5I7G3JQL / Dexamethasone; RWM8CCW8GP / Octreotide; VTD58H1Z2X / Dopamine

   

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[Title] Differential gene expression in models of pituitary prolactin-producing tumoral cells.

Although several genes and signalling pathways have been identified as important effectors in the development of pituitary tumours, our understanding of pituitary tumorigenesis remains incomplete and is the focus of much current research.

Use of the mRNA differential display technique in prolactinomas from D2-receptor knockout mice and in stable GH3 cell line clones with enhanced tumorigenicity in vivo has led to the identification of two genes that are involved in the pathogenic process--BMP-4 and RSUME.

In contrast, BMP-4 has an inhibitory role in corticotrophinomas.

RSUME (RWD-containing sumoylation enhancer) was identified from a transformed lactosomatotrophic cell line that had increased tumorigenic and angiogenic potential.

The differential expression and action of BMP-4 in prolactinomas and corticotrophinomas highlights the importance of studying a gene with contrasting actions in two cell lineages of the same organ in order to understand the pituitary transformation process.

Both BMP-4 and RSUME may be interesting targets for inhibiting steps involved in pituitary tumorigenesis.

[MeSH-major] Bone Morphogenetic Protein 4 / biosynthesis. Gene Expression Regulation, Neoplastic. Models, Biological. Neoplasm Proteins / biosynthesis. Prolactinoma / metabolism. Transcription Factors / biosynthesis

[MeSH-minor] Animals. Cell Hypoxia / genetics. Cell Line, Tumor. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / metabolism. Gene Expression Profiling. Humans. Mice. Mice, Knockout. Receptors, Dopamine D2 / genetics. Receptors, Dopamine D2 / metabolism. Signal Transduction / genetics

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[Copyright] Copyright 2009 S. Karger AG, Basel.

(PMID = 19407504.001).

[ISSN] 1423-0046

[Journal-full-title] Hormone research

[ISO-abbreviation] Horm. Res.

[Language] eng

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

[Publication-country] Switzerland

[Chemical-registry-number] 0 / BMP4 protein, human; 0 / Bone Morphogenetic Protein 4; 0 / Neoplasm Proteins; 0 / RSUME protein, human; 0 / Receptors, Dopamine D2; 0 / Transcription Factors

[Number-of-references] 56

   

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[Title] Immunohistochemical detection of PPARgamma receptors in the human pituitary adenomas: correlation with PCNA.

The occurrence of peroxisome proliferator-activated receptors gamma (PPARgamma) was investigated in 51 human pituitary adenomas and in 6 non-tumoral human pituitary tissue samples.

The mean percentage of cells with positive nuclear reaction was 3-fold higher in pituitary adenomas in comparison with non-tumoral pituitary tissues.

It was clearly stronger in pituitary adenomas than in non-tumoral pituitary tissues.

A slight, statistically insignificant tendency towards negative correlation between PPARgamma and PCNA was found in somatotropinomas, prolactinomas, corticotropinomas and gonadotropinomas.

On the other hand, in null cell adenomas and "silent" corticotropinomas, a strong positve correlation between the expression of PPARgamma and PCNA was observed.

The strong expression of PPARgamma in human pituitary adenomas and its possible involvement in control of cell proliferation in these tumors give a good reason for the attempts of their treatment with PPARgamma ligands.

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(PMID = 16201313.001).

[ISSN] 0239-8508

[Journal-full-title] Folia histochemica et cytobiologica

[ISO-abbreviation] Folia Histochem. Cytobiol.

[Language] ENG

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

[Publication-country] Poland

[Chemical-registry-number] 0 / PPAR gamma; 0 / Proliferating Cell Nuclear Antigen

   

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[Title] Unusual causes of Cushing's syndrome.

Although in the majority of the patients with Cushing's syndrome (CS), hypercortisolism is due to ACTH hypersecretion by a pituitary tumour or to ectopic ACTH secretion from an extrapituitary neoplastic lesion or to autonomous cortisol secretion by an adrenal tumour, in occasional patients a much rarer entity may be the cause of the syndrome.

The following unusual forms of CS were identified: (i) ACTH hyperesecretion due to ectopic corticotroph adenomas in the parasellar region or the neurohypophysis, or as part of double adenomas, or gangliocytomas;.

(ii) ACTH hypersecretion due to ectopic CRH or CRH-like peptide secretion by various neoplasms;.

(iii) ACTH-independent cortisol hypersecretion from ectopic or bilateral adrenal adenomas;.

Such unusual presentations of CS illustrate why Cushing's syndrome represents one of the most puzzling endocrine syndromes.

[MeSH-minor] ACTH Syndrome, Ectopic / complications. Adrenal Gland Neoplasms / complications. Female. Glucocorticoids / adverse effects. Humans. Liver Neoplasms / complications. Megestrol Acetate / adverse effects. Ovarian Neoplasms / complications. Pituitary Neoplasms / complications. Ritonavir / adverse effects

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(PMID = 18209862.001).

[ISSN] 0004-2730

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

[ISO-abbreviation] Arq Bras Endocrinol Metabol

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] Brazil

[Chemical-registry-number] 0 / Glucocorticoids; O3J8G9O825 / Ritonavir; TJ2M0FR8ES / Megestrol Acetate

[Number-of-references] 58

   

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[Title] [Recent trends in the pathophysiology and treatment of pituitary adenomas].

Recent molecular pathological investigations have elucidated the cytodifferentiation of pituitary cells and identified several transcriptional factors that regulate this cytodifferentiation of pituitary cells.

The patterns of cytodifferentiation are closely related to the pathogenesis of pituitary adenomas.

Meanwhile, the role of hypothalamic hormones in the development of pituitary adenomas has recently attracted the attention of investigators.

The expression of growth hormone-releasing hormone and corticotrophin releasing hormone in corticotroph adenomas have been demonstrated in somatotroph adenomas and corticotropin adenomas, respectively.

This finding indicates that the endogenous expression of hypothalamic hormones and their receptors in human pituitary adenoma cells has ample significance in the autocrine or paracrine regulation of pituitary hormone production and tumor extension induced by hypothalamic hormones produced by adenoma cells.

The recent progress in surgical techniques for treatment of pituitary adenomas has provided several alternatives: transsphenoidal surgery vs. transcranial surgery, sublabial approach vs. endonasal approach, and microsurgery vs. endoscopic surgery.

There have also been developments in the medical treatment of pituitary adenomas.

The frequently used dopamine agonist, cabergoline, is very effective for treating prolactin-producing adenoma.

Long-acting octreotide and pegvisomant are now available for the treatment of growth hormone producing adenoma.

Cabergoline is also used for growth hormone producing adenoma.

Temozolomide has recently been used for atypical adenomas or pituitary carcinomas.

Adult growth hormone deficiency sometimes occurs in postoperative patients with pituitary adenomas.

[MeSH-major] Adenoma / etiology. Adenoma / therapy. Pituitary Neoplasms / etiology. Pituitary Neoplasms / therapy

[MeSH-minor] Antineoplastic Agents / therapeutic use. Corticotropin-Releasing Hormone. Dacarbazine / analogs & derivatives. Dacarbazine / therapeutic use. Ergolines / therapeutic use. Growth Hormone-Releasing Hormone. Human Growth Hormone / analogs & derivatives. Human Growth Hormone / therapeutic use. Humans. Hypothalamic Hormones. Incidental Findings. Neurosurgical Procedures / methods. Neurosurgical Procedures / trends. Octreotide / therapeutic use. Prolactinoma. Receptors, Neuropeptide. Receptors, Pituitary Hormone-Regulating Hormone

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(PMID = 19697885.001).

[ISSN] 1881-6096

[Journal-full-title] Brain and nerve = Shinkei kenkyū no shinpo

[ISO-abbreviation] Brain Nerve

[Language] jpn

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

[Publication-country] Japan

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Ergolines; 0 / Hypothalamic Hormones; 0 / Receptors, Neuropeptide; 0 / Receptors, Pituitary Hormone-Regulating Hormone; 0 / pegvisomant; 0 / somatotropin releasing hormone receptor; 12629-01-5 / Human Growth Hormone; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; 9015-71-8 / Corticotropin-Releasing Hormone; 9034-39-3 / Growth Hormone-Releasing Hormone; LL60K9J05T / cabergoline; RWM8CCW8GP / Octreotide

[Number-of-references] 32

   

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[Title] [The value of corticotropin-releasing hormone (CRH) test for differential diagnosis of Cushing's syndrome].

INTRODUCTION: Diagnosis and differential diagnosis of Cushing's syndrome (CS) remain considerable challenge in endocrinology.

Following the CRH administration, the majority of patients with ACTH secreting pituitary adenoma show a significant rise of plasma cortisol and ACTH, whereas those with ectopic ACTH secretion characteristically do not.

OBJECTIVE: The aim of our study was to assess the value of CRF test for differential diagnosis of CS using the ROC (receiver operating characteristic) curve method.

ACTH secreting pituitary adenoma was found in 18, ectopic ACTH secretion in 3 and cortisol secreting adrenal adenoma in 9 of all patients with CS.

Cortisol and ACTH were determined -15.0, 15, 30, 45, 60, 90 and 120 min. after i.v. administration of 100 microg of ovine CRH.

Cortisol and ACTH were determined by commercial RIA.

Due to small number, the patients with ectopic ACTH secretion were excluded from test evaluation by ROC curve method.

Consequently, basal ACTH was (100.9 +/- 85.0 vs. 138.0 +/- 123.7 vs. 4.8 +/- 4.3 pg/mL) and maximal stimulated ACTH (203.8 +/- 160.1 vs. 288.0 +/- 189.5 vs. 7.4 +/- 9.2 pg/mL).

For ACTH, determination area under ROC curve was 0.637 +/- 0.142 (CI 95% 0.359-0.916).

For ACTH increase cut-off level of 30%, test sensitivity was 70%, with specificity of 57%.

CONCLUSION: Determination of cortisol and ACTH levels in CRH test remains reliable tool in differential diagnosis of Cushing's syndrome.

[MeSH-major] Corticotropin-Releasing Hormone. Cushing Syndrome / diagnosis

[MeSH-minor] ACTH Syndrome, Ectopic / diagnosis. ACTH-Secreting Pituitary Adenoma / diagnosis. Adenoma / diagnosis. Adrenocorticotropic Hormone / blood. Adult. Diagnosis, Differential. Female. Humans. Hydrocortisone / blood. Male. ROC Curve. Sensitivity and Specificity

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(PMID = 17503565.001).

[ISSN] 0370-8179

[Journal-full-title] Srpski arhiv za celokupno lekarstvo

[ISO-abbreviation] Srp Arh Celok Lek

[Language] srp

[Publication-type] English Abstract; Journal Article

[Publication-country] Serbia and Montenegro

[Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone; 9015-71-8 / Corticotropin-Releasing Hormone; WI4X0X7BPJ / Hydrocortisone

   

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[Title] Silent corticotroph adenomas have unique recurrence characteristics compared with other nonfunctioning pituitary adenomas.

OBJECTIVE: The prevalence of silent corticotroph adenomas (SCAs) is not rare among nonfunctioning pituitary adenomas (NFPAs); however, it is unknown whether the clinical significance of SCAs differs from that of NFPAs without ACTH immunoreactivity (non-SCAs).

MEASUREMENTS: We analysed whether clinical manifestations at diagnosis, postoperative recurrence rate and recurrence characteristics differed between SCA and non-SCA patients.

The mean age at the time of diagnosis was 44 years (range, 13-67 years) in the SCA group and 50 years (18-79 years) in the non-SCA group (P = 0.026), with respective follow-up periods of 5.2 (range, 1.0-16.0 years) and 4.2 years (0.5-16.1 years) (P = 0.255).

[MeSH-major] Adenoma / pathology. Adrenocorticotropic Hormone / analysis. Neoplasm Recurrence, Local. Pituitary Neoplasms / pathology

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(PMID = 19650787.001).

[ISSN] 1365-2265

[Journal-full-title] Clinical endocrinology

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

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] England

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

   

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[Title] [Cushing's syndrome. II. New forms of treatment].

Several new therapeutic options both medicinal and surgical, have emerged for the treatment of Cushing's syndrome.

In Cushing's disease caused by an adrenocorticotropin (ACTH) secreting pituitary adenoma, the introduction ofendoscopic pituitary surgery offers better visualization of the sella than does the traditional explorative surgery.

These agents may also be effective for the medicinal treatment of ectopic ACTH-secretion.

The primary treatment for ACTH-independent Cushing's syndrome is laparoscopic adrenalectomy.

[MeSH-major] ACTH-Secreting Pituitary Adenoma / therapy. Adenoma / therapy. Cushing Syndrome / therapy

[MeSH-minor] Adrenalectomy. Adrenergic Antagonists / therapeutic use. Humans. Pituitary Gland / surgery. Treatment Outcome

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[CommentIn] Ned Tijdschr Geneeskd. 2006 Oct 28;150(43):2345-9 [17100122.001]

[CommentIn] Ned Tijdschr Geneeskd. 2007 Feb 3;151(5):330; author reply 331 [17326480.001]

(PMID = 17100127.001).

[ISSN] 0028-2162

[Journal-full-title] Nederlands tijdschrift voor geneeskunde

[ISO-abbreviation] Ned Tijdschr Geneeskd

[Language] dut

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

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Adrenergic Antagonists

[Number-of-references] 24

   

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[Title] Malignant pituitary corticotroph adenomas: report of two cases and a comprehensive review of the literature.

Corticotroph pituitary carcinomas are tumors, defined by the presence of distant metastases that determine their poor prognosis.

The diagnosis and therapy of malignant corticotroph adenomas remains a clinical challenge.

The molecular mechanisms of malignant transformation of pituitary adenomas are unclear, although they are believed to arise in an adenoma-to-carcinoma sequence.

We describe two cases of malignant Cushing's disease with metastases in liver and bone, respectively.

The primary pituitary tumors were treated by a combination of radiotherapy and transsphenoidal surgery, but recurred several times in both patients.

The time interval between the diagnosis of Cushing's disease and the discovery of metastases was 32 and 17 years, respectively.

In the first case the patient died within 6 months after diagnosis of metastasis, whereas the second patient is alive at a follow-up of 2 years after the discovery of the metastasis.

Furthermore, we reviewed all available cases of corticotroph pituitary carcinomas reported in the literature and analyzed their clinical features and therapeutical management.

In conclusion, frequent relapses of Cushing's disease, aggressive growth of macroadenoma, Nelson's syndrome after adrenalectomy or persistently high ACTH levels should prompt the clinician to consider the possibility of pituitary corticotroph carcinomas.

[MeSH-major] ACTH-Secreting Pituitary Adenoma / diagnosis. ACTH-Secreting Pituitary Adenoma / pathology. Pituitary ACTH Hypersecretion / complications

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(PMID = 18176844.001).

[ISSN] 1573-7403

[Journal-full-title] Pituitary

[ISO-abbreviation] Pituitary

[Language] eng

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

[Publication-country] United States

[Number-of-references] 62

   

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[Title] Corticotroph adenoma of the pituitary in a patient with X-linked adrenal hypoplasia congenita due to a novel mutation of the DAX-1 gene.

We report the occurrence of an ACTH-secreting adenoma in a patient with X-linked congenital adrenal hypoplasia.

DESIGN AND METHODS: Detailed clinical, radiological and pathological investigation of the pituitary adenoma.

ACTH was 24 980 pg/ml and nuclear magnetic resonance disclosed a huge pituitary adenoma.

Three transsphenoidal operations and radiotherapy were necessary to remove the tumor mass and control ACTH secretion.

Histologically, the adenoma was composed of chromophobic and basophilic neoplastic cells with positive immunostaining for ACTH.

CONCLUSIONS: This case suggests that in adrenal hypoplasia congenita the development of a pituitary adenoma should be considered when a sudden rise of ACTH occurs despite adequate steroid substitution.

[MeSH-major] Adenoma / complications. Adrenal Insufficiency / complications. Adrenal Insufficiency / genetics. DNA-Binding Proteins / genetics. Pituitary Neoplasms / complications. Receptors, Retinoic Acid / genetics. Repressor Proteins / genetics

[MeSH-minor] Adrenocorticotropic Hormone / metabolism. Adult. Chromosomes, Human, X. DAX-1 Orphan Nuclear Receptor. Family Health. Female. Frameshift Mutation. Humans. Magnetic Resonance Imaging. Male. Pituitary ACTH Hypersecretion / complications. Pituitary ACTH Hypersecretion / metabolism. Pituitary ACTH Hypersecretion / pathology

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(PMID = 16061826.001).

[ISSN] 0804-4643

[Journal-full-title] European journal of endocrinology

[ISO-abbreviation] Eur. J. Endocrinol.

[Language] eng

[Grant] Italy / Telethon / / B.38

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

[Publication-country] England

[Chemical-registry-number] 0 / DAX-1 Orphan Nuclear Receptor; 0 / DNA-Binding Proteins; 0 / NR0B1 protein, human; 0 / Receptors, Retinoic Acid; 0 / Repressor Proteins; 9002-60-2 / Adrenocorticotropic Hormone

   

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[Title] Cushing's disease arising from a clinically nonfunctioning pituitary adenoma.

A 49-yr-old woman with a large pituitary tumor leading to visual loss and galactorrhea- amenorrhea was submitted to transcranial pituitary surgery, when a clinically nonfunctioning pituitary adenoma was partially removed.

Histopathology and immunohistochemistry confirmed the diagnosis of "non-secreting atypical adenoma."

Two years later, she presented high free urinary cortisol levels and a positive ACTH response to desmopressin testing on dexametasone 2 mg overnight.

A pituitary biopsy confirmed aggressive growth as well as positive immunoreactivity for ACTH, p53, Ki-67, and c-erb-B2.

The overall clinical, laboratory, and pathological data suggest a transition from a clinically nonfunctioning to a hypersecreting ACTH-producing tumor.

Putative mechanisms of tumor transformation and the possibility of a silent corticotropinoma evolving into clinical Cushing s syndrome are discussed.

[MeSH-major] Adenoma / complications. Adenoma / pathology. Pituitary ACTH Hypersecretion / etiology. Pituitary Neoplasms / complications. Pituitary Neoplasms / pathology

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(PMID = 17159252.001).

[ISSN] 1046-3976

[Journal-full-title] Endocrine pathology

[ISO-abbreviation] Endocr. Pathol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

   

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AREAS COVERED IN THIS REVIEW: The scope of this review is primarily focused upon recent insights in sst(5)-receptor physiology, novel sst(5)-targeted treatment options predominantly directed towards pituitary adenomas, and gastroenteropancreatic neuroendocrine tumours.

WHAT THE READER WILL GAIN: An understanding of the potential that novel sst(5)-targeted SRIF analogues might have in the medical treatment of Cushing's disease and acromegaly, as demonstrated by translational research, based on pathophysiological data combined with results from clinical trials.

Finally, absence of sst(5) in corticotroph adenomas could be related to tumour aggressiveness in Cushing's disease.

[MeSH-minor] Adenoma / drug therapy. Adenoma / physiopathology. Animals. Drug Design. Gastrointestinal Neoplasms / drug therapy. Gastrointestinal Neoplasms / physiopathology. Humans. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / physiopathology. Pituitary Neoplasms / drug therapy. Pituitary Neoplasms / physiopathology

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(PMID = 20151855.001).

[ISSN] 1744-7658

[Journal-full-title] Expert opinion on investigational drugs

[ISO-abbreviation] Expert Opin Investig Drugs

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] England

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

[Number-of-references] 101

   

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[Title] Expression of p16(INK4A) gene in human pituitary tumours.

Pituitary adenomas comprise 10-15% of primary intracranial tumours but the mechanisms leading to tumour development are yet to be clearly established.

The retinoblastoma pathway, which regulates the progression through the cell cycle, is often deregulated in different types of tumours.

We studied the cyclin-dependent kinase inhibitor p16(INK4A) gene expression at mRNA level in human pituitary adenomas.

Forty-six tumour specimens of different subtypes, 21 clinically non-functioning, 12 growth hormone-secreting, 6 prolactin-secreting, 6 adrenocorticotropin-secreting, and 1 thyrotropin-secreting tumours were studied.

All clinically non-functioning and most of the hormone-secreting tumours were macroadenomas (38/46).

The RT-PCR assay and electrophoresis of the PCR-products showed that p16(INK4A) mRNA was undetectable in: 62% of non-functioning, 8% of growth hormone-secreting, 17% of prolactin-secreting and 17% of adrenocorticotropin-secreting adenomas.

Within the non-functioning adenomas 63% were "null cell" and 37% were positive for some hormone, both subgroups showed similar percentage of cases with absence of p16(INK4A) mRNA.

Our results show that clinically non-functioning macroadenomas have impaired p16(INK4A) expression in a clearly higher proportion than any other pituitary tumour subtype investigated.

[MeSH-major] Adenoma / genetics. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Gene Expression Regulation, Neoplastic. Pituitary Neoplasms / genetics

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(PMID = 18058237.001).

[ISSN] 1573-7403

[Journal-full-title] Pituitary

[ISO-abbreviation] Pituitary

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / RNA, Messenger

   

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[Title] Clinicopathologic correlates of giant pituitary adenomas.

Giant adenomas comprise a clinical/therapeutic subset of pituitary adenomas that pose a surgical challenge.

The study population consisted of 28 patients who had giant pituitary adenomas, which are defined as tumors with a diameter greater than 5cm.

Clinically, five tumors (18%) were endocrinologically functional and 23 (82%) were not.

During surgery, one tumor was radically excised, four were subtotally excised, 12 were partially excised, and 11 were biopsied.

All of the tumors showed typical histological features of pituitary adenoma.

Of the 23 clinically non-functional adenomas, 18 were gonadotrophic tumors, four were null cell adenomas and one was a silent corticotroph adenoma.

The present study found giant adenomas to be invasive but slow growing, histologically benign and often gonadotrophic in subtype.

[MeSH-major] Adenoma / pathology. Adenoma / therapy. Pituitary Neoplasms / pathology. Pituitary Neoplasms / therapy

[MeSH-minor] Adolescent. Adrenocorticotropic Hormone / metabolism. Adult. Antigens, CD34 / metabolism. Female. Follow-Up Studies. Humans. Ki-67 Antigen / metabolism. Magnetic Resonance Imaging / methods. Male. Middle Aged. Neoplasm Invasiveness. Retrospective Studies. Treatment Outcome. Young Adult

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(PMID = 19285407.001).

[ISSN] 0967-5868

[Journal-full-title] Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia

[ISO-abbreviation] J Clin Neurosci

[Language] eng

[Publication-type] Clinical Trial; Journal Article

[Publication-country] Scotland

[Chemical-registry-number] 0 / Antigens, CD34; 0 / Ki-67 Antigen; 9002-60-2 / Adrenocorticotropic Hormone

   

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[Title] Pitfalls in the management of Cushing's disease.

Cushing's disease is caused by functional corticotroph adenomas of the pituitary gland, most commonly noninvasive microadenomas.

Transsphenoidal microsurgery is an effective means of control for patients with adrenocorticotrophic hormone-producing microadenomas.

The major causes of surgical failure in the treatment of Cushing's disease lies in inadequate preoperative evaluation, unsuccessful identification of the adenoma and inexperience of the surgeon.

For optimal results in this rare disease, endocrinological, radiological and surgical procedures should be co-ordinated in a specialized center.

[MeSH-major] Pituitary ACTH Hypersecretion / therapy. Treatment Failure

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(PMID = 17386367.001).

[ISSN] 0967-5868

[Journal-full-title] Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia

[ISO-abbreviation] J Clin Neurosci

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] Scotland

[Number-of-references] 82

   

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[Title] No effect of the PPAR-gamma agonist rosiglitazone on ACTH or cortisol secretion in Nelson's syndrome and Cushing's disease in vitro and in vivo.

OBJECTIVE: Surgical tumor resection remains the primary treatment strategy in ACTH-secreting pituitary adenomas, i.e.

Cushing's disease (CD) and Nelson's syndrome (NS).

However, an effective long-term pharmacological regime is not available in patients with persistent ACTH-hypersecretion.

The nuclear receptor peroxisome proliferator-activated receptor gamma (PPAR-gamma) is abundantly expressed in most pituitary adenomas.

First encouraging data reported that the PPAR-gamma ligand rosiglitazone antagonizes ACTH hypersecretion and exerts also antiproliferative effects in pituitary cell lines.

Herein, we studied the potential therapeutical effects of rosiglitazone in patients with ACTH-secreting pituitary adenomas in vitro and in vivo.

MATERIALS AND METHODS: Seven patients with persistent ACTH-hypersecretion (3 with NS, 4 with persistent CD) were treated 5 months with rosiglitazone (4 - 16 mg/day).

In vitro assays were performed in primary cell cultures obtained from eight additional patients with ACTH-secreting pituitary adenomas applying 80 microM rosiglitazone repeatedly over a time period of 14 days.

RESULTS: Our long-term clinical trial with the PPAR-gamma activator rosiglitazone showed no amelioration of clinical symptoms nor an inhibiting effect on ACTH-secretion in vivo.

In vitro, rosiglitazone treatment led to a statistically significant decrease of ACTH levels in 2 out of 8 primary cell cultures after 14 days compared to untreated controls.

CONCLUSION: In contrast to the initially promising laboratory data gathered in pituitary cell line experiments and nude mice models, our experimental data obtained in primary human ACTH-expressing pituitary adenoma cell cultures as well as our clinical experience with a long-term rosiglitazone trial in approved antidiabetic doses support the recently reported disappointing reports on acute or short-term medical treatment of ACTH-hypersecretion with PPAR-gamma activators.

[MeSH-major] Adrenocorticotropic Hormone / secretion. Hydrocortisone / secretion. Nelson Syndrome / blood. PPAR gamma / agonists. Pituitary ACTH Hypersecretion / blood. Thiazolidinediones / pharmacology

[MeSH-minor] Adenoma / pathology. Adenoma / secretion. Adult. Female. Humans. In Vitro Techniques. Magnetic Resonance Imaging. Male. Middle Aged. Pituitary Neoplasms / pathology. Pituitary Neoplasms / secretion. Treatment Outcome. Tumor Cells, Cultured

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(PMID = 19919817.001).

[ISSN] 0722-5091

[Journal-full-title] Clinical neuropathology

[ISO-abbreviation] Clin. Neuropathol.

[Language] eng

[Publication-type] Clinical Trial; Journal Article

[Publication-country] Germany

[Chemical-registry-number] 0 / PPAR gamma; 0 / Thiazolidinediones; 05V02F2KDG / rosiglitazone; 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone

   

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[Title] Immunohistochemical detection of dopamine D2 receptors in human pituitary adenomas.

Thirty one pituitary adenomas and 3 samples of peritumoral anterior pituitary tissue were immunostained with an antibody raised against dopamine D2 receptor protein.

The positive reactions were found in cell cytoplasm, a subpopulation of cell nuclei and the intratumoral blood vessels walls.

As expected, the positive immunostaining was shown in cytoplasm and/or cell nuclei of all examined prolactinomas (7/7).

In acromegaly the positive D2 staining occurred in 5/7 samples, in gonadotropinomas in 6/8 and in plurihormonal adenomas 2/4.

The lowest expression was observed in corticotropinomas (1/5).

Moreover, the presence of D2 receptors in intratumoral blood vessels walls constitutes the possibility of the anti-angiogenic action of D2 agonists in pituitary adenomas.

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(PMID = 21071344.001).

[ISSN] 1897-5631

[Journal-full-title] Folia histochemica et cytobiologica

[ISO-abbreviation] Folia Histochem. Cytobiol.

[Language] ENG

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

[Publication-country] Poland

[Chemical-registry-number] 0 / Receptors, Dopamine D2

   

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[Title] [Nelson's syndrome: course of aggressive pituitary corticotroph adenoma].

[Transliterated title] Syndrome de Nelson: évolution d'un adénome hypophysaire corticotrope agressif.

Nelson's syndrome was defined in 1958 as the association of an expanding pituitary tumor with high ACTH secretion after bilateral adrenalectomy for Cushing's disease.

Pituitary MRI and ACTH measurements led to the definition of Nelson's syndrome as the proliferation of a corticotrophic microadenoma or an aggressive and highly proliferative tumor residue induced by the decreased glucocorticoid inhibition after bilateral adrenalectomy.

Now, the problem is not the definition of Nelson's syndrome but rather the identification of markers predictive of tumor growth.

Based on a typical case and a review of the literature, we point out some predictive markers of tumor growth after bilateral adrenalectomy: young age at diagnosis, presence of tumor residue on pituitary MRI before adrenalectomy, markers of tumor aggressiveness (Ki-67>3%, mitoses, nuclear PTTG) and increase of ACTH levels during the first months following adrenalectomy.

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

[MeSH-minor] Adrenocorticotropic Hormone / analysis. Adrenocorticotropic Hormone / secretion. Adult. Female. Humans. Magnetic Resonance Imaging. Pituitary Gland / pathology

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(PMID = 17306208.001).

[ISSN] 0003-4266

[Journal-full-title] Annales d'endocrinologie

[ISO-abbreviation] Ann. Endocrinol. (Paris)

[Language] fre

[Publication-type] Case Reports; English Abstract; Journal Article

[Publication-country] France

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

   

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[Title] Magmas, a gene newly identified as overexpressed in human and mouse ACTH-secreting pituitary adenomas, protects pituitary cells from apoptotic stimuli.

Pituitary tumors are mostly benign, being locally invasive in 5-35% of cases.

Deregulation of several genes has been suggested as a possible alteration underlying the development and progression of pituitary tumors.

We here report the identification of a cDNA, corresponding to Magmas gene (mitochondria-associated protein involved in granulocyte-macrophage colony-stimulating factor signal transduction), which is highly expressed in two different ACTH-secreting mouse pituitary adenoma cell lines as compared with normal pituitary as well as in two thirds of 64 examined pituitary adenomas as compared with human normal pituitary.

Tim 16, the mitochondrial protein encoded by Magmas, was indeed expressed in a mouse ACTH-secreting pituitary adenoma cell line, AtT-20 D16v-F2 cells, in a subcellular compartment likely corresponding to mitochondria.

Our data demonstrate that Magmas is overexpressed in mouse and human ACTH-secreting pituitary adenomas.

Moreover, our results show that Magmas protects pituitary cells from apoptosis, suggesting its possible involvement in neoplastic transformation.

[MeSH-major] ACTH-Secreting Pituitary Adenoma / genetics. Adenoma / genetics. Apoptosis / genetics. Mitochondrial Proteins / physiology

[MeSH-minor] Animals. Cell Proliferation. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / pathology. Cells, Cultured. Cytoprotection / drug effects. Cytoprotection / genetics. Gene Expression Regulation, Neoplastic / drug effects. Humans. Mice. Pituitary Gland / metabolism. RNA, Small Interfering / pharmacology. Up-Regulation / drug effects

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(PMID = 20719856.001).

[ISSN] 1945-7170

[Journal-full-title] Endocrinology

[ISO-abbreviation] Endocrinology

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Mitochondrial Proteins; 0 / RNA, Small Interfering; 0 / magmas protein, human

   

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[Title] Magnetic resonance imaging characteristics and surgical results of adrenocorticotropin-secreting pituitary adenomas.

OBJECTIVE: To evaluate magnetic resonance imaging (MRI) characteristics and surgical results of adrenocorticotropin (ACTH)-secreting pituitary adenomas.

METHODS: MRI characteristics and relationship between MRI positive rate and surgical results of 266 patients with pathologically confirmed Cushing's disease were analyzed retrospectively.

All patients underwent thin-section sagittal and coronal scans of the pituitary gland before and after administration of gadolinium-diethylene triamine pentaacetic acid (Gd-DTPA) on a 1.5 Tesla MRI scanner, and dynamic enhanced MRI was performed in 39 patients.

RESULTS: Preoperative MRI revealed normal results in 41 (15.4%) cases, microadenoma in 179 (67.3%), macroadenoma in 42 (15.8%), and huge adenoma in 4 (1.5%).

Pituitary apoplexy was found in 13 (4.9%) cases.

Positive rate of ACTH-secreting adenomas was 84.6% (225/266) on MRI scans, and that of small microadenomas was 87.2% (34/39) on dynamic enhanced MRI scans.

Preoperative endocrinological tests of 199 cases supported the diagnosis of typical Cushing's disease, while the other 67 cases had atypical endocrinological results.

CONCLUSIONS: Enhanced coronal pituitary MRI is helpful for preoperative localization of ACTH-secreting pituitary microadenoma.

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(PMID = 18437910.001).

[ISSN] 1001-9294

[Journal-full-title] Chinese medical sciences journal = Chung-kuo i hsueh k'o hsueh tsa chih

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

[Language] ENG

[Publication-type] Journal Article

[Publication-country] China

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

   

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[Title] Loss of neuronatin expression is associated with promoter hypermethylation in pituitary adenoma.

The imprinted gene, neuronatin (NNAT), is one of the most abundant transcripts in the pituitary and is thought to be involved in the development and maturation of this gland.

In a recent whole-genome approach, exploiting a pituitary tumour cell line, we identified hypermethylation associated loss of NNAT.

In this report, we determined the expression pattern of NNAT in individual cell types of the normal gland and within each of the different pituitary adenoma subtypes.

Immunohistochemical (IHC) co-localization studies of normal pituitaries showed that each of the hormone secreting cells (GH, PRL, ACTH, FSH and TSH) expressed NNAT.

However, 33 out of 47 adenomas comprising, 11 somatotrophinomas, 10 prolactinomas, 12 corticotrophinomas and 14 non-functioning tumours, irrespective of subtype failed to express either NNAT transcript or protein as determined by quantitative real-time RT-PCR and IHC respectively.

In normal pituitaries and adenomas that expressed NNAT the promoter-associated CpG island showed characteristics of an imprinted gene where approximately 50% of molecules were densely methylated.

However, in the majority of adenomas that showed loss or significantly reduced expression of NNAT, relative to normal pituitaries, the gene-associated CpG island showed significantly increased methylation.

Collectively, these findings point to an important role for NNAT in the pituitary and perhaps tumour development in this gland.

[MeSH-major] DNA Methylation. Membrane Proteins / genetics. Nerve Tissue Proteins / genetics. Pituitary Gland / pathology. Pituitary Neoplasms / genetics. Promoter Regions, Genetic / genetics

[MeSH-minor] Animals. CpG Islands. Gene Silencing. Humans. Immunoenzyme Techniques. Loss of Heterozygosity. Mice. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured

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(PMID = 19218280.001).

[ISSN] 1351-0088

[Journal-full-title] Endocrine-related cancer

[ISO-abbreviation] Endocr. Relat. Cancer

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / Membrane Proteins; 0 / NNAT protein, human; 0 / Nerve Tissue Proteins; 0 / RNA, Messenger

   

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[Title] Differential gene expression in ACTH -secreting and non-functioning pituitary tumors.

OBJECTIVE: Differential expression of several genes between ACTH-secreting pituitary tumors causing Cushing' disease (CD), silent corticotroph adenoma (SCA), and non-functioning pituitary tumors (NFT) was investigated.

DESIGN AND METHODS: We used tissue specimens from 35 pituitary tumors (12 CD, 8 SCA, and 15 NFT).

Steady-state mRNA levels of the genes related to proopiomelanocortin (POMC) transcription, synthesis, processing, and secretion, such as neurogenic differentiation 1 (NeuroD1), T-box 19 (Tpit), corticotropin releasing hormone receptor (CRHR), vasopressin receptor 1b (V1bR), prohormone convertase (PC) 1/3 and PC2, 11beta-hydroxysteroid dehydrogenase (11beta-HSD) type 1 and type 2, glucocorticoid receptor alpha (GRalpha), annexin A1, histone deacetylase 2 (HDAC2), and BRM/SWI2-related gene 1, were determined by real-time RT-PCR.

In conclusion, our study demonstrated that the genes related to transcription, synthesis, processing, and secretion of POMC are differentially regulated in ACTH-secreting pituitary tumors causing CD and SCA compared with those in NFT.

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(PMID = 18057378.001).

[ISSN] 1479-683X

[Journal-full-title] European journal of endocrinology

[ISO-abbreviation] Eur. J. Endocrinol.

[Language] ENG

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

[Publication-country] England

[Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / CRF receptor type 1; 0 / Homeodomain Proteins; 0 / NEUROD1 protein, human; 0 / RNA, Messenger; 0 / Receptors, Corticotropin-Releasing Hormone; 0 / Receptors, Glucocorticoid; 0 / Receptors, Vasopressin; 0 / T-Box Domain Proteins; 0 / TBX19 protein, human; 0 / glucocorticoid receptor alpha; 66796-54-1 / Pro-Opiomelanocortin; 9002-60-2 / Adrenocorticotropic Hormone; EC 1.1.1.146 / 11-beta-Hydroxysteroid Dehydrogenases; EC 3.4.21.94 / Proprotein Convertase 2

   

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[Title] Repeated transsphenoidal pituitary surgery (TS) via the endoscopic technique: a good therapeutic option for recurrent or persistent Cushing's disease (CD).

BACKGROUND: No data on results of repeated transsphenoidal surgery via the endoscopic technique for patients with persistent or recurrent Cushing's disease are available.

DESIGN AND PATIENTS: We retrospectively evaluated the remission rates and complications of repeated transsphenoidal surgery via the endoscopic technique in 14 patients with persistent (N = 6) or recurrent (N = 8) Cushing's disease treated in our centre between 1999 and 2007.

The success of repeated transsphenoidal surgery could not be predicted by visualization of an adenoma on MRI before first or second surgery, histopathological confirmation of an ACTH secreting adenoma after first or second surgery, treatment with cortisol lowering agents before first or second surgery, the operation technique used during the first surgery, persistent vs. recurrent disease after the first surgery, age, gender and interval between the two surgeries.

CONCLUSION: Repeated transsphenoidal surgery via the endoscopic technique is a good treatment option for selected patients with recurrent or persistent Cushing's disease following primary pituitary surgery.

[MeSH-major] Endoscopy / methods. Neurosurgical Procedures / methods. Pituitary ACTH Hypersecretion / surgery. Pituitary Gland / surgery

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(PMID = 18616702.001).

[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] WI4X0X7BPJ / Hydrocortisone

   

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[Title] Detection of adrenocorticotropin-secreting pituitary adenomas by magnetic resonance imaging in children and adolescents with cushing disease.

CONTEXT: We recently showed that pre- and postcontrast spoiled gradient-recalled acquisition in the steady-state (SPGR) was superior to conventional pre- and postcontrast T-1 weighted spin echo (SE) acquisition magnetic resonance imaging (MRI) for the diagnostic evaluation of pituitary tumors in adult patients.

OBJECTIVE: The present investigation assessed the use of SPGR vs. SE-MRI in the diagnostic evaluation of ACTH-secreting tumors in children and adolescents with Cushing disease.

PATIENTS: Thirty children with Cushing disease (13 females and 17 males with a mean age of 12 +/- 3 yr) were studied.

Postcontrast SPGR-MRI identified the location of the tumor in 18 of 28 patients, whereas postcontrast SE-MRI identified the location and accurately estimated the size of the tumor in only five patients (P < 0.001).

CONCLUSIONS: We conclude that conventional MRI, even with contrast enhancement, mostly failed to identify ACTH-secreting microadenomas in children and adolescents with Cushing disease.

Postcontrast SPGR-MRI was superior to SE-MRI and should be used in addition to conventional SE-MRI in the pituitary evaluation of children and adolescents with suspected Cushing disease.

[MeSH-major] Adenoma / diagnosis. Adenoma / secretion. Adrenocorticotropic Hormone / secretion. Cushing Syndrome / diagnosis. Magnetic Resonance Imaging. Pituitary Neoplasms / diagnosis. Pituitary Neoplasms / secretion

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(PMID = 15941871.001).

[ISSN] 0021-972X

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

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

[Language] eng

[Publication-type] Evaluation Studies; Journal Article

[Publication-country] United States

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

   

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[Title] P53 gene mutation in an atypical corticotroph adenoma with Cushing's disease.

[MeSH-major] ACTH-Secreting Pituitary Adenoma / complications. ACTH-Secreting Pituitary Adenoma / genetics. Adenoma / genetics. Mutation / genetics. Pituitary ACTH Hypersecretion / etiology. Pituitary Neoplasms / genetics. Tumor Suppressor Protein p53 / genetics

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(PMID = 18771563.001).

[ISSN] 1365-2265

[Journal-full-title] Clinical endocrinology

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

[Language] eng

[Publication-type] Case Reports; Letter

[Publication-country] England

[Chemical-registry-number] 0 / Tumor Suppressor Protein p53

   

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CONTEXT: Hypertension (HTN) has been reported in up to 60% of children with Cushing syndrome (CS), but its course, side effects, and potential differences among various causes of CS have not been adequately studied.

DESIGN: Data from 86 children with corticotropinomas [Cushing disease (CD)] and 27 children with ACTH-independent CS (AICS) were analyzed.

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(PMID = 19293264.001).

[ISSN] 1945-7197

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

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

[Language] ENG

[Grant] United States / NICHD NIH HHS / HD / Z01 HD000642; United States / Intramural NIH HHS / /

[Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, N.I.H., Intramural

[Publication-country] United States

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

[Other-IDs] NLM/ PMC2690429

   

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[Title] [Corticotroph adenoma].

[Transliterated title] Adénome corticotrope.

Corticotroph adenomas cause ACTH oversecretion responsible for Cushing's disease.

This represents the most frequent cause of Cushing's syndrome, or chronic excess of endogenous glucocorticoids.

Ninety percent of corticotroph adenomas are microadenomas, sometime not visible on MRI.

Corticotroph macroadenomas are rare, but can be responsible for an aggressive tumor.

Cushing's disease diagnosis requires careful hormonal and imaging investigations, aiming first at the diagnosis of Cushing's syndrome and in a second step at the diagnosis of its pituitary origin.

The treatment of corticotroph adenoma is mainly based on pituitary surgery.

In case of failure of pituitary surgery, or in patients in whom surgery is not appropriate as a first line treatment, medical therapy (mainly anticortisolic drugs), pituitary radiotherapy or surgical bilateral adrenalectomy can be discussed.

[MeSH-major] ACTH-Secreting Pituitary Adenoma / complications. Pituitary ACTH Hypersecretion / etiology. Pituitary Neoplasms / complications

[MeSH-minor] Adrenalectomy. Adrenocorticotropic Hormone / analysis. Chemotherapy, Adjuvant. Corticotropin-Releasing Hormone / analysis. Cushing Syndrome / diagnosis. Cushing Syndrome / etiology. Cushing Syndrome / therapy. Diagnosis, Differential. Humans. Hydrocortisone / analysis. Hydrocortisone / antagonists & inhibitors. Magnetic Resonance Imaging. Neoadjuvant Therapy. Radiotherapy, Adjuvant

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(PMID = 19041214.001).

[ISSN] 2213-0276

[Journal-full-title] Presse medicale (Paris, France : 1983)

[ISO-abbreviation] Presse Med

[Language] fre

[Publication-type] English Abstract; Journal Article

[Publication-country] France

[Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone; 9015-71-8 / Corticotropin-Releasing Hormone; WI4X0X7BPJ / Hydrocortisone

   

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[Title] Defective expression of prohormone convertase 1/3 in silent corticotroph adenoma.

Silent corticotroph adenoma (SCA) is defined as an ACTH-producing pituitary tumor not associated with clinical and endocrine feartures of Cushing's syndrome, but its underlying molecular mechanism(s) remains unknown thus far.

We tested the hypothesis that reduced expression of prohormone convertase (PC) 1/3 responsible for proteolytic processing of proopiomelanocortin (POMC) in SCA may lead to production of unprocessed, biologically inactive POMC and/or precursor of ACTH.

Among 30 non-functioning pituitary macroadenomas (NFA) examined, we found 6 SCAs by immunohistochemical study using anti-ACTH antibody.

Preoperative endocrine and diagnostic image tests did not reveal any differences between SCA and the remaining NFA except for the higher recurrence rate of SCA.

Our data suggest that defective PC1/3 expression may lead to preferential production of unprocessed, biologically inactive ACTH variants in SCA.

[MeSH-major] ACTH-Secreting Pituitary Adenoma / genetics. Adenoma / genetics. Proprotein Convertase 1 / genetics

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(PMID = 17917309.001).

[ISSN] 1348-4540

[Journal-full-title] Endocrine journal

[ISO-abbreviation] Endocr. J.

[Language] eng

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

[Publication-country] Japan

[Chemical-registry-number] 0 / Protein Isoforms; 66796-54-1 / Pro-Opiomelanocortin; 9002-60-2 / Adrenocorticotropic Hormone; EC 3.4.21.93 / Proprotein Convertase 1

   

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[Title] Bone morphogenetic protein-4 control of pituitary pathophysiology.

Bone morphogenetic protein-4 (BMP-4), a member of the transforming growth factor-Beta(TGF-Beta) family, is overexpressed in different prolactinoma models and induces the development of these lineage adenomas.

SMAD proteins activated by growth factors of the TGF-Beta and BMP family interact with estrogen receptors to stimulate the proliferation of prolactin and growth hormone-secreting cells.

Furthermore, BMP-4 presents differential expression in normal and adenomatous corticotropes and inhibitory action on corticotropinoma cell proliferation.

The present review highlights not only the crucial and opposite role of BMP-4 in the progression of pituitary adenomas but also that BMP-4 and retinoic acid interaction might serve as a potential new mechanism target for therapeutic approaches for Cushing disease.

[MeSH-major] Bone Morphogenetic Proteins / physiology. Pituitary Diseases / etiology

[MeSH-minor] Adrenocorticotropic Hormone / secretion. Animals. Bone Morphogenetic Protein 4. Gene Expression. Humans. Models, Biological. Neurons / secretion. Pituitary Gland / cytology. Pituitary Gland / growth & development. Pituitary Gland / metabolism. Pituitary Gland / secretion. Receptors, Transforming Growth Factor beta / metabolism. Transforming Growth Factor beta / physiology. Tretinoin / pharmacology

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(PMID = 16809920.001).

[ISSN] 0301-3073

[Journal-full-title] Frontiers of hormone research

[ISO-abbreviation] Front Horm Res

[Language] eng

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

[Publication-country] Switzerland

[Chemical-registry-number] 0 / BMP4 protein, human; 0 / Bone Morphogenetic Protein 4; 0 / Bone Morphogenetic Proteins; 0 / Receptors, Transforming Growth Factor beta; 0 / Transforming Growth Factor beta; 5688UTC01R / Tretinoin; 9002-60-2 / Adrenocorticotropic Hormone

[Number-of-references] 42

   

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[Title] A comparative study by age and gender of the pituitary adenoma and ACTH and alpha-MSH secretion in dogs with pituitary-dependent hyperadrenocorticism.

Pituitary-dependent hyperadrenocorticism (PDH) is frequent in dogs.

Using magnetic resonance, pituitary tumours were intra-sellar (IS) in 30.8% and extra-sellar (ES) in 62.6% and the pars intermedia (PI) was affected in 6.5%.

ACTH concentration was greater in the ES vs. IS (p<0.05).

alpha-MSH did not present significant differences according to tumour size, showing a negative correlation (r=-0.47; p<0.01) vs. ACTH.

Differences in adenoma size according to gender and their age-related frequency of apparition could be because of different origins of the corticotrophinoma.

[MeSH-major] ACTH-Secreting Pituitary Adenoma / veterinary. Adrenocortical Hyperfunction / veterinary. Adrenocorticotropic Hormone / secretion. Dog Diseases / pathology. Pituitary Neoplasms / veterinary. alpha-MSH / secretion

[MeSH-minor] Age Factors. Animals. Dogs. Female. Magnetic Resonance Imaging. Male. Pituitary Gland / pathology. Pituitary Gland / physiopathology. Pituitary Gland / secretion. Retrospective Studies. Sex Factors

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[Copyright] Copyright 2009 Elsevier Ltd. All rights reserved.

(PMID = 19683322.001).

[ISSN] 1532-2661

[Journal-full-title] Research in veterinary science

[ISO-abbreviation] Res. Vet. Sci.

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 581-05-5 / alpha-MSH; 9002-60-2 / Adrenocorticotropic Hormone

   

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[Title] Potential of retinoic acid derivatives for the treatment of corticotroph pituitary adenomas.

Cushing's disease is a severe clinical condition caused by hypersecretion of corticosteroids due to excessive ACTH secretion from a pituitary adenoma.

This complex endocrine disorder still represents a major challenge for the physician in terms of efficient treatment.

In the last years there was only little progress in elucidating the molecular mechanisms responsible for the constitutive and autonomous ACTH secretion of pituitary corticotrophinomas.

As a consequence, no effective drug therapy is currently available, particularly if surgical excision is not successful.

In the present article we examine recent studies that have investigated the therapeutic potential of retinoic acid receptors as nuclear receptor targets for the treatment of Cushing's disease.

Retinoic acid is an efficient drug used for the treatment of different types of cancers and it proved to act in animal models of Cushing's disease.

The efficiency of this treatment in patients with this disorder still needs to be tested in clinical trials.

[MeSH-major] ACTH-Secreting Pituitary Adenoma / drug therapy. Antineoplastic Agents / therapeutic use. Pituitary Neoplasms / drug therapy. Tretinoin / therapeutic use

[MeSH-minor] Animals. Humans. Pituitary ACTH Hypersecretion / drug therapy. Pituitary ACTH Hypersecretion / metabolism

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(PMID = 18604646.001).

[ISSN] 1573-2606

[Journal-full-title] Reviews in endocrine & metabolic disorders

[ISO-abbreviation] Rev Endocr Metab Disord

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] Germany

[Chemical-registry-number] 0 / Antineoplastic Agents; 5688UTC01R / Tretinoin

[Number-of-references] 62

   

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[Title] Galectin-3 as a marker distinguishing functioning from silent corticotroph adenomas.

OBJECTIVE: Galectin-3 (Gal-3) belongs to the family of carbohydrate-binding proteins with high affinity for galactoside and is involved in many biological processes including cell growth and differentiation, cell adhesion, tumor progression, apoptosis and metastasis.

The aim of this study was to disclose differences in the expression of Gal-3 in silent and functioning corticotroph pituitary adenomas.

DESIGN: We examined 30 pituitary adenomas (19 functioning corticotroph, 11 silent corticotroph adenomas).

Two prolactinomas and 2 functioning somatotroph adenomas served as positive controls.

The independent variables t-test was used for comparison of the mean expression of Gal-3 in the two different corticotroph adenoma subgroups.

RESULTS: Eighteen of the functioning corticotroph adenomas (94.73%) were positive for Gal-3 with a cytoplasmic and focally membranous distribution; two cases also exhibited nuclear expression, whereas 9 of the silent corticotroph adenomas (81.81%) had zero or<1% expression of Gal-3 (p=0.001).

CONCLUSIONS: Gal-3 is highly expressed in functioning corticotroph adenomas of the pituitary gland, while silent adenomas exhibit very focal to null expression of Gal-3.

This observation can be used in the pathological diagnosis to separate functioning from silent corticotroph adenomas of the pituitary.

[MeSH-major] ACTH-Secreting Pituitary Adenoma / diagnosis. Adenoma / diagnosis. Biomarkers, Tumor / metabolism. Galectin 3 / metabolism

[MeSH-minor] Humans. Immunohistochemistry. Pituitary Gland / metabolism

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(PMID = 17724007.001).

[ISSN] 1109-3099

[Journal-full-title] Hormones (Athens, Greece)

[ISO-abbreviation] Hormones (Athens)

[Language] eng

[Publication-type] Journal Article

[Publication-country] Greece

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Galectin 3

   

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Nelson's syndrome is a potentially life-threatening condition that does not infrequently develop following total bilateral adrenalectomy (TBA) for the treatment of Cushing's disease.

In this review article, we discuss some controversial aspects of Nelson's syndrome including diagnosis, predictive factors, aetiology, pathology and management based on data from the existing literature and the experience of our own tertiary centre.

We propose that Nelson's syndrome should be diagnosed in any patient with prior TBA for the treatment of Cushing's disease and with at least one of the following criteria: i) an expanding pituitary mass lesion compared with pre-TBA images;.

ii) an elevated 0800 h plasma level of ACTH (>500 ng/l) in addition to progressive elevations of ACTH (a rise of >30%) on at least three consecutive occasions.

Regarding predictive factors for the development of Nelson's syndrome post TBA, current evidence favours the presence of residual pituitary tumour on magnetic resonance imaging (MRI) post transsphenoidal surgery (TSS); an aggressive subtype of corticotrophinoma (based on MRI growth rapidity and histology of TSS samples); lack of prophylactic neoadjuvant pituitary radiotherapy at the time of TBA and a rapid rise of ACTH levels in year 1 post TBA.

Finally, more studies are needed to assess the efficacy of therapeutic strategies in Nelson's syndrome, including the alkylating agent, temozolomide, which holds promise as a novel and effective therapeutic agent in the treatment of associated aggressive corticotroph tumours.

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(PMID = 20668020.001).

[ISSN] 1479-683X

[Journal-full-title] European journal of endocrinology

[ISO-abbreviation] Eur. J. Endocrinol.

[Language] ENG

[Publication-type] Journal Article; Review

[Publication-country] England

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

[Number-of-references] 101

   

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[Title] Nelson syndrome: comprehensive review of pathophysiology, diagnosis, and management.

Nelson syndrome (NS) is a rare clinical manifestation of an enlarging pituitary adenoma that can occur following bilateral adrenal gland removal performed for the treatment of Cushing disease.

It is characterized by excess adreno-corticotropin secretion and hyperpigmentation of the skin and mucus membranes.

The authors present a comprehensive review of the pathophysiology, diagnosis, and management of NS.

Corticotroph adenomas in NS remain challenging tumors that can lead to significant rates of morbidity and mortality.

Although the primary treatment for each tumor type may vary, it is important to consider all of the available options and select the one that is most appropriate for the individual case, particularly in cases of lesions resistant to intervention.

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(PMID = 17961028.001).

[ISSN] 1092-0684

[Journal-full-title] Neurosurgical focus

[ISO-abbreviation] Neurosurg Focus

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Neurotransmitter Agents

[Number-of-references] 123

   

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[Title] Cushing's syndrome due to a pituitary corticotropinoma in a child with tuberous sclerosis: an association or a coincidence?

[MeSH-major] ACTH-Secreting Pituitary Adenoma / complications. Cushing Syndrome / etiology. Pituitary Neoplasms / complications. Tuberous Sclerosis / complications

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(PMID = 17596199.001).

[ISSN] 0300-0664

[Journal-full-title] Clinical endocrinology

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

[Language] eng

[Grant] United States / NICHD NIH HHS / HD / Z01-HD-000642-04; United States / Intramural NIH HHS / /

[Publication-type] Case Reports; Letter; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural

[Publication-country] England

   

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[Title] Somatostatin and dopamine-somatostatin multiple ligands directed towards somatostatin and dopamine receptors in pituitary adenomas.

AIM: We report the comparative efficacy of octreotide, cabergoline and multiple ligands directed towards the different somatostatin subtypes (ssts), such as BIM-23A779 and SOM-230, and of chimeric analogs which bind both somatostatin and the dopamine D2 receptors (D2R), such as BIM-23A760 and BIM-23A781, in cell cultures from human growth hormone (GH)-secreting pituitary adenomas.

PROCEDURES: RT-PCR analysis of the quantitative expression of the different ssts and D2R mRNAs was performed on tumor fragments of 22 GH-secreting adenomas collected after surgery.

Pharmacological studies, using the different ligands, were performed on cell cultures of such tumors.

In each tumor tested, 3 patterns of response, in terms of GH suppression, were observed.

Among the compounds tested, the most potent inhibitors of GH secretion were the sst2, sst5, D2R chimeric compound BIM-23A760, followed by the sst universal ligand SOM-230.

The effect of multiple receptor activation on the functions of other pituitary tumor types, such as prolactinomas and corticotropinomas, is not presently analyzed, and the efficacy of multireceptor ligands remains to be elucidated.

[MeSH-major] Adenoma / drug therapy. Antineoplastic Agents, Hormonal / therapeutic use. Dopamine / analogs & derivatives. Pituitary Neoplasms / drug therapy. Somatostatin / analogs & derivatives

[MeSH-minor] Adult. Drug Screening Assays, Antitumor. Ergolines / therapeutic use. Female. Human Growth Hormone / drug effects. Human Growth Hormone / metabolism. Humans. Ligands. Male. Octreotide / therapeutic use. RNA, Messenger / analysis. Receptors, Dopamine D2 / drug effects. Receptors, Dopamine D2 / genetics. Receptors, Dopamine D2 / metabolism. Receptors, Somatostatin / classification. Receptors, Somatostatin / drug effects. Receptors, Somatostatin / genetics. Receptors, Somatostatin / metabolism. Recombinant Fusion Proteins / therapeutic use. Tumor Cells, Cultured

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(PMID = 17047391.001).

[ISSN] 0028-3835

[Journal-full-title] Neuroendocrinology

[ISO-abbreviation] Neuroendocrinology

[Language] eng

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

[Publication-country] Switzerland

[Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / BIM 23268; 0 / Ergolines; 0 / Ligands; 0 / RNA, Messenger; 0 / Receptors, Dopamine D2; 0 / Receptors, Somatostatin; 0 / Recombinant Fusion Proteins; 12629-01-5 / Human Growth Hormone; 51110-01-1 / Somatostatin; LL60K9J05T / cabergoline; RWM8CCW8GP / Octreotide; VTD58H1Z2X / Dopamine

   

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[Title] Pituitary-hormone secretion by thyrotropinomas.

Hormone secretion by somatotropinomas, corticotropinomas and prolactinomas exhibits increased pulse frequency, basal and pulsatile secretion, accompanied by greater disorderliness.

Regulation of non-TSH pituitary hormones in this context is not well understood.

Cross-ApEn synchrony between TSH and GH did not differ between patients and controls, but TSH and PRL synchrony was reduced in patients.

We conclude that TSH secretion by thyrotropinomas shares many characteristics of other pituitary hormone-secreting adenomas.

In addition, abnormalities in GH and PRL secretion exist ranging from decreased (joint) regularity to overt hypersecretion, although not always clinically obvious, suggesting tumoral transformation of thyrotrope lineage cells.

[MeSH-major] Adenoma / physiopathology. Pituitary Hormones / blood. Pituitary Hormones / secretion. Pituitary Neoplasms / blood

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(PMID = 19051037.001).

[ISSN] 1573-7403

[Journal-full-title] Pituitary

[ISO-abbreviation] Pituitary

[Language] eng

[Grant] United States / NCRR NIH HHS / RR / M01 RR000585

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Pituitary Hormones; 67763-96-6 / Insulin-Like Growth Factor I; 9002-62-4 / Prolactin; 9002-71-5 / Thyrotropin; 9002-72-6 / Growth Hormone

[Other-IDs] NLM/ PMC2712623

   

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[Title] Cushing's disease in dogs: cabergoline treatment.

The treatment of pituitary-dependent hyperadrenocorticism (PDH) in dogs has for a long time been focused on inhibiting the adrenal gland using drugs such as o-p'-DDD, Ketoconazole and Trilostane, without attacking the primary cause: the corticotrophinoma.

Corticotroph cells can express the D2 dopaminergic receptor; therefore cabergoline (Cbg) could be effective as a treatment.

A year after the treatment, there was a significant decrease in ACTH (p<0.0001), alpha-MSH (p<0.01), urinary cortisol/creatinine ratio (p<0.001), and of the tumor size (p<0.0001) evaluated by nuclear magnetic resonance.

[MeSH-major] Dog Diseases / drug therapy. Dopamine Agonists / therapeutic use. Ergolines / therapeutic use. Pituitary ACTH Hypersecretion / veterinary

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(PMID = 17910968.001).

[ISSN] 0034-5288

[Journal-full-title] Research in veterinary science

[ISO-abbreviation] Res. Vet. Sci.

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / Dopamine Agonists; 0 / Ergolines; 581-05-5 / alpha-MSH; 9002-60-2 / Adrenocorticotropic Hormone; LL60K9J05T / cabergoline; R9400W927I / Ketoconazole

   

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[Title] Management of ACTH-secreting supradiaphragmatic adenomas.

Supradiaphragmatic adrenocorticotropic hormone (ACTH) secreting pituitary adenomas are exceptionally encountered (14 cases previously described) and raise issues concerning their nosology and management.

To illustrate this issue, we presented two cases of supradiaphragmatic ACTH secreting pituitary adenomas successfully excised via a subfrontal approach.

Both patients were female (20 and 41 years) and had a typical Cushing's syndrome.

MRI revealed, in both cases, a suprasellar mass in contact with the pars tuberalis of the pituitary.

One year later, the patient was operated on again via a subfrontal approach, allowing excision of a supradiaphragmatic adenoma and a complete cure of Cushing's disease.

In both cases, the diaphragma sellae was found to be intact and the pituitary stalk could be preserved.

Postoperative MRI demonstrated a clearly visible intact pituitary stalk in conjunction with normal aspect of the pituitary.

Supradiaphragmatic pituitary adenomas are most likely adenomas of the pituitary stalk with extra-axial development.

[MeSH-major] ACTH-Secreting Pituitary Adenoma / pathology. ACTH-Secreting Pituitary Adenoma / surgery. Adenoma / pathology. Adenoma / surgery

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(PMID = 17532556.001).

[ISSN] 0303-8467

[Journal-full-title] Clinical neurology and neurosurgery

[ISO-abbreviation] Clin Neurol Neurosurg

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Netherlands

   

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[Title] Influence of the fibroblast growth factor receptor 4 expression and the G388R functional polymorphism on Cushing's disease outcome.

CONTEXT: Abnormal FGFR4 expression has been detected in pituitary tumors, especially in larger and invasive adenomas.

Then, we hypothesized that FGFR4 expression and genotype could be markers of adverse outcome of Cushing's disease after transsphenoidal surgery.

OBJECTIVES: The objective was to investigate whether there is an association between the postoperative outcome of Cushing's disease (remission/recurrence) and the FGFR4 G388R genotype or the FGFR4 expression in corticotrophinomas.

FGFR4 expression was assessed by real-time PCR in 18 corticotrophinomas.

MAIN OUTCOME MEASURES: The outcome measures included the FGFR4 G388R genotype and FGFR4 expression in postoperative remission and recurrence of Cushing's disease.

RESULTS: Homozygosis for FGFR4 glycine (Gly(388)) allele was associated with reduced disease-free survival, in the univariate analysis (hazard ratio of 6.91; 95% confidence interval of 1.14-11.26; P = 0.028).

Male gender (P = 0.036), lack of pathology confirmation (P = 0.009), and cortisol levels more than 2 μg/dl in the early postoperative period (P < 0.001) were also significant predictors of Cushing's disease recurrence in the univariate analysis.

FGFR4 overexpression was found in 44% of the corticotrophinomas, and it was associated with lower postoperative remission rate (P = 0.009).

CONCLUSIONS: Our data suggest that homozygosis for FGFR4 Gly(388) allele and FGFR4 overexpression are associated with higher frequency of postoperative recurrence and persistence of Cushing's disease, respectively.

[MeSH-major] Pituitary ACTH Hypersecretion / genetics. Polymorphism, Single Nucleotide. Receptor, Fibroblast Growth Factor, Type 4 / genetics

[MeSH-minor] ACTH-Secreting Pituitary Adenoma / diagnosis. ACTH-Secreting Pituitary Adenoma / genetics. ACTH-Secreting Pituitary Adenoma / surgery. Adolescent. Adult. Amino Acid Substitution / genetics. Arginine / genetics. Child. Female. Gene Expression / physiology. Glycine / genetics. Humans. Hypophysectomy. Male. Middle Aged. Pituitary Neoplasms / diagnosis. Pituitary Neoplasms / genetics. Pituitary Neoplasms / surgery. Prognosis. Recurrence. Retrospective Studies. Treatment Outcome. Young Adult

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(PMID = 20660043.001).

[ISSN] 1945-7197

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

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

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 94ZLA3W45F / Arginine; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 4; TE7660XO1C / Glycine

   

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OBJECTIVES: To review the clinical data of a group of patients with pancreatic neuroendocrine tumors (pNETs) and to investigate the role of surgery in the treatment for pNETs by analyzing clinical manifestations and postoperative course of this rare disease.

Patients' data related to demographics and characteristics, diagnostic studies, surgical and tumor characteristics and survival were retrospectively reviewed.

RESULTS: Forty-six patients (41.1%) had a well-differentiated neuroendocrine tumor (WDT), 44 (48.2%) a well-differentiated neuroendocrine carcinoma (WD-Ca) and 12 (10.7%) a poorly differentiated neuroendocrine carcinoma (PD-Ca).

Nonfunctional tumors were seen in 65 (58.0%) patients, whereas functional tumors were found in 47 (42.0%) patients, including 26 insulinomas, 17 gastrinomas, 2 VIPomas, 1 glucagonoma, and 1 ACTHoma.

Survival was significantly related to the type of neuroendocrine tumor (p = 0.001).

The 5-year survival rate differed significantly between patients with tumor node metastasis (TNM) stage I and II disease and those with stage III and IV tumors (p = 0.011).

Malignant cases should be treated with aggressive radical surgery to achieve complete tumor resection and potential for long-term survival.

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(PMID = 20571266.001).

[ISSN] 1421-9883

[Journal-full-title] Digestive surgery

[ISO-abbreviation] Dig Surg

[Language] eng

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

[Publication-country] Switzerland

   

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[Title] A change in pituitary magnetic resonance imaging protocol detects ACTH-secreting tumours in patients with previously negative results.

OBJECTIVE: While detection of pituitary tumours with magnetic resonance imaging (MRI) may reduce diagnostic costs and improve surgical outcomes for patients with Cushing's disease, the optimal T1-weighted spin-echo (SE) MRI protocol remains unknown.

We hypothesized that specific MR scanning parameters influence detection of corticotropinomas.

DESIGN AND PATIENTS: Between December 1997 and November 2004, 21 of 84 consecutive patients with Cushing's disease had a falsely negative initial pituitary MRI study and a lesion identified subsequently at the National Institutes of Health Clinical Center.

This study retrospectively reviewed and compared technical parameters used for the two pituitary T1-weighted SE MRIs in 18 patients with available scans.

Immunohistochemistry of tumours resected at transsphenoidal surgery confirmed all to be corticotropinomas.

CONCLUSIONS: Not all 'T1-weighted SE' scans are equally accurate.

We recommend that endocrinologists consider pituitary MRI parameters when interpreting the results.

[MeSH-major] ACTH-Secreting Pituitary Adenoma / diagnosis. Magnetic Resonance Imaging / methods. Pituitary Neoplasms / diagnosis

[MeSH-minor] Adult. False Negative Reactions. Female. Humans. Male. Middle Aged. Pituitary ACTH Hypersecretion / pathology. Pituitary Gland / pathology. Retrospective Studies

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(PMID = 19500112.001).

[ISSN] 1365-2265

[Journal-full-title] Clinical endocrinology

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

[Language] eng

[Grant] United States / Intramural NIH HHS / / Z01 HD008833-01

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural

[Publication-country] England

[Other-IDs] NLM/ NIHMS139974; NLM/ PMC2866063

   

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[Title] Endoscopic endonasal transsphenoidal surgery: surgical results of 228 pituitary adenomas treated in a pituitary center.

Pituitary tumors are challenging tumors in the sellar region.

Surgical approaches to the pituitary have undergone numerous refinements over the last 100 years.

The introduction of the endoscope have revolutionized pituitary surgery.

The aim of this study is to report the results of a consecutive series of patients undergoing pituitary surgery using a pure endoscopic endonasal approach and to evaluate the efficacy and safety of this procedure.

We reviewed the data of 228 consecutive patients who underwent endonasal transsphenoidal adenoma removal over an 10-year period.

Tumor removal rate, endocrinological outcomes, and complications were retrospectively assessed in 228 patients with pituitary adenomas who underwent 251 procedures between December 1998 and December 2007.

There were 93 nonfunctioning adenomas, 58 growth hormone-secreting, 41 prolactin-secreting, 28 adrenocorticotropin hormone secreting, 7 FSH-LH secreting and 1 thyroid-stimulating hormone-secreting adenomas.

The remission results for patients with nonfunctioning adenomas was 83% and for functioning adenomas were 76.3% (70.6% for GH hormone-secreting, 85.3% for prolactin hormone-secreting, 71.4% for ACTH hormone-secreting, 85.7% for FSH-LH hormone-secreting and 100% for TSH hormone-secreting), with no recurrence at the time of the last follow-up.

The endoscopic endonasal approach for resection of pituitary adenomas, provides acceptable results representing a safe alternative procedure to the microscopic approach.

This less invasive method, associated with a small number of complications, provides excellent tumor removal rates and represents an important tool for the achievement of good results in the pituitary surgery, mainly for the complete removal of large adenomas.

[MeSH-major] Adenoma / surgery. Endoscopy / methods. Pituitary Neoplasms / surgery

[MeSH-minor] Humans. Pituitary Hormones / blood. Postoperative Complications. Retrospective Studies

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(PMID = 19697135.001).

[ISSN] 1573-7403

[Journal-full-title] Pituitary

[ISO-abbreviation] Pituitary

[Language] eng

[Publication-type] Evaluation Studies; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Pituitary Hormones