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1. Kuo SF, Chen JY, Chuang WY, Jung SM, Chang YC, Lin JD: Concurrent papillary thyroid cancer with pituitary ACTH-secreting tumor. J Formos Med Assoc; 2007 Apr;106(4):330-5
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  • [Title] Concurrent papillary thyroid cancer with pituitary ACTH-secreting tumor.
  • Concomitant thyroid cancer with pituitary tumor is uncommon.
  • This study reports a case of advanced papillary thyroid carcinoma with pituitary adrenocorticotropic hormone (ACTH)-secreting tumor.
  • A 58-year-old male patient had thyroid cancer in 1991 and presented with headache caused by pituitary tumor with apoplexy in 1993.
  • During follow-up for thyroid cancer, (201)thallium scan proved to be an effective tool for detecting metastatic thyroid cancer in the patient without pituitary TSH reserve.
  • Pituitary ACTH-secreting tumor was confirmed in 2001 based on the high serum ACTH level and positive immunohistochemical stain for ACTH.
  • Moreover, serum ACTH levels were 337 and 232 pg/mL with normal serum cortisol and urine-free cortisol.


2. Hashiba T, Saitoh Y, Asanuma N, Kouhara H, Maruo T, Fujinaka T, Kasayama S, Yoshimine T: Reduction of a pancreatic tumor after total removal of an ACTH secreting pituitary tumor: differential diagnosis of Cushing's syndrome. Endocr J; 2006 Apr;53(2):203-8
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  • [Title] Reduction of a pancreatic tumor after total removal of an ACTH secreting pituitary tumor: differential diagnosis of Cushing's syndrome.
  • Endocrinologic tests sometimes fail to distinguish adrenocorticotropic hormone (ACTH)-secreting pituitary adenoma from ectopic ACTH-secreting tumor.
  • The authors experienced a case of Cushing's disease associated with a pancreatic tumor.
  • 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


3. Tateno T, Izumiyama H, Doi M, Akashi T, Ohno K, Hirata Y: Defective expression of prohormone convertase 1/3 in silent corticotroph adenoma. Endocr J; 2007 Dec;54(5):777-82
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  • 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.
  • 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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4. Sugiyama M, Sugiyama T, Yamaguchi M, Izumiyama H, Yoshimoto T, Kishino M, Akashi T, Hirata Y: Successful localization of ectopic ACTH-secreting bronchial carcinoid by selective pulmonary arterial sampling. Endocr J; 2010;57(11):959-64
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  • [Title] Successful localization of ectopic ACTH-secreting bronchial carcinoid by selective pulmonary arterial sampling.
  • Among patient with ACTH-dependent Cushing's syndrome, about 10-20% of those with ectopic ACTH syndromes (EAS) have occult or unknown tumors.
  • Despite the intensive search for the culprit tumors by dynamic endocrine tests and imaging tests, it is often difficult to localize and confirm the source of occult ectopic ACTH secretion.
  • We report a patient with EAS caused by a small bronchial carcinoid tumor, which was successfully localized by a selective pulmonary arterial sampling for the first time.
  • A 69-year-old woman presented with typical Cushingoid features and elevated plasma ACTH and cortisol levels, which showed lack of circadian rhythm, no suppression by high-dose dexamethasone, and no response to CRH stimulation.
  • No mass lesion was detected by pituitary MRI, and inferior petrosal sinus sampling showed no central to peripheral ACTH gradient.
  • Selective pulmonary arterial sampling of the wedged blood from a pulmonary artery branch affecting the nodule showed a marked ACTH gradient, and the lobectomy of the right middle lung resulted in dramatic decreases in plasma ACTH and cortisol levels.
  • The resected tumor was diagnosed as a bronchial carcinoid tumor with positive immunostaining for ACTH.
  • Thus, selective pulmonary arterial sampling, because of its more site-selective measurement of hormonal secretion, could be one of the useful tools to localize and confirm the ectopic ACTH production by a small pulmonary tumor.
  • [MeSH-major] Adrenocorticotropic Hormone / secretion. Bronchial Neoplasms / secretion. Carcinoid Tumor / secretion. Pulmonary Artery / radionuclide imaging
  • [MeSH-minor] ACTH Syndrome, Ectopic / blood. ACTH Syndrome, Ectopic / etiology. ACTH Syndrome, Ectopic / radionuclide imaging. ACTH Syndrome, Ectopic / surgery. Aged. Female. Humans. Hydrocortisone / blood

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  • (PMID = 20890054.001).
  • [ISSN] 1348-4540
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
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5. Tani Y, Inoshita N, Sugiyama T, Kato M, Yamada S, Shichiri M, Hirata Y: Upregulation of CDKN2A and suppression of cyclin D1 gene expressions in ACTH-secreting pituitary adenomas. Eur J Endocrinol; 2010 Oct;163(4):523-9
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  • [Title] Upregulation of CDKN2A and suppression of cyclin D1 gene expressions in ACTH-secreting pituitary adenomas.
  • OBJECTIVE: Cushing's disease (CD) is usually caused by ACTH-secreting pituitary microadenomas, while silent corticotroph adenomas (SCA) are macroadenomas without Cushingoid features.
  • However, the molecular mechanism(s) underlying their different tumor growth remains unknown.
  • DESIGN AND METHODS: Tumor tissue specimens resected from 43 pituitary tumors were studied: CD (n=10), SCA (n=11), and NFA (n=22).
  • Thus, it is suggested that upregulated CDKN2A with the concomitant downregulated cyclin gene family is partly involved in the small size of ACTH-secreting adenoma.


6. Tateno T, Kato M, Tani Y, Oyama K, Yamada S, Hirata Y: Differential expression of somatostatin and dopamine receptor subtype genes in adrenocorticotropin (ACTH)-secreting pituitary tumors and silent corticotroph adenomas. Endocr J; 2009;56(4):579-84
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  • [Title] Differential expression of somatostatin and dopamine receptor subtype genes in adrenocorticotropin (ACTH)-secreting pituitary tumors and silent corticotroph adenomas.
  • Somatostatin analogs and dopamine agonists are clinically used for medical therapy of functioning pituitary tumors, such as growth hormone- and prolactin-secreting tumors, however, their effects on ACTH-secreting tumors are controversial.
  • This study was aimed to determine whether somatostatin receptor (SSTR) subtype (1-5) and dopamine receptor type 2 (D2R) are differentially expressed in pituitary tumors causing Cushing's disease (CD), silent corticotroph adenoma (SCA), and non-functioning pituitary tumor (NFT).
  • Tissue specimens were obtained from 35 pituitary tumors during transsphenoidal surgery.
  • [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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7. Suzuki K, Hattori Y, Aoki C, Nakano A, Tomizawa A, Kase H, Kasai K: An ACTH-secreting pituitary adenoma within the sphenoid sinus. Intern Med; 2010;49(8):763-6
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  • [Title] An ACTH-secreting pituitary adenoma within the sphenoid sinus.
  • She was found to have a markedly elevated plasma ACTH-cortisol level.
  • We decided to proceed with radiation therapy to shrink the tumor.
  • We describe a rare case of an ACTH-secreting pituitary adenoma within the sphenoid sinus.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / diagnosis. Paranasal Sinus Neoplasms / diagnosis. Sphenoid Sinus / pathology

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  • (PMID = 20424367.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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8. Pimentel-Filho FR, Silva ME, Nogueira KC, Berger K, Cukiert A, Liberman B: Pituitary-adrenal dynamics after ACTH-secreting pituitary tumor resection in patients receiving no steroids post-operatively. J Endocrinol Invest; 2005 Jun;28(6):502-8
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  • [Title] Pituitary-adrenal dynamics after ACTH-secreting pituitary tumor resection in patients receiving no steroids post-operatively.
  • We compared the dynamics of ACTH and cortisol from a group of CD patients (cured and not cured), receiving no steroids post-operatively, with a control group of acromegalic patients who presented normal hypothalamic-pituitary-adrenal (HPA) axis.
  • Blood samples for ACTH and cortisol determination were obtained immediately before, at the end of surgery and at 4, 8, 12, 16, 24, 48 and 72 h after surgery, in 8 cured CD patients (Group I), 9 not cured CD patients (Group II) and in 7 subjects with acromegaly (Group III) who presented normal HPA axis (control group).
  • The mean ACTH level in Group I was significantly lower than in Group III from 4 to 12 h and lower than in Group II from 8 to 12 h post-operatively.
  • [MeSH-major] Adrenal Glands / physiopathology. Adrenocorticotropic Hormone / secretion. Glucocorticoids / administration & dosage. Pituitary Gland / physiopathology. Pituitary Neoplasms / secretion. Pituitary Neoplasms / surgery
  • [MeSH-minor] Adenoma / physiopathology. Adenoma / secretion. Adenoma / surgery. Adrenal Insufficiency / drug therapy. Adrenal Insufficiency / etiology. Adult. Female. Humans. Hydrocortisone / blood. Male. Pituitary ACTH Hypersecretion / physiopathology. Pituitary ACTH Hypersecretion / surgery. Postoperative Care. Postoperative Complications. Time Factors

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  • (PMID = 16117190.001).
  • [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 / Glucocorticoids; 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
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9. Amaral FC, Torres N, Saggioro F, Neder L, Machado HR, Silva WA Jr, Moreira AC, Castro M: MicroRNAs differentially expressed in ACTH-secreting pituitary tumors. J Clin Endocrinol Metab; 2009 Jan;94(1):320-3
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  • [Title] MicroRNAs differentially expressed in ACTH-secreting pituitary tumors.
  • OBJECTIVE: The aim of the study was to analyze the differential expression of let-7a, miR-15a, miR-16, miR-21, miR-141, miR-143, miR-145, and miR-150 in corticotropinomas and normal pituitary tissue and verify whether their profile of expression correlates with tumor size or remission after treatment.
  • MATERIAL AND METHODS: ACTH-secreting pituitary tumor samples were obtained during transphenoidal surgery from patients with Cushing disease and normal pituitary tissues from autopsies.
  • RESULTS: We found underexpression of miR-145 (2.0-fold; P = 0.04), miR-21 (2.4-fold; P = 0.004), miR-141 (2.6-fold; P = 0.02), let-7a (3.3-fold; P = 0.003), miR-150 (3.8-fold; P = 0.04), miR-15a (4.5-fold; P = 0.03), miR-16 (5.0-fold; P = 0.004), and miR-143 (6.4-fold; P = 0.004) in ACTH-secreting pituitary tumors when compared to normal pituitary tissues.
  • There were no differences between miRNA expression and tumor size as well as miRNA expression and ratio of remission after surgery, except in patients presenting lower miR-141 expression who showed a better chance of remission.
  • [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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10. Illouz F, Dubois-Ginouves S, Laboureau S, Rohmer V, Rodien P: [Use of cabergoline in persisting Cushing's disease]. Ann Endocrinol (Paris); 2006 Sep;67(4):353-6
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  • [Transliterated title] Utilisation de la cabergoline dans la maladie de Cushing non contrôlée.
  • Cabergoline is a dopaminergic agonist with demonstrated efficiency of for the treatment of prolactin-secreting pituitary tumors.
  • We describe the use of cabergoline in three patients with Cushing's disease, one of them presenting a silent ACTH-secreting pituitary tumor.
  • We describe a decrease or a normalization in hypercortisolism; for one of the subjects, tumor growth seemed to be stopped.
  • While cabergoline can induce a suppression of cortisol secretion or a corticotroph tumor shrinkage, the sites of action remain unclear.
  • [MeSH-major] Adrenocortical Hyperfunction / drug therapy. Ergolines / therapeutic use. Pituitary ACTH Hypersecretion / diagnosis

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  • (PMID = 17072242.001).
  • [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] 0 / Dopamine Agonists; 0 / Ergolines; LL60K9J05T / cabergoline; WI4X0X7BPJ / Hydrocortisone
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11. Liu JK, Fleseriu M, Delashaw JB Jr, Ciric IS, Couldwell WT: Treatment options for Cushing disease after unsuccessful transsphenoidal surgery. Neurosurg Focus; 2007;23(3):E8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Cushing disease is considered an aggressive pituitary endocrinopathy because of the devastating effects from untreated hypercortisolemia.
  • Although they are histologically benign, these adrenocorticotropic hormone (ACTH)-secreting pituitary tumors are associated with significant morbidity and premature death.
  • Currently, transsphenoidal surgery is the primary treatment of Cushing disease associated with an ACTH-secreting pituitary tumor, resulting in remission rates ranging from about 50 to 90%.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / surgery. Adenoma / surgery. Pituitary ACTH Hypersecretion / therapy

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  • (PMID = 17961031.001).
  • [ISSN] 1092-0684
  • [Journal-full-title] Neurosurgical focus
  • [ISO-abbreviation] Neurosurg Focus
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 67
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12. Castillo V, Giacomini D, Páez-Pereda M, Stalla J, Labeur M, Theodoropoulou M, Holsboer F, Grossman AB, Stalla GK, Arzt E: Retinoic acid as a novel medical therapy for Cushing's disease in dogs. Endocrinology; 2006 Sep;147(9):4438-44
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  • Cushing's disease is almost always caused by an ACTH-secreting pituitary tumor, but effective medical therapy is currently limited.
  • Clinical signs, plasma ACTH and alpha-MSH, the cortisol/creatinine urine ratio, and pituitary magnetic resonance imaging were assessed and compared at different time points.
  • We recorded a significant reduction in plasma ACTH and alpha-MSH, and also in the cortisol/creatinine urine ratio, of the dogs treated with retinoic acid.
  • Pituitary adenoma size was also significantly reduced at the end of retinoic acid treatment.
  • Retinoic acid treatment controls ACTH and cortisol hyperactivity and tumor size in dogs with ACTH-secreting tumors, leading to resolution of the clinical phenotype.
  • This study highlights the possibility of using retinoic acid as a novel therapy in the treatment of ACTH-secreting tumors in humans with Cushing's disease.
  • [MeSH-major] Dog Diseases / drug therapy. Pituitary ACTH Hypersecretion / veterinary. Tretinoin / therapeutic use
  • [MeSH-minor] Adenoma / pathology. Adrenocorticotropic Hormone / blood. Animals. Body Weight. Creatinine / urine. Dogs. Female. Hydrocortisone / urine. Ketoconazole / therapeutic use. Magnetic Resonance Imaging / veterinary. Male. Pituitary Gland / pathology. Pituitary Neoplasms / pathology. Survival Rate. alpha-MSH / blood

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  • (PMID = 16740975.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 5688UTC01R / Tretinoin; 581-05-5 / alpha-MSH; 9002-60-2 / Adrenocorticotropic Hormone; AYI8EX34EU / Creatinine; R9400W927I / Ketoconazole; WI4X0X7BPJ / Hydrocortisone
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13. Suri D, Weiss RE: Effect of pioglitazone on adrenocorticotropic hormone and cortisol secretion in Cushing's disease. J Clin Endocrinol Metab; 2005 Mar;90(3):1340-6
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  • Peroxisomal proliferator-activated receptors (PPAR)-gamma are abundantly expressed in ACTH-secreting pituitary tumors.
  • Treatment with PPARgamma agonists inhibits ACTH-secreting pituitary tumor growth, proliferation, and ACTH secretion in vitro in human and murine models and in vivo in murine corticotroph tumors.
  • It was hypothesized that treatment with the PPARgamma agonist pioglitazone would normalize the hypothalamic-pituitary-adrenal axis of patients with CD.
  • We evaluated the hypothalamic pituitary adrenal axis in five patients with CD in whom we measured:.
  • 2) the 24-h profile of serum cortisol and plasma ACTH; and 3) the ACTH and cortisol response to CRH stimulation.
  • At baseline, before low-dose dexamethasone, all five patients had elevated 24-h urine free cortisol, elevated 24-h serum cortisol and plasma ACTH levels, and robust responses to CRH, consistent with their diagnosis of CD.
  • Furthermore, there was no significant difference in the number of cortisol or ACTH spikes or in their diurnal rhythms.
  • In summary, pioglitazone treatment (45 mg daily for 30 d) of patients with CD was not found to be effective at attenuating either ACTH or cortisol levels and does not appear to be an alternative to surgical therapy.
  • [MeSH-major] Adrenocorticotropic Hormone / blood. Hydrocortisone / blood. Hypoglycemic Agents / administration & dosage. Pituitary ACTH Hypersecretion / drug therapy. Pituitary ACTH Hypersecretion / metabolism. Thiazolidinediones / administration & dosage
  • [MeSH-minor] Adult. Circadian Rhythm. Female. Humans. Hypothalamo-Hypophyseal System / drug effects. Male. Middle Aged. PPAR gamma / metabolism. Pituitary-Adrenal System / drug effects. Treatment Failure

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  • (PMID = 15585550.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK 58258; United States / NIDDK NIH HHS / DK / DK07011; United States / NIDDK NIH HHS / DK / DK17050; United States / NIDDK NIH HHS / DK / DK58258; United States / NCRR NIH HHS / RR / RR00055; United States / NCRR NIH HHS / RR / RR18372
  • [Publication-type] Clinical Trial; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hypoglycemic Agents; 0 / PPAR gamma; 0 / Thiazolidinediones; 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone; X4OV71U42S / pioglitazone
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14. Bush ZM, Lopes MB, Hussaini IM, Jane JA Jr, Laws ER Jr, Vance ML: Immunohistochemistry of COUP-TFI: an adjuvant diagnostic tool for the identification of corticotroph microadenomas. Pituitary; 2010;13(1):1-7
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  • Cushing's disease is caused by an ACTH-producing pituitary tumor, and accounts for 10-15% of pituitary tumors.
  • The majority of corticotroph tumors are microadenomas (<10 mm), and accurate histologic identification of these tumors can be challenging because of their small size and the presence of nests of normal corticotroph cells in the anterior pituitary.
  • Retinoic acid has been shown to inhibit ACTH production and induce apoptosis in corticotroph tumor cells.
  • The expression of the orphan nuclear receptor COUP-TFI antagonizes retinoic acid signaling and has been shown to be expressed in normal corticotroph cells, but absent in corticotroph tumor cell lines.
  • We analyzed 34 corticotroph tumor specimens by immunohistochemistry using a goat polyclonal IgG antibody with epitope mapping to the N-terminus of human COUP-TFI.
  • Segments of normal pituitary in each of the 34 specimens demonstrate COUP-TFI immunoreactivity in normal corticotroph cells.
  • Twenty-nine of 34 ACTH producing tumors were immunonegative for COUP-TFI.
  • Immunohistochemistry of COUP-TFI may be a useful adjuvant diagnostic tool in distinguishing corticotroph microadenomas from nests of normal corticotroph cells in the anterior pituitary.
  • Furthermore, this study identifies two unique corticotroph tumor populations which differ in their expression of COUP-TFI, the presence of which occurs more frequently in macroadenomas.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / diagnosis. Adenoma / diagnosis. COUP Transcription Factor I / analysis

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  • (PMID = 19526345.001).
  • [ISSN] 1573-7403
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / 1-T32-DK-07646; United States / NIDDK NIH HHS / DK / T32 DK007646; United States / NCRR NIH HHS / RR / M01RR000847; United States / NIDDK NIH HHS / DK / 1-F32-DK082159-01; United States / NINDS NIH HHS / NS / 5R01NS035122-10
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / COUP Transcription Factor I
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15. Salehi F, Scheithauer BW, Moyes VJ, Drake WM, Syro LV, Manoranjan B, Sharma S, Horvath E, Kovacs K: Low immunohistochemical expression of MGMT in ACTH secreting pituitary tumors of patients with Nelson syndrome. Endocr Pathol; 2010 Dec;21(4):227-9
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  • [Title] Low immunohistochemical expression of MGMT in ACTH secreting pituitary tumors of patients with Nelson syndrome.
  • The aim of the present study was to assess immunohistochemical expression of MGMT in ACTH-secreting pituitary adenomas of patients with Nelson syndrome.
  • Our material consisted of eight specimens from ACTH-secreting pituitary adenomas of patients with Nelson syndrome.
  • Absent or low MGMT staining in brain and other neoplasms has been shown to correlate with successful treatment with temozolomide, and recent reports of aggressive pituitary adenomas suggest similar outcomes.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / metabolism. Adenoma / metabolism. DNA Modification Methylases / biosynthesis. DNA Repair Enzymes / biosynthesis. Nelson Syndrome / metabolism. Tumor Suppressor Proteins / biosynthesis

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  • (PMID = 21061089.001).
  • [ISSN] 1559-0097
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Tumor Suppressor Proteins; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 6.5.1.- / DNA Repair Enzymes
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16. Candrina R, Sleiman I, Zorzi F: ACTH-secreting pituitary adenoma within an ovarian teratoma. Eur J Intern Med; 2005 Sep;16(5):359-60
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  • [Title] ACTH-secreting pituitary adenoma within an ovarian teratoma.
  • The differential diagnosis of Cushing's syndrome is one of the most difficult tasks in medicine, and it is especially problematic in cases with "occult" ectopic ACTH syndrome.
  • We describe the case of a 26-year-old woman who was found to suffer from ectopic ACTH syndrome due to pituitary microadenoma, localized within a mature ovarian teratoma.
  • 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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17. Bucciarelli LG, Pecori Giraldi F, Cavagnini F: No mutations in TPIT, a corticotroph-specific gene, in human tumoral pituitary ACTH-secreting cells. J Endocrinol Invest; 2005 Dec;28(11):1015-8
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  • [Title] No mutations in TPIT, a corticotroph-specific gene, in human tumoral pituitary ACTH-secreting cells.
  • BACKGROUND: TPIT is a recently identified transcription factor specific to proopiomelanocortin (POMC)-expressing cells within the pituitary and plays a pivotal role in the embryonal development of POMC lineage.
  • As with other transcription factors, TPIT could theoretically also be involved in corticotroph adenomatous transformation and ACTH hypersecretion and published data indicate that TPIT is present in normal and adenomatous human corticotrophs.
  • 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.
  • CONCLUSIONS: Aberrant TPIT is unlikely to play a role in corticotroph tumoral trasformation, ie, Cushing's disease, as the entire coding sequence is expressed without any mutation by human pituitary ACTH-secreting adenomas.
  • Conversely, the significance of this transcription factor in tumoral ACTH hypersecretion remains to be clarified.
  • [MeSH-major] Adrenocorticotropic Hormone / secretion. Homeodomain Proteins / genetics. Mutation / genetics. Pituitary Neoplasms / genetics. Transcription Factors / genetics
  • [MeSH-minor] Humans. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism. Reverse Transcriptase Polymerase Chain Reaction. T-Box Domain Proteins. Tumor Cells, Cultured

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  • (PMID = 16483181.001).
  • [ISSN] 0391-4097
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [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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18. Hernández I, Espinosa-de-los-Monteros AL, Mendoza V, Cheng S, Molina M, Sosa E, Mercado M: Ectopic ACTH-secreting syndrome: a single center experience report with a high prevalence of occult tumor. Arch Med Res; 2006 Nov;37(8):976-80
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  • [Title] Ectopic ACTH-secreting syndrome: a single center experience report with a high prevalence of occult tumor.
  • BACKGROUND: Differentiation between the two forms of ACTH-dependent Cushing's syndrome is a challenging task.
  • Although the majority of these cases will be diagnosed as Cushing's disease secondary to an ACTH-secreting pituitary adenoma, 10-15% result from the ectopic ACTH secretion syndrome (EAS), which is usually due to neuroendocrine tumors.
  • The latter included a standard biochemical assessment (urinary free cortisol, low- and high-dose dexamethasone suppression tests), petrosal sinus sampling when indicated and imaging techniques such as pituitary MRI, total body CT and somatostatin receptor scintigraphy.
  • RESULTS: The ectopic nature of the ACTH hypersecretion was confirmed with inferior petrosal sinus samplings in all cases.
  • CT scanning localized a putative tumor in 6/8 patients, whereas octreotide scintigraphy was positive in only five.
  • However, upon performing thoracotomy, a documented ACTH-secreting bronchial carcinoid tumor was found in only four patients.
  • CONCLUSIONS: EAS is a rare cause of ACTH-dependent Cushing's syndrome.
  • [MeSH-major] ACTH Syndrome, Ectopic / diagnosis. ACTH-Secreting Pituitary Adenoma / diagnosis. Adenoma / diagnosis. Adenoma / therapy

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  • (PMID = 17045113.001).
  • [ISSN] 0188-4409
  • [Journal-full-title] Archives of medical research
  • [ISO-abbreviation] Arch. Med. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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19. Stilling G, Sun Z, Zhang S, Jin L, Righi A, Kovācs G, Korbonits M, Scheithauer BW, Kovacs K, Lloyd RV: MicroRNA expression in ACTH-producing pituitary tumors: up-regulation of microRNA-122 and -493 in pituitary carcinomas. Endocrine; 2010 Aug;38(1):67-75
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  • [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.
  • 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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20. Gruszka A, Kunert-Radek J, Pawlikowski M: Rosiglitazone, PPAR-gamma receptor ligand, decreases the viability of rat prolactin-secreting pituitary tumor cells in vitro. Neuro Endocrinol Lett; 2005 Feb;26(1):51-4
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  • [Title] Rosiglitazone, PPAR-gamma receptor ligand, decreases the viability of rat prolactin-secreting pituitary tumor cells in vitro.
  • PPAR-gamma ligands thiazolidinediones (TZDs) have been shown to inhibit the growth and secretory activity of several rat and murine pituitary tumors in vivo as well as in vitro (ACTH-secreting AtT20, PRL- and GH-secreting GH3, LH-secreting LbetaT2 and alpha-T3 cells).
  • TZDs have been demonstrated to induce G0-G1 cell-cycle arrest and apoptosis in human, rat somatolactotroph, murine corticotroph and gonadotroph pituitary tumor cells.
  • In the present study we have investigated for the first time the effects of PPAR-gamma receptor ligand rosiglitazone on the rat estrogens-induced, PRL-secreting pituitary tumor cells in vitro.
  • Pituitary tumors were induced by subcutaneous implantation of capsules containing diethylstilboestrol (DES).
  • Eight weeks after the implantation of capsules the rats were sacrificed and pituitary tumors were collected.
  • RESULTS: We have demonstrated that rosiglitazone at the concentrations 10(-10) - 10(-4)M significantly decreases the number of viable rat PRL-secreting pituitary tumor cells in vitro.
  • CONCLUSION: These results suggest that PPAR-gamma receptor agonists thiazolidinediones may be useful in the medical treatment of pituitary tumors.
  • [MeSH-major] Hypoglycemic Agents / pharmacology. PPAR gamma / drug effects. Pituitary Neoplasms / metabolism. Prolactin / metabolism. Thiazolidinediones / pharmacology
  • [MeSH-minor] Animals. Carcinogens / administration & dosage. Carcinogens / pharmacology. Cell Survival / drug effects. Diethylstilbestrol / administration & dosage. Diethylstilbestrol / pharmacology. Drug Implants. Ligands. Male. Rats. Rats, Inbred F344. Tumor Cells, Cultured

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  • [CommentIn] Neuro Endocrinol Lett. 2005 Dec;26(6):763-4; author reply 765 [16380670.001]
  • (PMID = 15726020.001).
  • [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 / Carcinogens; 0 / Drug Implants; 0 / Hypoglycemic Agents; 0 / Ligands; 0 / PPAR gamma; 0 / Thiazolidinediones; 05V02F2KDG / rosiglitazone; 731DCA35BT / Diethylstilbestrol; 9002-62-4 / Prolactin
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21. Singer J, Werner F, Koch CA, Bartels M, Aigner T, Lincke T, Fasshauer M, Paschke R: Ectopic Cushing's syndrome caused by a well differentiated ACTH-secreting neuroendocrine carcinoma of the ileum. Exp Clin Endocrinol Diabetes; 2010 Aug;118(8):524-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ectopic Cushing's syndrome caused by a well differentiated ACTH-secreting neuroendocrine carcinoma of the ileum.
  • Cushing's syndrome can be caused by adrenocorticotropic hormone-secreting solid tumors.
  • We report a rare case of an ileal endocrine carcinoma that produced ACTH and induced hypercortisolism.
  • The search for the primary tumor was difficult.
  • The patient underwent subtotal thyroidectomy and surgical removal of a pituitary lesion.
  • After resection of an ACTH-producing metastasis of the mesentery, temporary remission of Cushing's syndrome ensued.
  • At the age 45 the primary tumor was detected in the ileum by Ga-68 DOTATOC-PET scan and explorative laparotomy.
  • Ectopic ACTH secretion within the small bowel is very rare.
  • This case underscores the difficulty in locating the source of ectopic ACTH secretion and suggests using small bowel barium study, tubus endoscopy or video endoscopy for preoperative localization if the small bowel is suspected as tumor source.
  • [MeSH-major] ACTH Syndrome, Ectopic / diagnosis. Adrenocorticotropic Hormone / secretion. Carcinoma / diagnosis. Cushing Syndrome / diagnosis. Ileal Neoplasms / diagnosis. Neuroendocrine Tumors / diagnosis
  • [MeSH-minor] Blood Pressure. Diabetes Mellitus / etiology. Humans. Male. Mesentery / surgery. Middle Aged. Muscle Strength. Pituitary Gland / surgery

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  • [Copyright] © J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart · New York.
  • (PMID = 20162505.001).
  • [ISSN] 1439-3646
  • [Journal-full-title] Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association
  • [ISO-abbreviation] Exp. Clin. Endocrinol. Diabetes
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone
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22. Santoro A, Minniti G, Ruggeri A, Esposito V, Jaffrain-Rea ML, Delfini R: Biochemical remission and recurrence rate of secreting pituitary adenomas after transsphenoidal adenomectomy: long-term endocrinologic follow-up results. Surg Neurol; 2007 Nov;68(5):513-8; discussion 518
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  • [Title] Biochemical remission and recurrence rate of secreting pituitary adenomas after transsphenoidal adenomectomy: long-term endocrinologic follow-up results.
  • BACKGROUND: Transsphenoidal surgery is safe and effective in patients with secreting pituitary adenomas; however, variable outcomes have been reported according to the different criteria used to define the biochemical remission of hormone hypersecretion.
  • We report the long-term endocrinologic follow-up results of a large cohort of patients who underwent TSS for secreting pituitary adenomas according to the most recent stringent criteria of cure.
  • METHODS: Two hundred ten consecutive patients were operated on by TSS between 1995 and 2004 for a secreting pituitary adenoma (65 PRL-, 109 GH-, and 36 ACTH-secreting adenomas) and were considered for the study.
  • RESULTS: The overall remission rate was 65% for the whole series, being 64%, 61%, and 75% for PRL-, GH-, and ACTH-secreting adenomas, respectively.
  • Remission rates were significantly higher in GH- and ACTH-secreting pituitary macroadenomas than in macroprolactinomas.
  • At a median follow-up of 56 months, tumor recurrence was 0%, 11%, and 14% for GH-, ACTH-, and PRL-secreting tumors.
  • Tumor size, cavernous sinus invasion, and high hormone levels were negatively correlated to the outcome.
  • CONCLUSION: Transsphenoidal surgery remains an effective treatment for secreting pituitary tumors according to the most recent criteria of cure.
  • Patients with PRL- or ACTH-secreting adenomas may recur after apparently successful surgery, thereby justifying long-term careful endocrinologic follow-up.
  • [MeSH-major] Adenoma / surgery. Hyperpituitarism / prevention & control. Pituitary Neoplasms / surgery
  • [MeSH-minor] Adolescent. Adult. Aged. Female. Follow-Up Studies. Humans. Male. Middle Aged. Pituitary Hormones, Anterior / blood. Pituitary Hormones, Anterior / secretion. Recurrence. Remission Induction. Retrospective Studies. Time Factors. Treatment Outcome

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  • (PMID = 17961741.001).
  • [ISSN] 0090-3019
  • [Journal-full-title] Surgical neurology
  • [ISO-abbreviation] Surg Neurol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Pituitary Hormones, Anterior
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23. Brown RL, Wollman R, Weiss RE: Transformation of a pituitary macroadenoma into to a corticotropin-secreting carcinoma over 16 years. Endocr Pract; 2007 Sep;13(5):463-71
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Transformation of a pituitary macroadenoma into to a corticotropin-secreting carcinoma over 16 years.
  • OBJECTIVE: To describe a case of a pituitary macroadenoma that differentiated into a corticotropin (ACTH)-secreting carcinoma with metastasis to the thigh.
  • METHODS: We present a case report with a 16-year follow-up that includes anatomic and endocrine documentation of the history of an ACTH-secreting carcinoma.
  • The patient underwent surgical debulking followed by a course of radiation directed to the pituitary.
  • Results from retrospective immunohistochemical staining with antibodies against ACTH, prolactin, and MIB-1 were negative.
  • In 1995, she developed left facial palsy and diplopia caused by tumor growth.
  • The patient's clinical status continued to deteriorate because of local mass effect from tumor growth and uncontrolled hypercortisolism.
  • Biopsy results of the obturator muscle revealed metastatic tumor of neuroendocrine origin with strong reactivity to ACTH antibodies and MIB-1 labeling in 8% of tumor cell nuclei.
  • CONCLUSION: A pituitary tumor can transform into an ACTH-secreting carcinoma in an indolent manner.
  • Patients with invasive pituitary adenomas require long-term surveillance to monitor for differentiation into pituitary carcinoma.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / pathology. ACTH-Secreting Pituitary Adenoma / secretion. Adenoma / pathology. Adenoma / secretion. Adrenocorticotropic Hormone / secretion

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  • (PMID = 17872347.001).
  • [ISSN] 1934-2403
  • [Journal-full-title] Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists
  • [ISO-abbreviation] Endocr Pract
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK07011; United States / NCRR NIH HHS / RR / RR00055; United States / NCRR NIH HHS / RR / RR18372
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone
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24. Horiguchi K, Yamada M, Umezawa R, Satoh T, Hashimoto K, Tosaka M, Yamada S, Mori M: Somatostatin receptor subtypes mRNA in TSH-secreting pituitary adenomas: a case showing a dramatic reduction in tumor size during short octreotide treatment. Endocr J; 2007 Jun;54(3):371-8
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  • [Title] Somatostatin receptor subtypes mRNA in TSH-secreting pituitary adenomas: a case showing a dramatic reduction in tumor size during short octreotide treatment.
  • TSH-secreting adenoma is a rare pituitary adenoma, and the expression levels of the specific subtypes of somatostatin receptors (sstr) mRNAs have remained obscure.
  • To determine the quantitative expression of the sstr1-5 mRNAs in TSH-secreting adenomas that may be related to the efficacy of treatment with a somatostatin analogue, expression of the sstr1-5 mRNAs was examined and compared in TSH-secreting adenomas and other pituitary adenomas.
  • The pituitary adenomas were obtained at transsphenoidal surgery from 4 cases of TSH-secreting adenoma, including 1 patient showing a significant shrinkage of the tumor size after only 10 days of octreotide treatment, 2 patients without tumor size reduction and 1 patient without treatment, and 5 GH-secreting adenomas, 6 prolactinomas, 5 nonfunctioning adenomas, 4 ACTH-secreting adenomas and normal pituitaries at autopsy from 4 normal subjects.
  • In comparison to the normal pituitary, sstr2A>sstr1>sstr5>sstr3 mRNAs were expressed in the TSH-secreting adenomas examined.
  • The expression level of sstr2 mRNA was significantly higher than those in normal pituitary, prolactinomas, ACTH-secreting and nonfunctioning pituitary adenomas.
  • The patient with marked shrinkage of the tumor showed the highest expression of both sstr2 and sstr5 mRNAs among all the cases of pituitary adenoma.
  • A TSH-secreting tumor without shrinkage showed a similar expression level of sstr2 mRNA.
  • These findings demonstrated that TSH-secreting adenomas express sstr1, 2A, 3 and 5 mRNAs, predominantly sstr2A, and in addition to the expression of sstr2 mRNA, the expression level of sstr5 mRNA may be a factor affecting the tumor shrinkage by somatostatin analogues against TSH-secreting adenomas.
  • [MeSH-major] Adenoma / drug therapy. Adenoma / genetics. Octreotide / therapeutic use. Pituitary Neoplasms / drug therapy. Pituitary Neoplasms / genetics. Receptors, Somatostatin / genetics. Thyrotrophs / pathology. Tumor Burden / drug effects

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  • (PMID = 17420609.001).
  • [ISSN] 0918-8959
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Case Reports; Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / Receptors, Somatostatin; RWM8CCW8GP / Octreotide
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25. Batista D, Courkoutsakis NA, Oldfield EH, Griffin KJ, Keil M, Patronas NJ, Stratakis CA: Detection of adrenocorticotropin-secreting pituitary adenomas by magnetic resonance imaging in children and adolescents with cushing disease. J Clin Endocrinol Metab; 2005 Sep;90(9):5134-40
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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.
  • 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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26. McDermott JH, Thabit H, Hickey N, Thompson C, Gaffney E, Young V, Sreenan S: ACTH-secreting bronchial carcinoid: a diagnostic and therapeutic challenge. Ir J Med Sci; 2008 Sep;177(3):269-72
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  • [Title] ACTH-secreting bronchial carcinoid: a diagnostic and therapeutic challenge.
  • OBJECTIVE: We describe a case of Cushing's syndrome due to ectopic ACTH secretion, where the only potential source on conventional imaging was a tiny benign-appearing lung nodule, which failed to take up radiolabelled octreotide.
  • RESULTS: Compared to ACTH and cortisol levels on a control day, the levels following the test dose of octreotide were lower.
  • Histological examination of the resected specimen confirmed bronchial carcinoid staining positive for ACTH.
  • CONCLUSIONS: This is one of the few cases described where ectopic ACTH secretion secondary to bronchial carcinoid responded to somatostatin analogue therapy.
  • The case was also unusual in that the tumour responded despite not taking up radiolabelled octreotide.
  • [MeSH-major] ACTH Syndrome, Ectopic / etiology. Bronchial Neoplasms / diagnosis. Carcinoid Tumor / diagnosis. Pituitary ACTH Hypersecretion / etiology

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  • (PMID = 18516660.001).
  • [ISSN] 1863-4362
  • [Journal-full-title] Irish journal of medical science
  • [ISO-abbreviation] Ir J Med Sci
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Ireland
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27. Pinchot SN, Sippel R, Chen H: ACTH-producing carcinoma of the pituitary with refractory Cushing's Disease and hepatic metastases: a case report and review of the literature. World J Surg Oncol; 2009;7:39
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  • [Title] ACTH-producing carcinoma of the pituitary with refractory Cushing's Disease and hepatic metastases: a case report and review of the literature.
  • BACKGROUND: Pituitary carcinomas are rare neuroendocrine tumors affecting the adenohypophysis.
  • CASE PRESENTATION: Here, we report the case of a fatal pituitary carcinoma evolving within two years from an adrenocorticotrophic hormone (ACTH)-secreting macroadenoma and review the global literature regarding this rare neuroendocrine tumor.
  • CONCLUSION: Pituitary carcinomas are extremely rare neoplasms, representing only 0.1% to 0.2% of all pituitary tumors.
  • The latency period between initial presentation of a pituitary adenoma and the development of distal metastases marking carcinoma is extremely variable, and some patients may live well over 10 years with pituitary carcinoma.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / pathology. Liver Neoplasms / secondary. Pituitary ACTH Hypersecretion / complications

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  • (PMID = 19356251.001).
  • [ISSN] 1477-7819
  • [Journal-full-title] World journal of surgical oncology
  • [ISO-abbreviation] World J Surg Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Parathyroid Hormone
  • [Other-IDs] NLM/ PMC2678126
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28. De Tommasi C, Vance ML, Okonkwo DO, Diallo A, Laws ER Jr: Surgical management of adrenocorticotropic hormone-secreting macroadenomas: outcome and challenges in patients with Cushing's disease or Nelson's syndrome. J Neurosurg; 2005 Nov;103(5):825-30
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  • [Title] Surgical management of adrenocorticotropic hormone-secreting macroadenomas: outcome and challenges in patients with Cushing's disease or Nelson's syndrome.
  • OBJECT: Adrenocorticotropic hormone (ACTH)-secreting pituitary macroadenomas are an uncommon cause of Cushing's disease (CD) and, subsequently, Nelson's syndrome (NS).
  • The outcome of modern surgical treatment is unclear and thus was assessed in a series of 43 patients, with the goal of improving therapeutic results in patients with ACTH-secreting macroadenomas.
  • They represented 15% of the patients surgically treated at the authors' institution for ACTH-secreting adenomas.
  • Invasion of the dura mater by tumor was histologically demonstrated in 10 patients with CD and in two patients with NS.
  • CONCLUSIONS: Comprehensive management of CD caused by ACTH-secreting macroadenomas through the appropriate use of combination therapy, including surgery, radiotherapy, radiosurgery, and adrenalectomy, can lead to outcomes similar to those for microadenomas.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / surgery. Adenoma / surgery. Nelson Syndrome / surgery. Pituitary ACTH Hypersecretion / surgery


29. Wong M, Isa SH, Kamaruddin NA, Khalid BA: ACTH producing pulmonary carcinoid and pituitary macroadenoma: a fortuitous association? Med J Malaysia; 2007 Jun;62(2):168-70
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  • [Title] ACTH producing pulmonary carcinoid and pituitary macroadenoma: a fortuitous association?
  • We report a case of a 45 year-old man who presented initially with a non-functioning pituitary macroadenoma.
  • Four years later, he presented acutely with adrenocorticotrophic hormone (ACTH) dependent Cushing's syndrome which resolved following a right lobectomy.
  • To our knowledge, this is the first reported case of an ectopic ACTH secreting pulmonary carcinoid found in association with a non-functioning pituitary macroadenoma.
  • [MeSH-major] ACTH Syndrome, Ectopic / complications. Carcinoid Tumor / secretion. Lung Neoplasms / secretion. Pituitary Neoplasms / complications

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  • (PMID = 18705457.001).
  • [ISSN] 0300-5283
  • [Journal-full-title] The Medical journal of Malaysia
  • [ISO-abbreviation] Med. J. Malaysia
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Malaysia
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30. Vik-Mo EO, Øksnes M, Pedersen PH, Wentzel-Larsen T, Rødahl E, Thorsen F, Schreiner T, Aanderud S, Lund-Johansen M: Gamma knife stereotactic radiosurgery of Nelson syndrome. Eur J Endocrinol; 2009 Feb;160(2):143-8
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  • OBJECTIVE: Gamma knife radiosurgery (GKR) can be used as primary or adjuvant therapy for the treatment of an ACTH-producing pituitary tumor after bilateral adrenalectomy, called Nelson syndrome (NS).
  • We have examined the effect of GKR on tumor growth and ACTH-hypersecretion, and characterized the adverse events of this treatment in patients with NS.
  • RESULTS: Tumor growth was stopped in all patients.
  • The ACTH levels declined in eight patients, and normalized in one patient.
  • There was a significant drop in ACTH levels, with a half-time of 2.8 years.
  • The substitution therapy of three pituitary axes present at GKR treatment could be stopped during the same period.
  • As the radiation level was below 1Gy to this area, it is unlikely that the GKR treatment itself induced the malignant tumor.

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  • (PMID = 18996962.001).
  • [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] 9002-60-2 / Adrenocorticotropic Hormone
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31. Lee EJ, Ahn JY, Noh T, Kim SH, Kim TS, Kim SH: Tumor tissue identification in the pseudocapsule of pituitary adenoma: should the pseudocapsule be removed for total resection of pituitary adenoma? Neurosurgery; 2009 Mar;64(3 Suppl):ons62-9; discussion ons69-70
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  • [Title] Tumor tissue identification in the pseudocapsule of pituitary adenoma: should the pseudocapsule be removed for total resection of pituitary adenoma?
  • OBJECTIVE: The microsurgical pseudocapsule can be found in the transition zone between an adenoma and the surrounding normal pituitary tissue.
  • Furthermore, we evaluated the remission rate, the changes in pituitary function, and the recurrence rate after intensive resection of the pseudocapsule.
  • METHODS: In 616 patients with pituitary adenomas (Hardy Types I-III) over a period of 14 years, we introduced intensive resection of the microsurgical pseudocapsule to achieve complete tumor removal.
  • A combined pituitary function test and radiological study were performed on the patients before surgery, 1 year after surgery, and at subsequent 1.5-year intervals 2 to 13 years postoperatively.
  • Tumor cluster infiltration was present in the pseudocapsule in 71 (43.6%) of these patients.
  • The presence of a pseudocapsule was slightly more frequent in prolactin-secreting tumors (70.9%) than in growth hormone-secreting (55.0%) and adrenocorticotropic hormone-secreting (40.0%) tumors.
  • In the 243 patients of the total resection group who underwent combined pituitary function tests more than 2 times after surgery, the surgical remission rate was 99.1% in clinically nonfunctional tumors, 88% in growth hormone-secreting, 70.6% in prolactin-secreting, and 100% in adrenocorticotropic hormone-secreting tumors.
  • There was no statistical difference in improvement or deterioration of pituitary function according to the existence or absence of the pseudocapsule.
  • The tumor recurrence rate was 0.8% in the total resection group and was 42.1% in the subtotal resection group.
  • CONCLUSION: We have shown that tumor tissue is frequently present within the pseudocapsule, suggesting that any tumor remnant in the pseudocapsule could be a source of recurrence and an obstacle to achieving complete remission.
  • These results indicate that intensive resection of the pseudocapsule could result in a higher remission rate without deteriorating pituitary function.
  • [MeSH-major] Neurosurgical Procedures / methods. Pituitary Gland / pathology. Pituitary Gland / surgery. Pituitary Neoplasms / pathology. Pituitary Neoplasms / surgery
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / surgery. Follow-Up Studies. Growth Hormone-Secreting Pituitary Adenoma / surgery. Humans. Magnetic Resonance Imaging. Microsurgery. Neoplasm Recurrence, Local / epidemiology. Pituitary Function Tests. Postoperative Period. Prolactinoma / surgery. Prospective Studies. Treatment Outcome

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  • (PMID = 19240574.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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32. Bronstein MD, Melmed S: [Pituitary tumorigenesis]. Arq Bras Endocrinol Metabol; 2005 Oct;49(5):615-25
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  • [Title] [Pituitary tumorigenesis].
  • Pituitary adenomas, almost invariably adenomas, account for 10% to 15% of all intracranial neoplasms and are incidentally detected in up to 27% of non selected autopsies.
  • Functionally, they are classified as secreting adenomas (PRL, GH, ACTH, TSH, LH, and FSH, and those co-secreting two or more hormones), and clinically non secreting or "non functioning" tumors.
  • Pituitary tumorigenesis mechanisms include those of primary hypothalamic versus pituitary origin, the latter is supported by evidence of pituitary adenoma monoclonality, as well as the absence of hyperplastic tissue surrounding the surgically removed tumor, and the relative independence of tumor hypothalamic control.
  • Nevertheless, a permissive role of the hypothalamus on tumor progression is also postulated.
  • Several molecular mechanisms involved in pituitary tumorigenesis have been unraveled including oncogenes, tumor suppressor genes and growth factors involved in neoplastic development, and will be described in this review.
  • [MeSH-major] Adenoma. Pituitary Neoplasms

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  • (PMID = 16444345.001).
  • [ISSN] 0004-2730
  • [Journal-full-title] Arquivos brasileiros de endocrinologia e metabologia
  • [ISO-abbreviation] Arq Bras Endocrinol Metabol
  • [Language] por
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Brazil
  • [Number-of-references] 68
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33. Bode H, Seiz M, Lammert A, Brockmann MA, Back W, Hammes HP, Thomé C: SOM230 (pasireotide) and temozolomide achieve sustained control of tumour progression and ACTH secretion in pituitary carcinoma with widespread metastases. Exp Clin Endocrinol Diabetes; 2010 Nov;118(10):760-3
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  • [Title] SOM230 (pasireotide) and temozolomide achieve sustained control of tumour progression and ACTH secretion in pituitary carcinoma with widespread metastases.
  • Pituitary carcinomas are rare and neurosurgically challenging lesions, as they commonly relapse after surgical removal.
  • We report a patient with an ACTH-secreting pituitary carcinoma and widespread intracranial, spinal and systemic metastases despite repeated surgical treatment, bilateral adrenalectomy, medical treatment and radiotherapy.
  • Additionally to chemotherapy with temozolomide, the patient received SOM230 as salvage therapy with an improvement of the patient's clinical status, and a reduction of ACTH levels.
  • After 12 months of combination therapy a sustained tumor control was achieved and persisted upon monotherapy with SOM230 for more than 9 months thereafter.
  • Thus, temozolomide in combination with SOM230 seems to be promising in patients with ACTH-secreting metastasized pituitary carcinoma.
  • [MeSH-major] Adrenocorticotropic Hormone / secretion. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma / drug therapy. Carcinoma / secondary. Dacarbazine / analogs & derivatives. Pituitary Neoplasms / drug therapy. Somatostatin / analogs & derivatives

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  • [Copyright] © J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart · New York.
  • (PMID = 20496311.001).
  • [ISSN] 1439-3646
  • [Journal-full-title] Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association
  • [ISO-abbreviation] Exp. Clin. Endocrinol. Diabetes
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Antineoplastic Agents, Hormonal; 51110-01-1 / Somatostatin; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; 9002-60-2 / Adrenocorticotropic Hormone; 98H1T17066 / pasireotide
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34. Colao A, Ochoa AS, Auriemma RS, Faggiano A, Pivonello R, Lombardi G: Pituitary carcinomas. Front Horm Res; 2010;38:94-108
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  • [Title] Pituitary carcinomas.
  • Pituitary carcinoma is a extremely rare and is characterized by a very poor prognosis.
  • Even if at diagnosis the presence of metastases is required to define a pituitary carcinoma, the lesion was almost invariably diagnosed first as a benign pituitary tumor, that after a variable period of latency, ranging from few months to many years, changed its natural course to an aggressive pituitary tumor poorly responsive to therapy.
  • Most pituitary carcinomas are functioning, and ACTH- and PRL-secreting carcinomas are the most frequent.
  • [MeSH-major] Pituitary Neoplasms / therapy
  • [MeSH-minor] Biomarkers, Tumor / analysis. Genes, Tumor Suppressor. Humans. Oncogenes

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  • [Copyright] Copyright (c) 2010 S. Karger AG, Basel.
  • (PMID = 20616500.001).
  • [ISSN] 0301-3073
  • [Journal-full-title] Frontiers of hormone research
  • [ISO-abbreviation] Front Horm Res
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 88
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35. Tateno T, Kato M, Tani Y, Yoshimoto T, Oki Y, Hirata Y: Processing of high-molecular-weight form adrenocorticotropin in human adrenocorticotropin-secreting tumor cell line (DMS-79) after transfection of prohormone convertase 1/3 gene. J Endocrinol Invest; 2010 Feb;33(2):113-7
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  • [Title] Processing of high-molecular-weight form adrenocorticotropin in human adrenocorticotropin-secreting tumor cell line (DMS-79) after transfection of prohormone convertase 1/3 gene.
  • Ectopic ACTH-producing tumors preferentially secrete biologically inactive ACTH precursors and ACTH-related fragments.
  • DMS-79 is known to secrete unprocessed high-molecular-weight (HMW) form ACTH.
  • Molecular weights of ACTH-related peptides were determined by chromatographical analyses coupled with ACTH and beta-endorphin (beta-END) radioimmunoassays.
  • The steady-state mRNA levels of PC1/3 and 2 in DMS-79 were lower than those in ACTH-secreting and nonfunctioning pituitary tumors.
  • DMS-79 predominantly secreted HMW form with both ACTH and beta-END immunoreactivities by size-exclusion chromatography.
  • After purification by immunoaffinity chromatography with anti-ACTH antibody, the apparent molecular weight of HMW form ACTH was estimated to be 16 kDa by sodium dodecyl sulfate-polyacrylamide gel electrophoresis with silver staining.
  • After retroviral transfection of PC1/3 cDNA into DMS-79 and puromycin selection, PC1/3 stably-expressing cell line (DMS-79T) secreted two immunoreactive ACTH components, a major one coeluting with ACTH(1-39) and a minor one as a HMW form as well as two beta- END immunoreactive components coeluting with beta-lipotropic hormone and beta-END, respectively.
  • Thus, we have established PC1/3 stably-expressing cell line (DMS-79T) capable of proteolytically processing ACTH precursor molecule(s) into mature ACTH and beta-END.
  • [MeSH-minor] Adenoma / secretion. Cell Line, Tumor. Electrophoresis, Polyacrylamide Gel. Humans. Lung Neoplasms. Molecular Weight. Pituitary Neoplasms / secretion. Proprotein Convertase 2 / genetics. Proprotein Convertase 2 / metabolism. RNA, Messenger / analysis. Retroviridae / genetics. Small Cell Lung Carcinoma. Transfection. beta-Endorphin / metabolism

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  • (PMID = 19786827.001).
  • [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 / RNA, Messenger; 60617-12-1 / beta-Endorphin; 66796-54-1 / Pro-Opiomelanocortin; 9002-60-2 / Adrenocorticotropic Hormone; EC 3.4.21.93 / Proprotein Convertase 1; EC 3.4.21.94 / Proprotein Convertase 2
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36. Goh KP, Lee HY, Rajasoorya RC: Triple jeopardy in the pituitary. Pituitary; 2008;11(3):331-6
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  • [Title] Triple jeopardy in the pituitary.
  • Aggressive pituitary tumors are rare the pathogenesis is not well established.
  • The development of pituitary tumor after apoplexy has also been rarely reported.
  • We describe the sequential development of Cushing's disease, apoplexy and aggressive pituitary tumor in the same patient.
  • A 31-year old male presented with eutopic ACTH dependent Cushing's syndrome which failed initial pituitary surgery.
  • An episode of pituitary apoplexy then occurred which was followed by the development of a null-cell pituitary tumor.
  • This second tumor exhibited an aggressive behavior with invasion into the surrounding structures and systemic spread clinically.
  • This case provides important evidence for the hypotheses of the pathogenesis of aggressive pituitary tumors which could have arisen from surviving adenoma cells following apoplexy or as a de novo development of pituitary carcinoma from cells which were not part of the original adenoma.
  • This is the first report of a transformation of Cushing's disease to an aggressive and invasive null cell tumor after pituitary irradiation, apoplexy and surgery.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / complications. Adenoma / complications. Carcinoma / etiology. Neoplasms, Second Primary. Pituitary ACTH Hypersecretion / complications. Pituitary Apoplexy / complications. Pituitary Gland / pathology. Pituitary Neoplasms / etiology
  • [MeSH-minor] Adrenalectomy. Adult. Fatal Outcome. Humans. Magnetic Resonance Imaging. Male. Neoplasm Invasiveness. Radiotherapy, Adjuvant

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  • (PMID = 18058238.001).
  • [ISSN] 1386-341X
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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37. Moraes AB, Taboada GF, Carneiro MP, Neto LV, Wildemberg LE, Madi K, Domingues RC, Gadelha MR: Utility of [(18)F] fluoro-2-deoxy-D: -glucose positron emission tomography in the localization of ectopic ACTH-secreting tumors. Pituitary; 2009;12(4):380-3
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  • [Title] Utility of [(18)F] fluoro-2-deoxy-D: -glucose positron emission tomography in the localization of ectopic ACTH-secreting tumors.
  • Ectopically ACTH producing tumors may be difficult to localize by conventional radiology and functional imaging may be helpful.
  • Case 1: 31-year-old man was diagnosed with ectopic ACTH-dependent Cushing's syndrome (ECS).
  • Pathological examination confirmed an ACTH-positive carcinoid tumor.
  • Pituitary MRI was normal.
  • [(18)F] FDG PET scan revealed intense uptake in uterus, especially cervix, suggesting this to be the primary tumor site.
  • These cases illustrate the role of [(18)F] FDG PET in the investigation of an ECS where conventional imaging studies were not elucidative in the search for a responsible tumor.
  • [MeSH-minor] Adult. Carcinoid Tumor / diagnosis. Carcinoid Tumor / secretion. Carcinoma, Small Cell / diagnosis. Carcinoma, Small Cell / secretion. Female. Humans. Immunohistochemistry. Magnetic Resonance Imaging. Male. Middle Aged

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  • (PMID = 18459046.001).
  • [ISSN] 1573-7403
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0Z5B2CJX4D / Fluorodeoxyglucose F18
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38. Kim JP, Park BJ, Kim SB, Lim YJ: Pituitary Apoplexy due to Pituitary Adenoma Infarction. J Korean Neurosurg Soc; 2008 May;43(5):246-9
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  • [Title] Pituitary Apoplexy due to Pituitary Adenoma Infarction.
  • Cause of pituitary apoplexy has been known as hemorrhage, hemorrhagic infarction or infarction of pituitary adenoma or adjacent tissues of pituitary gland.
  • However, pituitary apoplexy caused by pure infarction of pituitary adenoma has been rarely reported.
  • Here, we present the two cases pituitary apoplexies caused by pituitary adenoma infarction that were confirmed by transsphenoidal approach (TSA) and pathologic reports.
  • Pathologic report of first case revealed total tumor infarction of a nonfunctioning pituitary macroadenoma and second case partial tumor infarction of ACTH secreting pituitary macroadenoma.
  • Patients with pituitary apoplexy which was caused by pituitary adenoma infarction unrelated to hemorrhage or hemorrhagic infarction showed good response to TSA treatment.
  • Further study on the predisposing factors of pituitary apoplexy and the mechanism of infarction in pituitary adenoma is necessary.

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  • (PMID = 19096606.001).
  • [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/ PMC2588219
  • [Keywords] NOTNLM ; Pituitary adenoma infarction / Pituitary apoplexy
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39. Pinto EM, Bronstein MD: [Molecular aspects of pituitary tumorigenesis]. Arq Bras Endocrinol Metabol; 2008 Jun;52(4):599-610
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  • [Title] [Molecular aspects of pituitary tumorigenesis].
  • [Transliterated title] Aspectos moleculares da tumorigênese hipofisária.
  • Pituitary tumors, almost invariably adenomas, are of frequent occurrence, accounting for 10% to 15% of all the intracranial neoplasm.
  • They are classified as microadenomas (< 10 mm) or macroadenomas (> 10 mm) and as secreting or clinically non-secreting (or not functioning) adenomas.
  • These tumors are autonomously capable to release pituitary hormones such as the growth hormone (GH), prolactin (PRL), adrenocorticotropic hormone (ACTH), thyroid stimulating hormone (TSH), follicle-stimulating hormone (FSH) and luteinizing hormone (LH).
  • The occurrence of metastases, characterizing a pituitary carcinoma, is exceedingly rare.
  • Although the pathogenesis of pituitary tumors is fully characterized, many molecular mechanisms of pituitary tumorigenesis had already been revealed.
  • This review intends to describe advances in the understanding of the involved advances that have been made in the last decade concerning pituitary tumors progression, including the participation of oncogenes, tumor suppressor genes and growth factors.
  • [MeSH-major] Genes, Tumor Suppressor / physiology. Intercellular Signaling Peptides and Proteins / genetics. Pituitary Neoplasms / genetics

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  • (PMID = 18604372.001).
  • [ISSN] 1677-9487
  • [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] 0 / Intercellular Signaling Peptides and Proteins
  • [Number-of-references] 73
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40. Colao A, Pivonello R, Di Somma C, Savastano S, Grasso LF, Lombardi G: Medical therapy of pituitary adenomas: effects on tumor shrinkage. Rev Endocr Metab Disord; 2009 Jun;10(2):111-23
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  • [Title] Medical therapy of pituitary adenomas: effects on tumor shrinkage.
  • The efficacy of dopamine-agonists (DA) in patients with prolactinomas and that of somatostatin analogues (SSA) in those with GH- and TSH-secreting adenomas is well established.
  • More recently, data are accumulating suggesting a potential therapeutic role of DA also in patients with ACTH-secreting and clinically non-functioning (NFA) pituitary adenomas.
  • This review aims at summarizing published results of DA and SSA on tumor shrinkage in patients with different histotypes of pituitary adenomas.
  • Results of tumor shrinkage are of clinical relevance as tumor size is the one of the most important determinant of surgical outcome.
  • While reduction of tumor size more than 50% of baseline size in macroprolactinomas treated with DA is a frequent finding in patients with GH-secreting adenomas treated with SSA tumor shrinkage only recently is becoming frequent thanks to the availability of depot formulations.
  • Data on tumor shrinkage in patients with TSH-secreting adenomas treated with SSA are limited because of the rarity of these tumors.
  • Very recently, DA have been reported of some efficacy also in patients with ACTH-secreting adenomas but data are still very limited.
  • NFA respond very scantly to both DA and SSA even if receptors targeting these drugs are present.
  • [MeSH-major] Hormones / therapeutic use. Pituitary Neoplasms / drug therapy. Somatostatin / analogs & derivatives. Somatostatin / therapeutic use

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  • (PMID = 18791829.001).
  • [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] United States
  • [Chemical-registry-number] 0 / Dopamine Agonists; 0 / Hormones; 51110-01-1 / Somatostatin; 9002-60-2 / Adrenocorticotropic Hormone; 9002-71-5 / Thyrotropin; 9002-72-6 / Growth Hormone
  • [Number-of-references] 103
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41. Jin L, Riss D, Ruebel K, Kajita S, Scheithauer BW, Horvath E, Kovacs K, Lloyd RV: Galectin-3 Expression in Functioning and Silent ACTH-Producing Adenomas. Endocr Pathol; 2005;16(2):107-14
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  • [Title] Galectin-3 Expression in Functioning and Silent ACTH-Producing Adenomas.
  • Galectin-3 (Gal-3), a beta galactoside-binding protein, has been implicated in a variety of biological functions including cell growth, differentiation, tumor cell adhesion, angiogenesis, tumor progression, and metastasis.
  • We recently reported that Gal-3 was expressed in a subset of normal pituitary cells and tumors including PRL, ACTH, and in folliculo-stellate (FS) cells and tumors and that Gal-3 had an important regulatory role in pituitary cell proliferation.
  • We further investigated the expression of Gal-3 protein in ACTH- and PRL-producing tumors and the expression of various galectin mRNAs by RT-PCR in pituitary adenomas and normal pituitary.
  • Most silent ACTH subtypes 1 and 2 adenomas were negative or only focally positive for Gal-3 expression compared to functioning ACTH tumors from patients with Cushing's disease and Nelson's syndrome.
  • In the normal pituitary, Gal-3 was expressed in less than 1% of the basophil-invading cells (ACTH cells present in the posterior pituitary) and in a subset of the anterior lobe ACTH-positive cells.
  • RT-PCR analyses showed that many members of the galectin family including galectins 1, 2, 3, 4, 5, 6, 7, 8, and 9 were expressed in normal pituitary and in functioning ACTH- and PRL-producing tumors.
  • These results indicate that Gal-3 is associated with functioning ACTH and PRL tumors and is expressed infrequently in silent ACTH adenomas, suggesting that Gal-3 protein and/or gene is altered in non-functioning ACTH tumors.
  • The use of ACTH and Gal-3 immunostaining should help in the diagnosis of silent ACTH adenomas.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / metabolism. Adenoma / metabolism. Adrenocorticotropic Hormone / secretion. Galectin 3 / biosynthesis. Pituitary Gland / metabolism. Pituitary Neoplasms / metabolism

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  • (PMID = 16199895.001).
  • [ISSN] 1046-3976
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA90249
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Galectin 3; 0 / RNA, Messenger; 9002-60-2 / Adrenocorticotropic Hormone; 9002-62-4 / Prolactin
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42. Castinetti F, Brue T: [Radiotherapy and radiosurgery of pituitary adenomas]. Presse Med; 2009 Jan;38(1):133-9
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  • [Title] [Radiotherapy and radiosurgery of pituitary adenomas].
  • There are two principal types of treatment for pituitary adenomas: fractionated conventional radiation therapy, based on biological selectivity, and radiosurgery, which is delivered in a single dose, based on anatomic selectivity and indicated preferentially for small tumors sufficiently distant from the optic chiasm.
  • Radiation therapy and radiosurgery make it possible to stabilize or diminish tumor volume in 70-100% of cases.
  • This is especially useful in the case of an active residue after surgery for non-secreting adenoma, but the long-term side effects of radiation must be borne in mind.
  • The principal side effect is the onset of a pituitary deficiency (in more than 50% of cases after radiation therapy, 20% after radiosurgery).
  • [MeSH-major] Adenoma / radiotherapy. Pituitary Neoplasms / radiotherapy. Radiosurgery
  • [MeSH-minor] Acromegaly / therapy. Antineoplastic Agents / therapeutic use. Decision Trees. Dose Fractionation. Humans. Hypopituitarism / etiology. Pituitary ACTH Hypersecretion / therapy. Pituitary Gland / radiation effects. Pituitary Gland / secretion. Postoperative Complications. Prolactinoma / radiotherapy. Prolactinoma / secretion. Prolactinoma / surgery. Radiation Injuries / etiology. Risk Factors. Time Factors. Treatment Outcome

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  • (PMID = 18954960.001).
  • [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] 0 / Antineoplastic Agents
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43. Salgado LR, Fragoso MC, Knoepfelmacher M, Machado MC, Domenice S, Pereira MA, de Mendonça BB: Ectopic ACTH syndrome: our experience with 25 cases. Eur J Endocrinol; 2006 Nov;155(5):725-33
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  • [Title] Ectopic ACTH syndrome: our experience with 25 cases.
  • OBJECTIVE: Ectopic ACTH syndrome (EAS) occurs in about 5-10% of all patients with ACTH-dependent hypercortisolism with most of them caused by intrathoracic neoplasms.
  • DESIGN AND SUBJECTS: Tumor markers, imaging, and outcome data from 25 patients (13F/12M) aged 18-72 years.
  • High dexamethasone suppression test (HDDST), desmopressin test, GHRP-6 test, corticotropin-releasing hormone (CRH) test, IPSS, computed tomography (CT), magnetic resonance imaging (MRI), and (111)In-pentetreotide scintigraphy were revised.
  • In 13 patients who underwent desmopressin test, ACTH- and cortisol-positive responses were seen in six and five patients respectively.
  • In the seven patients submitted to IPSS using desmopressin in six of them, none had ACTH gradients.
  • Fourteen patients had intrathoracic tumors, five had pheochromocytomas, three had pancreatic tumors, one had a glomic tumor, and had three occult tumors.

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  • (PMID = 17062889.001).
  • [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 / Oligopeptides; 7S5I7G3JQL / Dexamethasone; 87616-84-0 / growth hormone releasing hexapeptide; 9015-71-8 / Corticotropin-Releasing Hormone; ENR1LLB0FP / Deamino Arginine Vasopressin
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44. Sakihara S, Kageyama K, Matsumoto A, Ikeda H, Tsushima Y, Naraoka M, Terui K, Nigawara T, Suda T: Exaggerated response of adrenocorticotropic hormone to growth hormone-releasing peptide-2 test in Cushing's disease. Case report. Neurol Med Chir (Tokyo); 2009 Aug;49(8):365-9
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  • A 47-year-old woman presented with a pituitary microadenoma manifesting as typical Cushing's syndrome.
  • Plasma adrenocorticotropic hormone (ACTH) levels were greatly increased from 66 pg/ml to 2490 pg/ml (about 38-fold) in response to the administration of 100 microg human growth hormone-releasing peptide (GHRP)-2.
  • GHRP receptor type 1a messenger ribonucleic acid was detected in the tumor.
  • Therefore, GHRP-2 may stimulate ACTH via the GHRP receptor type 1a in pituitary ACTH-producing tumor.
  • [MeSH-major] Adenoma / metabolism. Adrenocorticotropic Hormone / blood. Oligopeptides. Pituitary ACTH Hypersecretion / diagnosis. Pituitary ACTH Hypersecretion / physiopathology. Pituitary Neoplasms / metabolism
  • [MeSH-minor] Biomarkers / analysis. Biomarkers / blood. Female. Humans. Hypothalamo-Hypophyseal System / metabolism. Hypothalamo-Hypophyseal System / physiopathology. Hypothalamo-Hypophyseal System / secretion. Middle Aged. Pituitary-Adrenal System / metabolism. Pituitary-Adrenal System / physiopathology. Pituitary-Adrenal System / secretion. Predictive Value of Tests. RNA, Messenger / metabolism. Receptors, Neuropeptide / genetics. Receptors, Pituitary Hormone-Regulating Hormone / genetics

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  • (PMID = 19707004.001).
  • [ISSN] 1349-8029
  • [Journal-full-title] Neurologia medico-chirurgica
  • [ISO-abbreviation] Neurol. Med. Chir. (Tokyo)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Oligopeptides; 0 / RNA, Messenger; 0 / Receptors, Neuropeptide; 0 / Receptors, Pituitary Hormone-Regulating Hormone; 0 / growth hormone-releasing peptide-2; 0 / somatocrinin receptor; 9002-60-2 / Adrenocorticotropic Hormone
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45. Rocha Filho PA, Galvão AC, Teixeira MJ, Rabello GD, Fortini I, Calderaro M, Carrocini D: SUNCT syndrome associated with pituitary tumor: case report. Arq Neuropsiquiatr; 2006 Jun;64(2B):507-10
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  • [Title] SUNCT syndrome associated with pituitary tumor: case report.
  • MRI revealed a pituitary tumor with little suprasellar extent.
  • The subjects serial assays of prolactin, GH, TSH and ACTH were within normal levels.
  • Following transsphenoidal hypophysectomy, with complete removal of the tumor, the subject no more presented pain.
  • The pathological diagnosis was non-secreting adenoma.
  • [MeSH-major] Adenoma / complications. Pituitary Neoplasms / complications. SUNCT Syndrome / etiology

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  • (PMID = 16917628.001).
  • [ISSN] 0004-282X
  • [Journal-full-title] Arquivos de neuro-psiquiatria
  • [ISO-abbreviation] Arq Neuropsiquiatr
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Brazil
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46. Mezosi E, Nemes O: [Treatment of pituitary adenomas]. Orv Hetil; 2009 Sep 27;150(39):1803-10
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Treatment of pituitary adenomas].
  • According to epidemiological studies, the prevalence of pituitary adenomas is 16.5% and the majority of them are "incidentalomas".
  • The symptoms of pituitary disorders are often non-specific; disturbances of pituitary function, compression symptoms, hypophysis apoplexy or accidental findings may help the diagnosis.
  • The hormonal evaluation of pituitary adenomas is different from the algorithm used in the disorders of peripheral endocrine organs.
  • The first-line therapy of prolactinomas are the dopamine agonists, and the aims of the treatment are to normalize the prolactin level, restore fertility in child-bearing age, decrease tumor mass, save or improve the residual pituitary function and inhibit the relapse of the disease.
  • Neurosurgery is the primary therapy of GH-, ACTH-, TSH-producing and inactive adenomas.
  • The rare TSH-producing tumor can respond to both dopamine agonist and somatostatin analog therapy.
  • Further studies are needed to elucidate the exact role of radiosurgery and fractionated stereotaxic irradiation in the treatment of pituitary tumors.
  • [MeSH-major] Adenoma / therapy. Pituitary Hormones / blood. Pituitary Neoplasms / therapy
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / therapy. Acromegaly / drug therapy. Acromegaly / etiology. Adrenocorticotropic Hormone / blood. Aminoquinolines / therapeutic use. Bromocriptine / therapeutic use. Cushing Syndrome / drug therapy. Cushing Syndrome / etiology. Dopamine Agonists / therapeutic use. Female. Growth Hormone-Secreting Pituitary Adenoma / therapy. Human Growth Hormone / analogs & derivatives. Human Growth Hormone / blood. Human Growth Hormone / therapeutic use. Humans. Hypophysectomy. Incidental Findings. Male. Pregnancy. Pregnancy Complications, Neoplastic / therapy. Prolactinoma / therapy. Radiosurgery. Receptors, Somatotropin / antagonists & inhibitors. Somatostatin / analogs & derivatives. Somatostatin / therapeutic use. Thyrotropin / blood

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  • (PMID = 19758960.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / Aminoquinolines; 0 / Dopamine Agonists; 0 / Pituitary Hormones; 0 / Receptors, Somatotropin; 0 / pegvisomant; 12629-01-5 / Human Growth Hormone; 3A64E3G5ZO / Bromocriptine; 51110-01-1 / Somatostatin; 80Q9QWN15M / quinagolide; 9002-60-2 / Adrenocorticotropic Hormone; 9002-71-5 / Thyrotropin; 98H1T17066 / pasireotide
  • [Number-of-references] 28
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47. Barahona MJ, Sojo L, Wägner AM, Bartumeus F, Oliver B, Cano P, Webb SM: Determinants of neurosurgical outcome in pituitary tumors. J Endocrinol Invest; 2005 Oct;28(9):787-94
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Determinants of neurosurgical outcome in pituitary tumors.
  • OBJECTIVE: Neurosurgery is one of the main therapies for pituitary tumors; optimising outcome is highly desirable for the patient and the health system.
  • We have analysed predictors of outcome in surgically treated pituitary adenomas operated in this centre.
  • DESIGN AND PATIENTS: A total of 289 patients underwent neurosurgery for a pituitary tumor, by the same two neurosurgeons, between 1982 and 2001.
  • Most tumors (70.2%) were macroadenomas; 28.4% were non-functioning, 27.3% secreted PRL, 26.3% GH of which 14 (4.8%) also secreted PRL, 17.3% ACTH, 0.3% FSH and 0.3% TSH.
  • RESULTS: A stepwise, forward logistic regression analysis revealed tumor size as the only significant predictor of radiological cure [odds ratio (OR) for macroadenoma 0.16 vs microadenoma, p=0.0005].
  • Hormonally, PRL-secretion by the tumor was a predictor of poor prognosis (OR 3.29 for cure of non-PRL-secreting tumors, p=0.005), as was tumor size (OR 0.45 for cure of macroadenomas, p=0.005).
  • Considering simultaneous radiological and hormonal remission, tumor size (OR 0.35 for macroadenoma, p=0.0002), and operation date (OR 0.40 for up to 1991, p=0.0002) were the only significant predictors.
  • CONCLUSIONS: PRL secretion, tumor size and operation date are the main predictors of neurosurgical outcome in pituitary tumors, the latter suggesting that neurosurgical experience plays an important role.
  • [MeSH-major] Adenoma / surgery. Neurosurgical Procedures / methods. Pituitary Neoplasms / surgery

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  • (PMID = 16370556.001).
  • [ISSN] 0391-4097
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 12629-01-5 / Human Growth Hormone; 9002-60-2 / Adrenocorticotropic Hormone
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48. Jankowska A, Wasko R, Waligorska-Stachura J, Andrusiewicz M, Jaskula M, Liebert W, Sowinski J: Survivin products in pituitary tumors. Neuro Endocrinol Lett; 2008 Dec;29(6):1033-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • 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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49. da Rocha AA, Giorgi RR, de Sa SV, Correa-Giannella ML, Fortes MA, Cavaleiro AM, Machado MC, Cescato VA, Bronstein MD, Giannella-Neto D: Hepatocyte growth factor-regulated tyrosine kinase substrate (HGS) and guanylate kinase 1 (GUK1) are differentially expressed in GH-secreting adenomas. Pituitary; 2006;9(2):83-92
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  • [Title] Hepatocyte growth factor-regulated tyrosine kinase substrate (HGS) and guanylate kinase 1 (GUK1) are differentially expressed in GH-secreting adenomas.
  • Pituitary tumors, adenomas in their vast majority, represent around 10-15% of the intracranial neoplasms.
  • Pituitary carcinomas are exceedingly rare.
  • Pituitary tumorigenesis is still poorly understood.
  • In order to investigate the expression of cancer-related genes in pituitary tumors, we employed a human cancer cDNA macroarray membrane with 1176 well-characterized human genes related to cancer and tumor biology.
  • We were able to identify several differentially expressed genes, among them hepatocyte growth factor-regulated tyrosine kinase substrate (HGS) and guanylate kinase 1 (GUK1) which were over expressed in a pool of clinically nonfunctioning pituitary adenomas, compared with a spinal cord metastasis of a nonfunctioning pituitary carcinoma.
  • HGS and GUK1 mRNA expression were chosen to be validated by quantitative RT-qPCR, however, only GUK1 had the differential expression confirmed between the adenomas and the metastasis of a pituitary carcinoma.
  • We have also investigated HGS and GUK1 mRNA expressions in a series of 46 pituitary adenomas (18 nonfunctioning, 12 GH-secreting, nine PRL-secreting, and seven ACTH-secreting adenomas).
  • HGS and GUK1 were significantly over expressed in GH-secreting adenomas, compared with ACTH-secreting adenomas and nonfunctioning tumors, and with PRL-secreting adenomas, respectively.
  • We have shown that these genes, involved in tumorigenesis in other tissues, are as well over expressed in the pituitary tumors, however, their role in the oncogenesis of these tumors need to be further investigated.
  • [MeSH-major] Adenoma / metabolism. Growth Hormone-Secreting Pituitary Adenoma / metabolism. Guanylate Kinase / metabolism. Phosphoproteins / metabolism
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / genetics. ACTH-Secreting Pituitary Adenoma / metabolism. Adolescent. Adult. Aged. DNA, Neoplasm / genetics. Endosomal Sorting Complexes Required for Transport. Female. Gene Expression Regulation, Neoplastic. Humans. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Prolactinoma / genetics. Prolactinoma / metabolism. RNA, Messenger / genetics

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  • (PMID = 16832584.001).
  • [ISSN] 1386-341X
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Endosomal Sorting Complexes Required for Transport; 0 / Phosphoproteins; 0 / RNA, Messenger; 0 / hepatocyte growth factor-regulated tyrosine kinase substrate; EC 2.7.4.8 / Guanylate Kinase
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50. Xu H, Zhang M, Zhai G, Zhang M, Ning G, Li B: The role of integrated (18)F-FDG PET/CT in identification of ectopic ACTH secretion tumors. Endocrine; 2009 Dec;36(3):385-91
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  • [Title] The role of integrated (18)F-FDG PET/CT in identification of ectopic ACTH secretion tumors.
  • The role of (18)F-Flurodeoxyglucose positron emission tomography ((18)F-FDG PET) scan in localization of ectopic Cushing's syndrome (EAS) tumor is still controversial.
  • Five patients, three men and two women, were reported, whose endocrine investigations and negative pituitary imaging were suggestive of ectopic ACTH secretion. (18)F-FDG PET/CT was performed to identify the source of ACTH secretion.
  • Four of them underwent lesion resection, whose plasma ACTH and serum cortisol levels returned to normal after the surgery.
  • Unfortunately, one patient died due to severe infection and electrolyte disorders. (18)F-FDG PET/CT technology integrates PET and CT imaging in one device so as to increase the accuracy of tumor localization and further improve the prognosis of the patients by curative resection.
  • [MeSH-major] ACTH Syndrome, Ectopic / radionuclide imaging. ACTH-Secreting Pituitary Adenoma / radionuclide imaging. Adenoma / radionuclide imaging. Carcinoid Tumor / radionuclide imaging. Fluorodeoxyglucose F18. Positron-Emission Tomography / methods. Tomography, Emission-Computed / methods

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  • (PMID = 19806477.001).
  • [ISSN] 1559-0100
  • [Journal-full-title] Endocrine
  • [ISO-abbreviation] Endocrine
  • [Language] eng
  • [Publication-type] Case Reports; Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0Z5B2CJX4D / Fluorodeoxyglucose F18; WI4X0X7BPJ / Hydrocortisone
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51. Giorgi RR, Chile T, Bello AR, Reyes R, Fortes MA, Machado MC, Cescato VA, Musolino NR, Bronstein MD, Giannella-Neto D, Corrêa-Giannella ML: Expression of neurotensin and its receptors in pituitary adenomas. J Neuroendocrinol; 2008 Sep;20(9):1052-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of neurotensin and its receptors in pituitary adenomas.
  • The neurotensin (NT) produced in the hypothalamus and in pituitary gonadotrophs and thyrotrophs participates in neuroendocrine regulation.
  • In the present study, we evaluated the expression of NT and its receptors (NTR1, 2 and 3) in a series of 50 pituitary adenomas [11 growth hormone (GH)-, eight prolactin (PRL)-, four adrenocorticotrophic hormone (ACTH)- and 27 nonfunctioning adenomas].
  • NT mRNA expression was significantly higher in functioning compared to nonfunctioning adenomas and with normal pituitary.
  • Nonfunctioning pituitary adenomas showed lower expression of NT mRNA than normal pituitary.
  • In the immunohistochemical study of functioning adenomas, NT was colocalised with GH, PRL and ACTH secreting cells.
  • NTR3 mRNA expression was observed in all examined samples and was higher in the adenomas, both functioning and nonfunctioning, compared to normal pituitary.
  • By contrast, NTR1 and NTR2 mRNA were not detected in either pituitary adenomas or normal tissue.
  • The higher expression of NTR3, as well as the expression of NT by tumoural corticotrophs, lactotrophs and somatotrophs, which are cells types that do not express this peptide in the normal pituitary, suggests that NT autocrine and/or paracrine stimulation mediated by NTR3 may be a mechanism associated with the tumourigenesis of functioning adenomas.
  • [MeSH-major] Adenoma / genetics. Neurotensin / genetics. Pituitary Neoplasms / genetics. Receptors, Neurotensin / genetics
  • [MeSH-minor] Adult. Aged. Autocrine Communication / genetics. Autocrine Communication / physiology. Female. Gene Expression Regulation, Neoplastic. Humans. Male. Middle Aged. Paracrine Communication / genetics. Paracrine Communication / physiology. RNA, Messenger / metabolism. Tumor Cells, Cultured. Young Adult

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  • (PMID = 18624930.001).
  • [ISSN] 1365-2826
  • [Journal-full-title] Journal of neuroendocrinology
  • [ISO-abbreviation] J. Neuroendocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Receptors, Neurotensin; 39379-15-2 / Neurotensin
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52. Walsh MT, Couldwell WT: Symptomatic cystic degeneration of a clinically silent corticotroph tumor of the pituitary gland. Skull Base; 2010 Sep;20(5):367-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Symptomatic cystic degeneration of a clinically silent corticotroph tumor of the pituitary gland.
  • Clinically silent corticotroph tumors of the pituitary gland are those tumors that stain for adrenocorticotropic hormone (ACTH) but do not manifest with clinical or laboratory features of Cushing disease.
  • These tumors have been described as exhibiting more aggressive behavior than other nonfunctional pituitary tumors.
  • We present an unusual case of a clinically silent corticotropic adenoma of the pituitary gland that underwent cystic degeneration following recurrence after transsphenoidal surgery and radiation therapy.
  • Patients with clinically silent ACTH-secreting tumors should be monitored for aggressive tumor behavior and may require closer follow-up than those patients harboring other nonfunctional tumors.

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  • [Cites] Nucleic Acids Res. 1983 Oct 25;11(20):7191-203 [6634412.001]
  • (PMID = 21359002.001).
  • [ISSN] 1532-0065
  • [Journal-full-title] Skull base : official journal of North American Skull Base Society ... [et al.]
  • [ISO-abbreviation] Skull Base
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC3023327
  • [Keywords] NOTNLM ; Cortisol / Cushing disease / adrenocorticotropic hormone / corticotroph cells / cystic degeneration / nonfunctional pituitary adenoma
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53. Katavetin P, Cheunsuchon P, Swearingen B, Hedley-Whyte ET, Misra M, Levitsky LL: Review: Pituitary adenomas in children and adolescents. J Pediatr Endocrinol Metab; 2010 May;23(5):427-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Review: Pituitary adenomas in children and adolescents.
  • Clinical manifestations and outcomes of pituitary adenomas in children are not clearly defined.
  • We retrospectively reviewed cases of pituitary adenomas in children 0-18 years treated at MassGeneral Hospital for Children over 15 years.
  • Patients with or without recurrence did not differ for age, tumor-size and hormone levels.
  • [MeSH-major] Adenoma / pathology. Pituitary Neoplasms / pathology
  • [MeSH-minor] Adolescent. Child. Combined Modality Therapy. Female. Growth Hormone-Secreting Pituitary Adenoma / pathology. Humans. Male. Pituitary ACTH Hypersecretion / pathology. Prolactinoma / pathology. Retrospective Studies

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  • (PMID = 20662340.001).
  • [ISSN] 0334-018X
  • [Journal-full-title] Journal of pediatric endocrinology & metabolism : JPEM
  • [ISO-abbreviation] J. Pediatr. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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54. Mauermann WJ, Sheehan JP, Chernavvsky DR, Laws ER, Steiner L, Vance ML: Gamma Knife surgery for adrenocorticotropic hormone-producing pituitary adenomas after bilateral adrenalectomy. J Neurosurg; 2007 Jun;106(6):988-93
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  • [Title] Gamma Knife surgery for adrenocorticotropic hormone-producing pituitary adenomas after bilateral adrenalectomy.
  • OBJECT: Patients with adrenocorticotropic hormone (ACTH)-secreting pituitary adenomas may require a bilateral adrenalectomy to treat their Cushing's disease.
  • Approximately one third of these patients, however, will experience progressive enlargement of the residual pituitary adenoma, develop hyperpigmentation, and have an elevated level of serum ACTH.
  • METHODS: The prospectively collected University of Virginia Gamma Knife database of patients with pituitary adenomas was reviewed to identify all individuals with Nelson's syndrome who were treated with GKS.
  • These patients were assessed for tumor control (that is, lack of tumor growth over time) with neuroimaging studies (median follow-up duration 22 months) and for biochemical normalization of their ACTH levels (median follow-up duration 50 months).
  • Neuroimaging follow-up studies were available for 22 patients, and endocrine follow up was available for 15 patients in whom elevation of ACTH levels was documented prior to GKS.
  • In the 22 patients in whom neuroimaging follow-up studies were available, 12 had a decrease in tumor size, eight had no tumor growth, and two had an increase in tumor volume.
  • Ten of 15 patients with elevated ACTH levels prior to GKS showed a decrease in their ACTH levels at last follow up; three of these 10 patients achieved normal ACTH levels (< 50 pg/ml) and the other five patients with initially elevated values had an increase in ACTH levels.
  • Ten patients were thoroughly evaluated for post-GKS pituitary function; four were found to have new pituitary hormone deficiency and six did not have hypopituitarism after GKS.
  • CONCLUSIONS: Gamma Knife surgery may control the residual pituitary adenoma and decrease ACTH levels in patients with Nelson's syndrome.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / surgery. Adenoma / surgery. Adrenalectomy. Nelson Syndrome / surgery. Radiosurgery

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  • (PMID = 17564169.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone
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55. Sidibé EH: [Pituitary carcinoma. Anatomic and clinical features of cases reported in literature]. Neurochirurgie; 2007 Aug;53(4):284-8
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  • [Title] [Pituitary carcinoma. Anatomic and clinical features of cases reported in literature].
  • [Transliterated title] Carcinome ou adénocarcinome de l'hypophyse. Profil anatomoclinique à travers quelques observations de la littérature.
  • BACKGROUND AND PURPOSE: Pituitary gland tumors that became aggressive, implying adjacent bone structure and the brain as metastases outside of the cranial box, are referred to as pituitary carcinomas.
  • METHODS: We reviewed 67 cases reported in the literature [44 corticotropic pituitary tumors, 11 PRL tumors, 3 GH tumors, 1 TSH tumor, 3 gonadotropic cell tumors and 5 non-functioning tumors].
  • ACTH, beta-lipotrophin, betaendorphin, alphamelano-stimulating hormone, CRH, and beta-gamma MSH were contributive while ultrastructural microscopy provided little information, as did an equimolar Lph/ACTH ratio.
  • [MeSH-major] Adenocarcinoma / pathology. Pituitary Neoplasms / pathology
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / diagnosis. ACTH-Secreting Pituitary Adenoma / metabolism. ACTH-Secreting Pituitary Adenoma / pathology. Adult. Aged. Female. Gonadotropins / metabolism. Growth Hormone-Secreting Pituitary Adenoma / diagnosis. Growth Hormone-Secreting Pituitary Adenoma / metabolism. Humans. Male. Middle Aged. Prolactinoma / diagnosis. Prolactinoma / metabolism. Prolactinoma / pathology. Thyrotropin / metabolism

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  • (PMID = 17524431.001).
  • [ISSN] 0028-3770
  • [Journal-full-title] Neuro-Chirurgie
  • [ISO-abbreviation] Neurochirurgie
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Gonadotropins; 9002-71-5 / Thyrotropin
  • [Number-of-references] 50
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56. Azevedo MF, Xekouki P, Keil MF, Lange E, Patronas N, Stratakis CA: An unusual presentation of pediatric Cushing disease: recurrent corticotropinoma of the posterior pituitary lobe. J Pediatr Endocrinol Metab; 2010 Jun;23(6):607-12
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  • [Title] An unusual presentation of pediatric Cushing disease: recurrent corticotropinoma of the posterior pituitary lobe.
  • We report the case of a 15-year-old girl with a recurrent corticotrophin (ACTH)-secreting adenoma, located in the posterior lobe of the pituitary gland.
  • At the age of 11, she presented with classic CS symptoms; biochemical investigation was compatible with ACTH-dependent Cushing disease, although pituitary gland imaging did not show any tumor.
  • Following transsphenoidal surgery (TSS), histopathological analysis identified an ACTH-secreting pituitary microadenoma arising from the posterior gland.
  • The patient went into remission but 4 years later she presented with recurrent CS; this time, pituitary gland imaging showed a microadenoma located in the posterior lobe, which was resected after TSS.
  • Posterior lobe pituitary adenomas are very rare and often hard to diagnose and treat; this is the first case of such a tumor causing recurrent Cushing's disease in a child.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / pathology. Adenoma / pathology. Pituitary ACTH Hypersecretion / diagnosis
  • [MeSH-minor] Child. Female. Humans. Magnetic Resonance Imaging. Neoplasm Recurrence, Local

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  • (PMID = 20662335.001).
  • [ISSN] 0334-018X
  • [Journal-full-title] Journal of pediatric endocrinology & metabolism : JPEM
  • [ISO-abbreviation] J. Pediatr. Endocrinol. Metab.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / ZIA HD000642-12
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] England
  • [Other-IDs] NLM/ NIHMS752367; NLM/ PMC4727444
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57. Waugh MS, Soler AP, Robboy SJ: Silent corticotroph cell pituitary adenoma in a struma ovarii. Int J Gynecol Pathol; 2007 Jan;26(1):26-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Silent corticotroph cell pituitary adenoma in a struma ovarii.
  • This is the first report of a silent corticotroph cell pituitary adenoma arising in a struma ovarii.
  • The patient, a 79-year-old woman, was found to have an asymptomatic left-sided adnexal mass confirmed by vaginal sonography to be a complex cystic and solid tumor.
  • The pituitary cells were predominantly immunoreactive for adrenocorticotropic hormone, in addition to synaptophysin.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / pathology. Corticotrophs / pathology. Struma Ovarii / pathology

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  • (PMID = 17197893.001).
  • [ISSN] 0277-1691
  • [Journal-full-title] International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists
  • [ISO-abbreviation] Int. J. Gynecol. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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58. Martínez-Fuentes AJ, Moreno-Fernández J, Vázquez-Martínez R, Durán-Prado M, de la Riva A, Tena-Sempere M, Diéguez C, Jiménez-Reina L, Webb SM, Pumar A, Leal-Cerro A, Benito-López P, Malagón MM, Castaño JP: Ghrelin is produced by and directly activates corticotrope cells from adrenocorticotropin-secreting adenomas. J Clin Endocrinol Metab; 2006 Jun;91(6):2225-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • 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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59. Saeger W, Hofmann BM, Buslei R, Buchfelder M: Silent ACTH cell adenoma in coincidence with granulomatous hypophysitis--a case report. Pathol Res Pract; 2007;203(4):221-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Silent ACTH cell adenoma in coincidence with granulomatous hypophysitis--a case report.
  • A 44-year-old male suffered from an inactive pituitary adenoma measuring 20mm in computed tomography (CT) scan and nuclear magnetic resonance tomography (NMR).
  • The tumor was surgically resected via the transnasal-transsphenoidal route.
  • Surgical specimens revealed a typical, sparsely granulated adrenocorticotropic hormone (ACTH) cell adenoma, but also a granulomatous inflammation mostly in the periphery of the tumor, corresponding to a granulomatous hypophysitis.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / complications. ACTH-Secreting Pituitary Adenoma / ultrastructure. Adenoma / complications. Adenoma / ultrastructure. Pituitary Diseases / complications. Pituitary Diseases / pathology

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  • (PMID = 17395399.001).
  • [ISSN] 0344-0338
  • [Journal-full-title] Pathology, research and practice
  • [ISO-abbreviation] Pathol. Res. Pract.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
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60. Haap M, Gallwitz B, Meyermann R, Mittelbronn M: Cushing's disease associated with both pituitary microadenoma and corticotroph hyperplasia. Exp Clin Endocrinol Diabetes; 2009 Jun;117(6):289-93
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  • [Title] Cushing's disease associated with both pituitary microadenoma and corticotroph hyperplasia.
  • Laboratory analysis demonstrated elevated plasma levels of ACTH and cortisol.
  • MRI imaging revealed a possible pituitary microadenoma.
  • To confirm the diagnosis a bilateral inferior petrosal sinus sampling was performed presenting higher ACTH levels on the right side.
  • Histological examination of the tumor revealed a microadenoma.
  • Neuropathological autopsy revealed nodular proliferations of corticotropic cells in the pituitary gland that are assumed to be morphological entities between diffuse hyperplasias and adenomas, termed as tumorlets.
  • In single reports, multiple pituitary lesions in patients with Cushing's disease have been demonstrated, but to our knowledge none of these cases presented the combination of an ACTH-producing microadenoma and corticotroph cell hyperplasia in the same patient.
  • Therefore, even after resection of a pituitary microadenoma one should be aware of the possibility of continuously elevated ACTH level being due to multifocal nodular corticotroph hyperplasia which is invisible by neuroradiological examination.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / pathology. Pituitary ACTH Hypersecretion / pathology. Pituitary Neoplasms / pathology

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  • [CommentIn] Exp Clin Endocrinol Diabetes. 2010 Jan;118(1):68 [20127571.001]
  • (PMID = 19085700.001).
  • [ISSN] 1439-3646
  • [Journal-full-title] Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association
  • [ISO-abbreviation] Exp. Clin. Endocrinol. Diabetes
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
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61. Labeur M, Refojo D, Wölfel B, Stalla J, Vargas V, Theodoropoulou M, Buchfelder M, Paez-Pereda M, Arzt E, Stalla GK: Interferon-gamma inhibits cellular proliferation and ACTH production in corticotroph tumor cells through a novel janus kinases-signal transducer and activator of transcription 1/nuclear factor-kappa B inhibitory signaling pathway. J Endocrinol; 2008 Nov;199(2):177-89
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  • [Title] Interferon-gamma inhibits cellular proliferation and ACTH production in corticotroph tumor cells through a novel janus kinases-signal transducer and activator of transcription 1/nuclear factor-kappa B inhibitory signaling pathway.
  • Moreover, IFNG modulates normal pituitary hormone secretion, and was shown to inhibit the expression of the ACTH precursor POMC in murine ACTH-secreting AtT-2010/21/2008 tumor cells.
  • We have studied the functional role of IFNG on pituitary tumor cells, focusing on the involvement of IFNG in the molecular events leading to the control of POMC transcriptional repression.
  • Herein, it is shown that IFNG inhibits AtT-20 tumor cell proliferation without inducing apoptosis.
  • 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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62. Raverot G, Sturm N, de Fraipont F, Muller M, Salenave S, Caron P, Chabre O, Chanson P, Cortet-Rudelli C, Assaker R, Dufour H, Gaillard S, François P, Jouanneau E, Passagia JG, Bernier M, Cornélius A, Figarella-Branger D, Trouillas J, Borson-Chazot F, Brue T: Temozolomide treatment in aggressive pituitary tumors and pituitary carcinomas: a French multicenter experience. J Clin Endocrinol Metab; 2010 Oct;95(10):4592-9
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  • [Title] Temozolomide treatment in aggressive pituitary tumors and pituitary carcinomas: a French multicenter experience.
  • CONTEXT: To date only 18 patients with aggressive pituitary tumors or carcinomas treated with temozolomide have been reported.
  • OBJECTIVES: The objective of the study was to describe the antitumoral efficacy and toxicity of temozolomide in patients with aggressive pituitary tumors or carcinomas and evaluate the possible prognostic value of MGMT promoter methylation and protein expression.
  • PATIENTS: Eight patients, five with pituitary carcinomas (three prolactin (PRL) and two ACTH) and three with aggressive pituitary tumors (one PRL and two ACTH), all treated with temozolomide administered orally for four to 24 cycles, were included in our French multicenter study.
  • RESULTS: Three of the eight patients (two ACTH adenomas and one PRL carcinoma) responded to temozolomide as demonstrated by significant tumor shrinkage and reduced hormone secretion.
  • CONCLUSION: Temozolomide treatment may be an effective option for some aggressive pituitary tumors or carcinomas.
  • [MeSH-major] Carcinoma / drug therapy. Dacarbazine / analogs & derivatives. Pituitary Neoplasms / drug therapy
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / drug therapy. ACTH-Secreting Pituitary Adenoma / genetics. ACTH-Secreting Pituitary Adenoma / pathology. Adult. Antineoplastic Agents, Alkylating / therapeutic use. DNA Methylation. Female. France. Humans. Male. Middle Aged. Neoplasm Invasiveness. O(6)-Methylguanine-DNA Methyltransferase / genetics. O(6)-Methylguanine-DNA Methyltransferase / metabolism. Prolactinoma / drug therapy. Prolactinoma / genetics. Prolactinoma / pathology. Retrospective Studies. Sequence Analysis, DNA


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

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  • (PMID = 16020484.001).
  • [ISSN] 0888-8809
  • [Journal-full-title] Molecular endocrinology (Baltimore, Md.)
  • [ISO-abbreviation] Mol. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenergic alpha-1 Receptor Antagonists; 0 / Adrenergic alpha-Antagonists; 0 / Antineoplastic Agents; 0 / I-kappa B Proteins; 0 / NF-kappa B; 0 / Receptors, Adrenergic, alpha-1; 0 / Tumor Necrosis Factor-alpha; 139874-52-5 / NF-kappaB inhibitor alpha; 66796-54-1 / Pro-Opiomelanocortin; 9002-60-2 / Adrenocorticotropic Hormone; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases; NW1291F1W8 / Doxazosin
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64. Kovacs K, Horvath E: Effects of medical therapy on pituitary tumors. Ultrastruct Pathol; 2005 May-Aug;29(3-4):163-7
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  • [Title] Effects of medical therapy on pituitary tumors.
  • Previously surgery and irradiation were the only available procedures to treat patients with pituitary tumors.
  • This paper summarizes the effect of medical therapy on the morphologic features of pituitary tumors and illustrates the ultrastructural alterations on electron micrographs.
  • Currently drugs can be used in the management of pituitary tumors secreting GH, PRL, and/or TSH in excess.
  • No medical therapy is available so far for ACTH-, FSH-, LH-, or alpha-subunit-secreting tumors as well as non-hormone-secreting pituitary tumors.
  • Dopamine agonists are effective in the management of PRL-secreting tumors; they cause marked reversible tumor shrinkage in the substantial majority of patients.
  • Long-acting somatostatin analogs are useful in the management of GH- and TSH-secreting pituitary tumors; they lead to mild to moderate tumor shrinkage in approximately 50% of cases.
  • Recently GH receptor blockers (pegvisomant) were introduced in the treatment of GH-producing pituitary adenomas.
  • To the authors' knowledge the effect of these drugs on the morphology of pituitary tumors has not been revealed so far.
  • [MeSH-major] Dopamine Agonists / therapeutic use. Human Growth Hormone / analogs & derivatives. Octreotide / therapeutic use. Pituitary Neoplasms / drug therapy

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  • (PMID = 16036872.001).
  • [ISSN] 0191-3123
  • [Journal-full-title] Ultrastructural pathology
  • [ISO-abbreviation] Ultrastruct Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dopamine Agonists; 0 / pegvisomant; 12629-01-5 / Human Growth Hormone; 9002-62-4 / Prolactin; 9002-71-5 / Thyrotropin; RWM8CCW8GP / Octreotide
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65. Kreutzer J, Jeske I, Hofmann B, Blumcke I, Fahlbusch R, Buchfelder M, Buslei R: 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. Clin Neuropathol; 2009 Nov-Dec;28(6):430-9
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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.
  • 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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66. Daly AF, Jaffrain-Rea ML, Ciccarelli A, Valdes-Socin H, Rohmer V, Tamburrano G, Borson-Chazot C, Estour B, Ciccarelli E, Brue T, Ferolla P, Emy P, Colao A, De Menis E, Lecomte P, Penfornis F, Delemer B, Bertherat J, Wémeau JL, De Herder W, Archambeaud F, Stevenaert A, Calender A, Murat A, Cavagnini F, Beckers A: Clinical characterization of familial isolated pituitary adenomas. J Clin Endocrinol Metab; 2006 Sep;91(9):3316-23
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  • [Title] Clinical characterization of familial isolated pituitary adenomas.
  • CONTEXT: Familial pituitary adenomas occur rarely in the absence of multiple endocrine neoplasia type 1 (MEN1) and Carney complex (CNC).
  • OBJECTIVE: Our objective was to characterize the clinical and genealogical features of non-MEN1/CNC familial isolated pituitary adenomas (FIPA).
  • RESULTS: Sixty-four FIPA families including 138 affected individuals were identified [55 prolactinomas, 47 somatotropinomas, 28 nonsecreting adenomas (NS), and eight ACTH-secreting tumors].
  • A single tumor phenotype occurred in 30 families (homogeneous), and heterogeneous phenotypes occurred in 34 families.
  • [MeSH-major] Adenoma / genetics. Adenoma / pathology. Pituitary Neoplasms / genetics. Pituitary Neoplasms / pathology
  • [MeSH-minor] Adrenocorticotropic Hormone / secretion. Adult. Cyclic AMP-Dependent Protein Kinase RIalpha Subunit. Cyclic AMP-Dependent Protein Kinases / genetics. Female. Gonadotropins, Pituitary / metabolism. Humans. Immunohistochemistry. Male. Middle Aged. Pedigree. Pituitary Hormones, Anterior / metabolism. Prolactinoma / genetics. Prolactinoma / pathology. Retrospective Studies. Sequence Analysis, DNA

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  • (PMID = 16787992.001).
  • [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; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit; 0 / Gonadotropins, Pituitary; 0 / PRKAR1A protein, human; 0 / Pituitary Hormones, Anterior; 9002-60-2 / Adrenocorticotropic Hormone; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases
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67. Lupi I, Manetti L, Caturegli P, Menicagli M, Cosottini M, Iannelli A, Acerbi G, Bevilacqua G, Bogazzi F, Martino E: Tumor infiltrating lymphocytes but not serum pituitary antibodies are associated with poor clinical outcome after surgery in patients with pituitary adenoma. J Clin Endocrinol Metab; 2010 Jan;95(1):289-96
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  • [Title] Tumor infiltrating lymphocytes but not serum pituitary antibodies are associated with poor clinical outcome after surgery in patients with pituitary adenoma.
  • CONTEXT: Serum pituitary antibodies (Pit Abs) and tumor-infiltrating lymphocytes (TILs) have been described in pituitary adenomas, but their clinical significance remains unknown.
  • OBJECTIVE: The objective of the study was to assess Pit Abs and TILs prevalence in pituitary adenomas and their influence on clinical outcome.
  • PATIENTS AND SETTING: Two hundred ninety-one pituitary adenoma cases (110 non-secreting, 30 ACTH-69 GH-71 prolactin- and 13 TSH-secreting adenoma; 177 operated and 114 untreated), 409 healthy controls, and 14 autoimmune hypophysitis were enrolled in a tertiary referral center.
  • MAIN OUTCOME MEASURE: Clinical response of pituitary adenoma after surgery was evaluated.
  • Similarly, TILs prevalence was higher in adenomas than normal pituitary (P = 0.01) and lower than in autoimmune hypophysitis (P < 0.0001).
  • Multivariate regression analysis identified the presence of TILs as independent prognostic factor for persistence/recurrence of pituitary adenoma.
  • CONCLUSIONS: TILs and Pit Abs are present in a significant number of pituitary adenoma patients.

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  • (PMID = 19875479.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R21 DK080351; United States / NIDDK NIH HHS / DK / DK080351
  • [Publication-type] Evaluation Studies; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Autoantibodies; 0 / Biomarkers
  • [Other-IDs] NLM/ PMC2805498
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68. Johnson MD, Fan X, Bourne P, Walters D: Neuronal differentiation and expression of neural epitopes in pituitary adenomas. J Histochem Cytochem; 2007 Dec;55(12):1265-71
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  • [Title] Neuronal differentiation and expression of neural epitopes in pituitary adenomas.
  • In this study we performed a retrospective morphological and immunohistochemical analysis of neurofilament, phosphoneurofilament, Neu-N, class III tubulin, and Hu in WHO grade I pituitary adenomas.
  • Limited numbers of cells with neuronal features and neuron-associated epitopes may be more common in pituitary adenomas than previously recognized.
  • [MeSH-major] Adenoma / metabolism. Biomarkers, Tumor / biosynthesis. Epitopes. Neurons / metabolism. Pituitary Neoplasms / metabolism
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / metabolism. ACTH-Secreting Pituitary Adenoma / pathology. Adult. Aged. Aged, 80 and over. Antibodies. Cell Differentiation. Female. Gonadotrophs / metabolism. Gonadotrophs / pathology. Human Growth Hormone / metabolism. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Staging. Prolactin / metabolism. Prolactinoma / metabolism. Prolactinoma / pathology. Retrospective Studies

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  • (PMID = 17875653.001).
  • [ISSN] 0022-1554
  • [Journal-full-title] The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society
  • [ISO-abbreviation] J. Histochem. Cytochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Biomarkers, Tumor; 0 / Epitopes; 12629-01-5 / Human Growth Hormone; 9002-62-4 / Prolactin
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69. Iino K, Oki Y, Yamashita M, Matsushita F, Hayashi C, Yogo K, Nishizawa S, Yamada S, Maekawa M, Sasano H, Nakamura H: Possible relevance between prohormone convertase 2 expression and tumor growth in human adrenocorticotropin-producing pituitary adenoma. J Clin Endocrinol Metab; 2010 Aug;95(8):4003-11
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  • [Title] Possible relevance between prohormone convertase 2 expression and tumor growth in human adrenocorticotropin-producing pituitary adenoma.
  • CONTEXT: Methods for preoperative diagnosis of prohormone convertase 2 (PC2)-positive ACTH-producing pituitary adenomas (APPAs) have not been established.
  • CONCLUSIONS: Our study suggests that PC2 expression and Akt phosphorylation are related at the molecular level, resulting in a change in cell cycle and an increase in pituitary adenoma size.
  • An elevation of plasma alphaMSH could conjecture the activation of the phosphatidylinositol 3/Akt cascade in PC2-positive APPAs and may become a valuable clinical marker of tumor growth in Cushing's disease.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / metabolism. Adenoma / metabolism. Proprotein Convertase 2 / metabolism. alpha-MSH / blood

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  • (PMID = 20501680.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 581-05-5 / alpha-MSH; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 3.4.21.94 / Proprotein Convertase 2
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70. Hu SM, Li F, Yu HM, Li RY, Ma QY, Ye TJ, Lu ZY, Chen JL, Song HD: The mimecan gene expressed in human pituitary and regulated by pituitary transcription factor-1 as a marker for diagnosing pituitary tumors. J Clin Endocrinol Metab; 2005 Dec;90(12):6657-64
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The mimecan gene expressed in human pituitary and regulated by pituitary transcription factor-1 as a marker for diagnosing pituitary tumors.
  • OBJECTIVE: We hypothesize that the mimecan gene expressed in the human pituitary and regulated by pituitary transcription factor-1 (Pit-1) might act as a marker for diagnosing pituitary tumors.
  • SETTING AND PATIENTS: In total, 20 pituitary tumor samples were collected from January 1, 2002, to December 30, 2002, in Ruijin Hospital, Shanghai, China.
  • INTERVENTION: The number of pituitary tumors was limited.
  • Collection of more pituitary tumor samples for additional observation will be necessary.
  • RESULTS: The mimecan gene was expressed at a moderate level in the mouse pituitary gland by Northern blot analysis.
  • Expression of mimecan mRNA and protein is also observed in the human anterior pituitary gland.
  • In addition, our data also show that almost all the ACTH- or GH-positive pituitary tumors likely express mimecan protein, and only a portion of prolactin-, TSH-, FSH-, and LH-positive pituitary tumors express mimecan protein.
  • CONCLUSIONS: This work provides insight into the regulating mechanism of mimecan in pituitary and suggests that mimecan may be an unidentified pituitary secretory protein, and certain pituitary cells secreting ACTH or GH also secrete mimecan.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Gene Expression Regulation. Glycoproteins / genetics. Pituitary Gland / metabolism. Pituitary Neoplasms / diagnosis. Transcription Factor Pit-1 / physiology

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  • (PMID = 16189248.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Glycoproteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / OGN protein, human; 0 / Ogn protein, mouse; 0 / Transcription Factor Pit-1
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71. Netea-Maier RT, van Lindert EJ, den Heijer M, van der Eerden A, Pieters GF, Sweep CG, Grotenhuis JA, Hermus AR: Transsphenoidal pituitary surgery via the endoscopic technique: results in 35 consecutive patients with Cushing's disease. Eur J Endocrinol; 2006 May;154(5):675-84
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  • [Title] Transsphenoidal pituitary surgery via the endoscopic technique: results in 35 consecutive patients with Cushing's disease.
  • OBJECTIVE AND DESIGN: The endoscopic technique has been recently introduced in the field of transsphenoidal pituitary surgery.
  • This technique allows inspection of sellar, supra- and parasellar structures and removal of the tumor under direct visualization, is minimally traumatic and permits easier reoperations.
  • Our aim was to retrospectively analyze the results of pituitary surgery in 35 consecutive patients with Cushing's disease operated in our hospital after the introduction of the endoscopic technique (1998-2004).
  • RESULTS: Pituitary MRI showed a macroadenoma in 6 patients, a microadenoma in 17 patients and no adenoma in 12 patients.
  • Three of them had a second endoscopic pituitary surgery resulting in remission in two patients.
  • In one patient a second endoscopic pituitary surgery will soon follow.
  • CONCLUSIONS: Endoscopic transsphenoidal pituitary surgery resulted in our series of patients with Cushings disease in an excellent postoperative remission rate.
  • A randomized clinical trial, comparing endoscopic and conventional pituitary surgery in patients with Cushings disease, is needed to determine the pros and cons of both techniques.

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  • (PMID = 16645014.001).
  • [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] WI4X0X7BPJ / Hydrocortisone
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72. Mannelli M, Cantini G, Poli G, Mangoni M, Nesi G, Canu L, Rapizzi E, Borgogni E, Ercolino T, Piccini V, Luconi M: Role of the PPAR-γ system in normal and tumoral pituitary corticotropic cells and adrenal cells. Neuroendocrinology; 2010;92 Suppl 1:23-7
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  • [Title] Role of the PPAR-γ system in normal and tumoral pituitary corticotropic cells and adrenal cells.
  • In this minireview, we summarize the current knowledge on PPAR-γ in normal and tumoral corticotropic pituitary and adrenal cells.
  • The receptor expression has been shown in ACTH-secreting cells in both normal and adenomal pituitary as well as in normal and tumor adrenal cortex.
  • Preclinical studies conducted both in vitro on tumor cells and in vivo on xenograft tumor models obtained by subcutaneous injection of cancer cells have evidenced the anticancer properties of TZD, in particular rosiglitazone (RGZ) and pioglitazone (PIO).
  • In both pituitary and adrenocortical cancer, RGZ treatment results in inhibition of cell proliferation, through G0/G1 cell-cycle arrest and induction of cell apoptosis, leading to significant inhibition of tumor growth in the xenograft tumor models.
  • In addition, since RGZ can reduce ACTH and corticosterone secretion in mouse corticotropic pituitary tumors, both RGZ and PIO have been used in the treatment of Cushing's disease with variable but generally unsatisfactory results.
  • [MeSH-major] Adrenal Cortex / metabolism. Corticotrophs / metabolism. PPAR gamma / metabolism. Pituitary ACTH Hypersecretion / metabolism. Pituitary Gland / metabolism
  • [MeSH-minor] Adrenal Cortex Neoplasms / drug therapy. Adrenal Cortex Neoplasms / metabolism. Humans. Pituitary Neoplasms / drug therapy. Pituitary Neoplasms / metabolism. Thiazolidinediones / therapeutic use

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  • [Copyright] Copyright © 2010 S. Karger AG, Basel.
  • (PMID = 20829614.001).
  • [ISSN] 1423-0194
  • [Journal-full-title] Neuroendocrinology
  • [ISO-abbreviation] Neuroendocrinology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / PPAR gamma; 0 / Thiazolidinediones; X4OV71U42S / pioglitazone
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73. Kovacs K, Horvath E, Coire C, Cusimano M, Smyth H, Scheithauer BW, Lloyd RV: Pituitary corticotroph hyperplasia preceding adenoma in a patient with Nelson's syndrome. Clin Neuropathol; 2006 Mar-Apr;25(2):74-80
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  • [Title] Pituitary corticotroph hyperplasia preceding adenoma in a patient with Nelson's syndrome.
  • 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.
  • [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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74. Weil RJ, Vortmeyer AO, Nieman LK, Devroom HL, Wanebo J, Oldfield EH: Surgical remission of pituitary adenomas confined to the neurohypophysis in Cushing's disease. J Clin Endocrinol Metab; 2006 Jul;91(7):2656-64
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  • [Title] Surgical remission of pituitary adenomas confined to the neurohypophysis in Cushing's disease.
  • CONTEXT: Partial or total removal of the pituitary cures 60-80% of patients with Cushing's disease (CD) in whom an adenoma cannot be identified at surgery.
  • Tumor was visible at surgery in 11 patients; all 12 tumors were positive for ACTH by immunohistochemistry.
  • CONCLUSION: We report a new subset of patients with CD, ACTH-secreting adenomas that arise wholly within the posterior lobe of the pituitary gland.
  • In cases of CD in which an adenoma is not identified in the adenohypophysis and in patients with persistent hypercortisolism after complete or partial excision of the anterior lobe, tumor within the neurohypophysis should be considered; selective adenomectomy of a neurohypophyseal, ACTH-secreting tumor can produce long-term remission.
  • [MeSH-major] Adenoma / surgery. Pituitary ACTH Hypersecretion / surgery. Pituitary Gland, Posterior / surgery. Pituitary Neoplasms / surgery

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  • (PMID = 16636117.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone
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75. Kobayashi T: Long-term results of stereotactic gamma knife radiosurgery for pituitary adenomas. Specific strategies for different types of adenoma. Prog Neurol Surg; 2009;22:77-95
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  • [Title] Long-term results of stereotactic gamma knife radiosurgery for pituitary adenomas. Specific strategies for different types of adenoma.
  • Long-term results of gamma knife radiosurgery for pituitary adenomas are presented and treatment strategies for different adenoma types are discussed.
  • Two hundred and sixty-seven patients with pituitary adenoma have been treated by gamma knife radiosurgery during the past 12 years.
  • There were 131 cases of nonfunctioning and 136 cases of functioning adenomas, in which 71 GH-producing, 33 PRL-producing and 32 ACTH-producing adenomas were included.
  • Surgical or chemical debulking was necessary before radiosurgery for a large tumor with extrasellar extension.
  • Cushing disease showed the best response because of the smallest tumor size with the highest dose treatment.
  • High-dose treatment was necessary for functioning adenomas to control tumor growth and oversecretion of hormones.
  • In conclusion, gamma knife radiosurgery was effective and safe for the treatment of pituitary adenomas.
  • However, the treatment strategies should be specific to each adenoma type according to the radiosensitivity, chemosensitivity and biological nature of the tumor.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / surgery. Acromegaly / surgery. Adenoma / surgery. Radiosurgery
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Child. Female. Follow-Up Studies. Growth Hormone-Secreting Pituitary Adenoma / pathology. Growth Hormone-Secreting Pituitary Adenoma / surgery. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Patient Satisfaction. Pituitary ACTH Hypersecretion / pathology. Pituitary ACTH Hypersecretion / surgery. Prolactinoma / pathology. Prolactinoma / surgery. Treatment Outcome. Young Adult

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  • (PMID = 18948721.001).
  • [ISSN] 0079-6492
  • [Journal-full-title] Progress in neurological surgery
  • [ISO-abbreviation] Prog Neurol Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
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76. Salgado LR, Machado MC, Cukiert A, Liberman B, Kanamura CT, Alves VA: Cushing's disease arising from a clinically nonfunctioning pituitary adenoma. Endocr Pathol; 2006;17(2):191-9
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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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77. Revill K, Dudley KJ, Clayton RN, McNicol AM, Farrell WE: Loss of neuronatin expression is associated with promoter hypermethylation in pituitary adenoma. Endocr Relat Cancer; 2009 Jun;16(2):537-48
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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.
  • In addition, we determined associations between expression and CpG island methylation and used colony forming efficiency assays (CFE) to gain further insight into the tumour-suppressor function of this gene.
  • Immunohistochemical (IHC) co-localization studies of normal pituitaries showed that each of the hormone secreting cells (GH, PRL, ACTH, FSH and TSH) expressed NNAT.
  • 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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78. Pandey P, Ojha BK, Mahapatra AK: Pediatric pituitary adenoma: a series of 42 patients. J Clin Neurosci; 2005 Feb;12(2):124-7
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  • [Title] Pediatric pituitary adenoma: a series of 42 patients.
  • Pituitary adenomas are uncommon in childhood.
  • This report describes the presentation, endocrinological profile, management and outcome of 42 children with pituitary adenomas.
  • Amongst the functioning tumors, there were 20 patients (47.6%) with prolactinomas, 11 patients (26.2%) with Cushing's disease and nine patients (21.4%) with growth hormone (GH)-secreting adenomas.
  • Transsphenoidal tumor decompression was performed in most cases (71.4%).
  • Of these, 89% of the children with GH-secreting tumors and 100% of the children with Cushing's disease achieved remission.
  • We conclude that the transsphenoidal approach is effective and safe in surgery for pituitary adenomas in children and is the procedure of choice if there is no contraindication.
  • [MeSH-major] Adenoma. Pituitary Neoplasms
  • [MeSH-minor] Adolescent. Child. Female. Humans. Male. Pituitary ACTH Hypersecretion / etiology

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  • (PMID = 15749410.001).
  • [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
  • [Publication-country] Scotland
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79. Bangaru ML, Woodliff J, Raff H, Kansra S: Growth suppression of mouse pituitary corticotroph tumor AtT20 cells by curcumin: a model for treating Cushing's disease. PLoS One; 2010;5(4):e9893
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  • [Title] Growth suppression of mouse pituitary corticotroph tumor AtT20 cells by curcumin: a model for treating Cushing's disease.
  • BACKGROUND: Pituitary corticotroph tumors secrete excess adrenocorticotrophic hormone (ACTH) resulting in Cushing's disease (CD).
  • Standard treatment includes surgery and, if not successful, radiotherapy, both of which have undesirable side effects and frequent recurrence of the tumor.
  • Our laboratory recently demonstrated that curcumin inhibited growth and induced apoptosis in prolactin- and growth hormone-producing tumor cells.
  • Subsequently, Schaaf et.al. confirmed our findings and also showed the in vivo effectiveness of curcumin to suppress pituitary tumorigenesis.
  • PRINCIPAL FINDINGS: Using the mouse corticotroph tumor cells, AtT20 cells, we report that curcumin had a robust, irreversible inhibitory effect on cell proliferation and clonogenic property.
  • Finally, curcumin had a concentration-dependent suppressive effect on ACTH secretion from AtT20 cells.
  • CONCLUSION: The ability of curcumin to inhibit NFkappaB and induce apoptosis in pituitary corticotroph tumor cells leads us to propose developing it as a novel therapeutic agent for the treatment of CD.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / drug therapy. Cell Proliferation / drug effects. Curcumin / pharmacology. Pituitary ACTH Hypersecretion / drug therapy
  • [MeSH-minor] Adrenocorticotropic Hormone / secretion. Animals. Antineoplastic Agents. Apoptosis / drug effects. Cell Line, Tumor. Dose-Response Relationship, Drug. Mice. NF-kappa B / antagonists & inhibitors

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  • [ErratumIn] PLoS One. 2010;5(4). doi:10.1371/annotation/38a101d6-a1f2-4a74-ab63-bc5c61e5f62b
  • (PMID = 20405005.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / NF-kappa B; 9002-60-2 / Adrenocorticotropic Hormone; IT942ZTH98 / Curcumin
  • [Other-IDs] NLM/ PMC2854133
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80. Gondim JA, Schops M, de Almeida JP, de Albuquerque LA, Gomes E, Ferraz T, Barroso FA: Endoscopic endonasal transsphenoidal surgery: surgical results of 228 pituitary adenomas treated in a pituitary center. Pituitary; 2010;13(1):68-77
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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.
  • 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
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81. Gejman R, Batista DL, Zhong Y, Zhou Y, Zhang X, Swearingen B, Stratakis CA, Hedley-Whyte ET, Klibanski A: Selective loss of MEG3 expression and intergenic differentially methylated region hypermethylation in the MEG3/DLK1 locus in human clinically nonfunctioning pituitary adenomas. J Clin Endocrinol Metab; 2008 Oct;93(10):4119-25
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  • [Title] Selective loss of MEG3 expression and intergenic differentially methylated region hypermethylation in the MEG3/DLK1 locus in human clinically nonfunctioning pituitary adenomas.
  • CONTEXT: MEG3 is an imprinted gene encoding a novel noncoding RNA that suppresses tumor cell growth.
  • Although highly expressed in the normal human pituitary, it is unknown which of the normal pituitary cell types and pituitary tumors express MEG3.
  • OBJECTIVES: Our objectives were 1) to investigate cell-type- and tumor-type-specific expression of MEG3 in the human pituitary and 2) to investigate whether methylation in the intergenic differentially methylated region (IG-DMR) at the DLK1/MEG3 locus is involved in the loss of MEG3 expression in tumors.
  • DESIGN AND METHODS: RT-PCR, quantitative RT-PCR, Northern blot, and a combination of in situ hybridization and immunofluorescence were used to determine the cell-type- and tumor-type-specific MEG3 expression.
  • Bisulfite treatment and PCR sequencing of genomic DNA were used to measure the CpG methylation status in the normal and tumor tissues.
  • Five normal human pituitaries and 17 clinically nonfunctioning, 11 GH-secreting, seven prolactin-secreting, and six ACTH-secreting pituitary adenomas were used.
  • RESULTS: All normal human pituitary cell types express MEG3.
  • However, loss of MEG3 expression occurs only in nonfunctioning pituitary adenomas of a gonadotroph origin.
  • All other pituitary tumor phenotypes examined express MEG3.
  • Hypermethylation of the IG-DMR at the DLK1/MEG3 locus is present in nonfunctioning pituitary adenomas.
  • CONCLUSIONS: MEG3 is the first human gene identified expressed in multiple normal human pituitary cell types with loss of expression specifically restricted to clinically nonfunctioning pituitary adenomas.

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  • (PMID = 18628527.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK040947; United States / NIDDK NIH HHS / DK / R01 DK-40947
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DLK1 protein, human; 0 / DNA, Intergenic; 0 / Intercellular Signaling Peptides and Proteins; 0 / MEG3 non-coding RNA, human; 0 / Membrane Proteins; 0 / Proteins; 0 / RNA, Long Noncoding
  • [Other-IDs] NLM/ PMC2579639
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82. Shah NA, Urusova IA, D'Agnolo A, Colquhoun SD, Rosenbloom BE, Vener SL, Geller SA, Younes M, Lechago J, Heaney AP: Primary hepatic carcinoid tumor presenting as Cushing's syndrome. J Endocrinol Invest; 2007 Apr;30(4):327-33
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  • [Title] Primary hepatic carcinoid tumor presenting as Cushing's syndrome.
  • ACTH-producing carcinoid tumors most commonly originate in the lung or thymus and present insidiously with bronchospasm and/or chest mass.
  • Occasionally, ectopic ACTH syndromes have been reported in association with pancreatic islet cell tumors, medullary thyroid cancer, pheochromocytoma, small-cell lung carcinoma, and rarely, ovarian and prostate tumors.
  • We report here a patient with an ectopic ACTH-secreting primary hepatic carcinoid tumor who presented with cushingoid appearance, profound proximal muscle weakness, severe lower extremity edema, and markedly elevated urinary free cortisol.
  • ACTH levels were in the low normal range.
  • Following surgical resection of the hepatic tumor, histopathology confirmed an ACTH-secreting neuroendocrine tumor (NET), the patient had complete resolution of hypercortisolemic symptoms and remains in remission, now 4 yr after hepatic tumor resection.
  • This case reports the first ACTH-secreting primary hepatic NET presenting as ectopic Cushing's syndrome.
  • Interesting aspects of this case include the presence of a pituitary incidentaloma, the low normal ACTH, and photopenia on 18FDG-PET imaging.
  • [MeSH-major] ACTH Syndrome, Ectopic / diagnosis. Carcinoid Tumor / diagnosis. Cushing Syndrome / diagnosis. Liver Neoplasms / diagnosis


83. Morris DG, Musat M, Czirják S, Hanzély Z, Lillington DM, Korbonits M, Grossman AB: Differential gene expression in pituitary adenomas by oligonucleotide array analysis. Eur J Endocrinol; 2005 Jul;153(1):143-51
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  • [Title] Differential gene expression in pituitary adenomas by oligonucleotide array analysis.
  • OBJECTIVES: Microarray technology allows for the expression profile of many thousands of genes to be quantified at the same time, and has resulted in novel discoveries about the tumour biology of a number of cancers.
  • We sought to do this in pituitary adenomas, the most common intracranial neoplasm.
  • METHODS: Affymetrix GeneChip HG-U133A oligonucleotide arrays covering 14 500 well-characterised genes from the human genome were used to study pooled RNA for each of the four major pituitary adenoma subtypes.
  • Individual gene-expression levels in the tumours were compared relative to the expression profile in normal pooled pituitary RNA.
  • RESULTS: Bioinformatic analysis showed that 3906 genes and 351 expressed sequence tags were differentially expressed among all pituitary tumour subtypes.
  • Lysosomal-associated protein transmembrane- 4-beta (LAPTM4B), a novel gene upregulated in hepatocellular carcinoma, was significantly over-expressed in adrenocorticotrophin (ACTH)-secreting adenomas and non-functioning pituitary adenomas (NFPAs).
  • Bcl-2-associated athanogene (BAG1), an anti-apoptotic protein found at high levels in a number of human cancers, was significantly over-expressed in growth hormone-secreting and prolactin-secreting adenomas and NFPAs.
  • The cyclin-dependent kinase inhibitor p18, in which murine gene deletion has been shown to produce pituitary ACTH cell hyperplasia and adenomas, was significantly under-expressed in ACTH-secreting adenomas.
  • CONCLUSIONS: Expression array analysis of pituitary adenomas using the Affymetrix GeneChip HG-U133A arrays appears to be a valid method of identifying genes that may be important in tumour pathogenesis.

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  • (PMID = 15994756.001).
  • [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 / BCL2-associated athanogene 1 protein; 0 / CDKN2C protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p18; 0 / DNA-Binding Proteins; 0 / LAPTM4B protein, human; 0 / Membrane Proteins; 0 / Oncogene Proteins; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 9002-60-2 / Adrenocorticotropic Hormone; 9002-62-4 / Prolactin
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84. Cristina C, Perez-Millan MI, Luque G, Dulce RA, Sevlever G, Berner SI, Becu-Villalobos D: VEGF and CD31 association in pituitary adenomas. Endocr Pathol; 2010 Sep;21(3):154-60
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  • [Title] VEGF and CD31 association in pituitary adenomas.
  • Pituitary tumors are usually less vascularized than the normal pituitary, and the role of angiogenesis in these adenomas is contentious.
  • We determined the protein expression of VEGF and CD31, an endothelial marker, in a series of 56 surgically removed pituitary adenomas using Western blot assay.
  • Prolactinomas had higher VEGF protein expression compared to nonfunctioning or ACTH- and GH-secreting adenomas, while CD31 was similar in the different adenoma histotypes.
  • The positive association of VEGF and CD31 expression suggests the participation of angiogenesis in adenoma development, while epithelial cell proliferation in pituitary tumors is not directly related to VEGF or CD31 expression, and other factors, such as primary genetic alterations may be involved.
  • [MeSH-major] Adenoma / metabolism. Antigens, CD31 / biosynthesis. Biomarkers, Tumor / analysis. Pituitary Neoplasms / metabolism. Vascular Endothelial Growth Factor A / biosynthesis

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  • (PMID = 20473646.001).
  • [ISSN] 1559-0097
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD31; 0 / Biomarkers, Tumor; 0 / Vascular Endothelial Growth Factor A
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85. Hanson JM, Mol JA, Leegwater PA, Bilodeau S, Drouin J, Meij BP: Expression and mutation analysis of Tpit in the canine pituitary gland and corticotroph adenomas. Domest Anim Endocrinol; 2008 Apr;34(3):217-22
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  • [Title] Expression and mutation analysis of Tpit in the canine pituitary gland and corticotroph adenomas.
  • Pituitary-dependent hyperadrenocorticism (PDH) in dogs is caused by a pituitary corticotroph adenoma.
  • 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.
  • 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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86. Gilliot O, Khalil T, Irthum B, Zasadny X, Verrelle P, Tauveron I, Pontvert D: Radiotherapy of pituitary adenomas: state of the art. Ann Endocrinol (Paris); 2007 Oct;68(5):337-48
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Radiotherapy of pituitary adenomas: state of the art.
  • Pituitary adenomas represent approximately 12% of intracranial tumors.
  • Prolactin-secreting adenomas are first treated with dopamine agonists, and GH-secreting adenomas are first treated by surgery if excising the complete tumor is possible; otherwise medical treatment is started.
  • The first-line treatment of ACTH-secreting adenomas is surgery; however, in many cases, insufficient control of either secretion or tumoral volume leads to consideration of irradiation.
  • Because the indications of radiotherapy are still debated, irradiation of pituitary adenomas must be decided by the complete team of endocrinologists, neurosurgeons, radiologists and radiotherapists.
  • [MeSH-major] Adenoma / radiotherapy. Pituitary Neoplasms / radiotherapy

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  • (PMID = 17512895.001).
  • [ISSN] 0003-4266
  • [Journal-full-title] Annales d'endocrinologie
  • [ISO-abbreviation] Ann. Endocrinol. (Paris)
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 12629-01-5 / Human Growth Hormone; 9002-62-4 / Prolactin
  • [Number-of-references] 94
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87. Mayberg M, Vermeulen S: Advances in stereotactic radiosurgery in the treatment of pituitary adenomas. Curr Opin Endocrinol Diabetes Obes; 2007 Aug;14(4):296-300
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  • [Title] Advances in stereotactic radiosurgery in the treatment of pituitary adenomas.
  • PURPOSE OF REVIEW: Stereotactic radiosurgery has become the preferred radiation treatment modality for secreting and nonsecreting pituitary adenomas, although randomized studies comparing delivery systems, fractionation and dose have not been performed.
  • With a reduction in acute and chronic side effects, the total dose to abnormal tissue can be increased allowing for greater tumor control.
  • SUMMARY: The radiobiology, control rates and normal tissue tolerances of stereotactic radiosurgery in the treatment of pituitary adenomas is reviewed.
  • [MeSH-major] Adenoma / surgery. Pituitary Neoplasms / surgery. Radiosurgery
  • [MeSH-minor] Acromegaly / radiotherapy. Acromegaly / surgery. Humans. Pituitary ACTH Hypersecretion / radiotherapy. Pituitary ACTH Hypersecretion / surgery. Prolactinoma / surgery. Prolactinoma / therapy

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  • (PMID = 17940455.001).
  • [ISSN] 1752-2978
  • [Journal-full-title] Current opinion in endocrinology, diabetes, and obesity
  • [ISO-abbreviation] Curr Opin Endocrinol Diabetes Obes
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 18
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88. Curtò L, Torre ML, Ferraù F, Pitini V, Altavilla G, Granata F, Longo M, Hofland LJ, Trimarchi F, Cannavò S: Temozolomide-induced shrinkage of a pituitary carcinoma causing Cushing's disease--report of a case and literature review. ScientificWorldJournal; 2010;10:2132-8
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  • [Title] Temozolomide-induced shrinkage of a pituitary carcinoma causing Cushing's disease--report of a case and literature review.
  • Temozolomide (TMZ) is an alkylating chemotherapeutic agent that has recently been used in some cases as a new therapeutic tool for pituitary carcinomas and aggressive pituitary adenomas.
  • In this report, we present the case of effective TMZ treatment in a 42-year-old man with ACTH-secreting carcinoma.
  • The tumor grew progressively over 4 years, from 2.2 to 31.1 cm³, despite three surgical approaches and γ-knife treatment.
  • Thereafter, four cycles of 5-day TMZ administration (200 mg/m²/day during the first, and 150 mg/m²/day during the following cycles) induced dramatic tumor size reduction (>90%).
  • [MeSH-major] Adenoma / drug therapy. Dacarbazine / analogs & derivatives. Pituitary ACTH Hypersecretion / drug therapy. Pituitary Neoplasms / drug therapy

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  • [CommentIn] Turk Neurosurg. 2015;25(4):679-80 [26242353.001]
  • (PMID = 21057727.001).
  • [ISSN] 1537-744X
  • [Journal-full-title] TheScientificWorldJournal
  • [ISO-abbreviation] ScientificWorldJournal
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [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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89. Rudnik A, Zawadzki T, Wojtacha M, Bazowski P, Zubgałuszka-Ignasiak B, Duda I: [Endoscopic transsphenoidal treatment of pituitary adenomas]. Neurol Neurochir Pol; 2005 Jan-Feb;39(1):17-23; discussion 24-5
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  • [Title] [Endoscopic transsphenoidal treatment of pituitary adenomas].
  • BACKGROUND AND PURPOSE: The aim of this study is to present a new endoscopic transnasal transsphenoidal method of surgical treatment of pituitary adenomas and to evaluate the results and complications of the method.
  • MATERIAL AND SURGICAL TECHNIQUE: From October 2001 to June 2003 in the Department of Neurosurgery of the Medical University of Silesia in Katowice 88 operations of pituitary adenomas were performed using the transnasal transsphenoidal endoscopic method.
  • RESULTS: In the group of 51 nonfunctioning adenomas, in 32 cases we obtained the total removal of the tumor, which amounts to 63%.
  • Among 37 of hyperfunctioning adenomas there were 11 prolactinomas, 19 GH secreting adenomas and 7 ACTH secreting adenomas.
  • In all cases of prolactinomas the tumor was removed totally and in the cases of GH secreting adenomas and ACTH secreting adenomas the total removal of the tumor was performed in 58% and 86% of the cases, respectively.
  • CONCLUSIONS: The endoscopic transnasal transsphenoidal approach is an efficient method of surgical treatment of pituitary adenomas.
  • [MeSH-major] Adenoma / surgery. Hypophysectomy / methods. Neuroendoscopy. Pituitary Neoplasms / surgery. Sphenoid Sinus / surgery
  • [MeSH-minor] Adolescent. Adult. Aged. Cavernous Sinus / surgery. Female. Humans. Male. Middle Aged. Neoplasm Invasiveness. Poland. Retrospective Studies. Time Factors. Treatment Outcome

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  • (PMID = 15735985.001).
  • [ISSN] 0028-3843
  • [Journal-full-title] Neurologia i neurochirurgia polska
  • [ISO-abbreviation] Neurol. Neurochir. Pol.
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Poland
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90. Zhang HW, Sun W, Yang J, Yan CX, Yu CJ: Diagnosis and treatment of pituitary microadenoma: report of 80 cases. Neurol Res; 2008 Jul;30(6):587-93
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  • [Title] Diagnosis and treatment of pituitary microadenoma: report of 80 cases.
  • OBJECTIVE: To analyse and discuss the diagnosis and treatment of pituitary microadenoma.
  • SUBJECTS AND METHODS: Eighty cases of pituitary microadenoma treated with transsphenoidal approach in our department were analysed retrospectively during the last 2 years.
  • RESULTS: During following-up of 13.0+/-3.2 months, neither remained tumor was found except one patients with microprolactinoma, nor recurrence.
  • Thirteen of 15 patients (86.7%) with ACTH-secreting microadenoma achieved chemical remission judged by plasma cortisol levels<or=2 microg/dl within 72 hours of surgery.
  • CONCLUSIONS:. (1) Transsphenoidal surgery (TSS) is safe and effective treatment for pituitary microadenoma;.
  • (2) TSS is considered to be definitive treatment for ACTH- and GH-secreting microadenoma once the diagnosis is established;.
  • (3) in order to obtain better effects, TSS could be offered as first-line treatment for patients with locally non-invasive PRL-secreting microadenoma (tumor larger than 3 mm in diameter) and non-functioning microadenoma.
  • [MeSH-major] Adenoma / diagnosis. Adenoma / therapy. Pituitary Neoplasms / diagnosis. Pituitary Neoplasms / therapy

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  • (PMID = 18647498.001).
  • [ISSN] 0161-6412
  • [Journal-full-title] Neurological research
  • [ISO-abbreviation] Neurol. Res.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone; 9002-62-4 / Prolactin
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91. Saeger W: [Effects of irradiation therapy and inhibiting drugs on the pituitary and its adenomas]. Pathologe; 2006 Feb;27(1):57-60
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  • [Title] [Effects of irradiation therapy and inhibiting drugs on the pituitary and its adenomas].
  • Radiation therapies of pituitary adenomas induce an increase in fibroses and nuclear pleomorphism.
  • Most growth hormone (GH) secreting pituitary adenomas react to somatostatin analogues by a distinct decrease of GH secretion.
  • Some cases show a shrinkage of adenomas that correlates with fibrosis of the tumor.
  • With these drugs, thyroid stimulating hormone secreting adenomas can also be treated.
  • Prolactin secreting adenomas are mostly treated primarily with dopamine agonists.
  • Long-term medication with high doses of glucocorticoids induces Crooke's cells in the anterior pituitary.
  • These are suppressed ACTH cells and characterized by increased numbers of large lysosomes and dense bundles of cytofilaments.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Pituitary Gland / pathology. Pituitary Neoplasms / drug therapy. Pituitary Neoplasms / radiotherapy. Radiotherapy / adverse effects

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  • (PMID = 16362259.001).
  • [ISSN] 0172-8113
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Dopamine Agonists; 0 / Glucocorticoids
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92. Paez-Pereda M, Giacomini D, Echenique C, Stalla GK, Holsboer F, Arzt E: Signaling processes in tumoral neuroendocrine pituitary cells as potential targets for therapeutic drugs. Curr Drug Targets Immune Endocr Metabol Disord; 2005 Sep;5(3):259-67
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  • [Title] Signaling processes in tumoral neuroendocrine pituitary cells as potential targets for therapeutic drugs.
  • Pituitary adenomas are neuroendocrine tumors that produce different endocrine and metabolic alterations, including hyperprolactinemia, acromegaly and Cushing's disease.
  • These different clinical features of pituitary tumors are the result of the overproduction of hormones produced by the different pituitary cell types.
  • Recent advances in the understanding of the signaling pathways that control hormone production in pituitary cells provide a source of potential therapeutic targets.
  • In ACTH-secreting cells, the mechanisms that control hormone biosynthesis have been clarified to a great extent, indicating a number of protein kinases and ligand-activated nuclear receptors as targets for experimental drugs.
  • ACTH production requires the activation of signal transduction through the PKA, the MAPK and the CamK pathways.
  • The inhibition of these kinases and nuclear receptors has been shown to produce therapeutic effects in mouse models of Cushing's syndrome.
  • It has been recently shown that 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.
  • The inhibition of both of these pathways results in the decrease of tumor growth in animal models of prolactinoma.
  • Therefore, the study of signaling pathways that control hormone production and proliferation is a good source of candidate targets in pituitary tumors.
  • [MeSH-major] Neurosecretory Systems / drug effects. Neurosecretory Systems / physiology. Pituitary Neoplasms / drug therapy. Pituitary Neoplasms / physiopathology. Signal Transduction / drug effects

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  • (PMID = 16178787.001).
  • [ISSN] 1568-0088
  • [Journal-full-title] Current drug targets. Immune, endocrine and metabolic disorders
  • [ISO-abbreviation] Curr. Drug Targets Immune Endocr. Metabol. Disord.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cytokines; 0 / Receptors, Cytokine; 0 / Transforming Growth Factor beta; 9002-60-2 / Adrenocorticotropic Hormone; 9002-62-4 / Prolactin
  • [Number-of-references] 77
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93. Maïza JC, Caron P: [Pituitary carcinomas and aggressive adenomas: an overview and new therapeutic options]. Ann Endocrinol (Paris); 2009 Sep;70 Suppl 1:S12-9
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  • [Title] [Pituitary carcinomas and aggressive adenomas: an overview and new therapeutic options].
  • Pituitary carcinomas are a rare disease with an estimated prevalence around 0.2 % of the pituitary tumours.
  • They are defined by the presence of intra or extra-cranial metastases but initially they can share the same features as aggressive pituitary adenomas.
  • The majority of carcinomas are prolactin or ACTH-secreting tumors.
  • Carcinomas require often repeated surgery and radiotherapy fail to control the tumor.
  • [MeSH-major] Adenoma / therapy. Pituitary Neoplasms / therapy

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  • (PMID = 19878763.001).
  • [ISSN] 0003-4266
  • [Journal-full-title] Annales d'endocrinologie
  • [ISO-abbreviation] Ann. Endocrinol. (Paris)
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents
  • [Number-of-references] 36
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94. Oldfield EH, Vortmeyer AO: Development of a histological pseudocapsule and its use as a surgical capsule in the excision of pituitary tumors. J Neurosurg; 2006 Jan;104(1):7-19
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  • [Title] Development of a histological pseudocapsule and its use as a surgical capsule in the excision of pituitary tumors.
  • OBJECT: The presence of a histological pseudocapsule around pituitary tumors was noted in the early 1900s.
  • Since that time there has been no emphasis on the sequence of the stages of its development or on the relationship between these stages and the capacity to identify very small pituitary tumors at surgery in patients in whom preoperative imaging has been nondiagnostic.
  • In addition, limited emphasis has been given to the pseudocapsule's use for selective and complete resection of pituitary adenomas.
  • METHODS: The development of the pseudocapsule was examined by performing histological analysis of portions of pituitary glands removed during 805 operations for Cushing disease.
  • Twenty-five adenomas, each measuring between 0.25 and 4 mm in maximum diameter, were detected in the excised specimens; 17 were adenocorticotropic hormone-positive adenomas and eight were incidental tumors (four prolactin-secreting and four nonsecreting lesions).
  • The distribution of tumor size in relation to the presence of a histological pseudocapsule indicates a transition from the absence of a reticulin capsule (tumor diameter < or =1 mm) through the initial compression of surrounding tissue (tumor diameter 1-2 mm) to the presence of a multilayered reticulin capsule observed when adenomas become larger (tumor diameter 2-3 mm).
  • CONCLUSIONS: The absence of a reticulin capsule in cases of very small tumors may contribute to limited localization of these lesions during surgical exploration of the pituitary gland.
  • In this article the authors describe surgical techniques in which the histological pseudocapsule is used as a surgical capsule during pituitary surgery.
  • In their experience, recognition of this surgical capsule and its use at surgery has contributed to the identification of microadenomas buried in the pituitary gland, aided the recognition of subtle invasion of the pituitary capsule and contiguous dura mater, and enhanced the consistency of complete tumor excision with small and large tumors.
  • [MeSH-major] Adenoma / complications. Adenoma / pathology. Neurosurgical Procedures / methods. Pituitary Gland / pathology. Pituitary Neoplasms / complications. Pituitary Neoplasms / pathology
  • [MeSH-minor] Humans. Pituitary ACTH Hypersecretion / etiology. Pituitary ACTH Hypersecretion / surgery. Retrospective Studies

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  • [CommentIn] J Neurosurg. 2006 Jan;104(1):1-2; discussison 2-3 [16509140.001]
  • (PMID = 16509142.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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95. Bogazzi F, Russo D, Locci MT, Chifenti B, Ultimieri F, Raggi F, Viacava P, Cecchetti D, Cosci C, Sardella C, Acerbi G, Gasperi M, Martino E: Peroxisome proliferator-activated receptor (PPAR)gamma is highly expressed in normal human pituitary gland. J Endocrinol Invest; 2005 Nov;28(10):899-904
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  • [Title] Peroxisome proliferator-activated receptor (PPAR)gamma is highly expressed in normal human pituitary gland.
  • OBJECTIVE: Expression of peroxisome proliferator-activated receptor (PPAR)gamma in normal pituitary seems to be restricted to ACTH-secreting cells.
  • The aim of the study was to evaluate the expression of PPARgamma in normal human pituitary tissue and to study its localization in the pituitary secreting cells.
  • MATERIALS AND METHODS: Normal pituitary tissue samples were obtained form 11 patients with non-secreting adenoma who underwent surgical excision of the tumor.
  • Expression of PPARgamma was evaluated by immunostaining and western blotting; localization of PPARgamma in each pituitary secreting cell lineage was evaluated by double immunofluorescence using confocal microscopy.
  • Pituitary non-functioning adenomas served as Controls.
  • RESULTS: PPARgamma was highly expressed in all pituitary samples with a (mean +/- SD) 81 +/- 6.5% of stained cells; expression of PPARgamma was confirmed by western blotting.
  • Non-functioning pituitary adenomas had 74 +/- 11% PPARgamma positive cells.
  • Double immunostaining revealed that every pituitary secreting cell (GH, TSH, LH, FSH, PRL and ACTH) had PPARgamma expressed.
  • DISCUSSION: The present study demonstrated that PPARgamma is highly expressed in every normal pituitary secreting cell lineage.
  • It can translocate into the nucleus by ligand binding; however, its role in pituitary hormone regulation remains to be elucidated.
  • [MeSH-major] PPAR gamma / analysis. Pituitary Gland / chemistry
  • [MeSH-minor] Adrenocorticotropic Hormone / metabolism. Adult. Aged. Animals. Blotting, Western. Cell Line, Tumor. Female. Follicle Stimulating Hormone / metabolism. Growth Hormone / metabolism. Humans. Immunohistochemistry. Luteinizing Hormone / metabolism. Male. Microscopy, Confocal. Middle Aged. Peptide Fragments / metabolism. Pituitary Hormones / metabolism. Pituitary Neoplasms / chemistry. Pituitary Neoplasms / metabolism. Pituitary Neoplasms / pathology. Prolactin / metabolism. Thyrotropin / metabolism

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  • (PMID = 16419492.001).
  • [ISSN] 0391-4097
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / PPAR gamma; 0 / Peptide Fragments; 0 / Pituitary Hormones; 0 / somatotropin (134-154); 9002-60-2 / Adrenocorticotropic Hormone; 9002-62-4 / Prolactin; 9002-67-9 / Luteinizing Hormone; 9002-68-0 / Follicle Stimulating Hormone; 9002-71-5 / Thyrotropin; 9002-72-6 / Growth Hormone
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96. Raica M, Coculescu M, Cimpean AM, Ribatti D: Endocrine gland derived-VEGF is down-regulated in human pituitary adenoma. Anticancer Res; 2010 Oct;30(10):3981-6
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  • [Title] Endocrine gland derived-VEGF is down-regulated in human pituitary adenoma.
  • BACKGROUND: Endocrine gland-derived vascular endothelial growth factor (EG-VEGF) is an angiogenic molecule restricted to endocrine glands and, particularly, to steroid-secreting cells.
  • MATERIALS AND METHODS: In this study, we investigated by immunohistochemistry the expression of EG-VEGF in 2 samples of normal adenohypophysis and 43 bioptic samples of pituitary adenoma.
  • Moreover, the expression of growth hormone (GH), prolactin (PRL), follicle-stimulating hormone (FSH), luteinizing hormone (LH), thyroid-stimulating hormone (TSH) and adrenocorticoprophic hormone (ACTH) were also estimated.
  • RESULTS: The results of this study for the first time demonstrate a down-regulation of EG-VEGF expression in human pituitary adenoma as compared to normal adenohypophysis, suggesting an impaired function of the neoplastic cells in terms of hormone release in the blood stream, as a consequence of impaired tumor angiogenesis in the tumor.
  • CONCLUSION: On the basis of our data showing a marked decrease in the expression of EG-VEGF in pituitary adenoma, with the exception of LH-secreting adenomas, we suggest that LH might be involved in the induction of EG-VEGF secretion.
  • [MeSH-major] Adenoma / metabolism. Pituitary Neoplasms / metabolism. Vascular Endothelial Growth Factor, Endocrine-Gland-Derived / biosynthesis
  • [MeSH-minor] Adrenocorticotropic Hormone / biosynthesis. Down-Regulation. Follicle Stimulating Hormone / biosynthesis. Human Growth Hormone / biosynthesis. Humans. Immunohistochemistry. Luteinizing Hormone / biosynthesis. Pituitary Gland, Anterior / metabolism. Prolactin / biosynthesis. Thyrotropin / biosynthesis

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  • (PMID = 21036711.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Vascular Endothelial Growth Factor, Endocrine-Gland-Derived; 12629-01-5 / Human Growth Hormone; 9002-60-2 / Adrenocorticotropic Hormone; 9002-62-4 / Prolactin; 9002-67-9 / Luteinizing Hormone; 9002-68-0 / Follicle Stimulating Hormone; 9002-71-5 / Thyrotropin
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97. Min HS, Lee SJ, Kim SK, Park SH: Pituitary adenoma with rich folliculo-stellate cells and mucin-producing epithelia arising in a 2-year-old girl. Pathol Int; 2007 Sep;57(9):600-5
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  • [Title] Pituitary adenoma with rich folliculo-stellate cells and mucin-producing epithelia arising in a 2-year-old girl.
  • Pituitary adenoma is a rare neoplasm in childhood, with prolactin and adrenocorticotropic hormone (ACTH)-secreting adenomas predominating in this age group.
  • Herein is reported a case of an ACTH-producing macroadenoma with an unusual histology that occurred in a 2-year-old girl.
  • Because of the patient's age and the macroadenoma's suprasellar location and large size (up to 4 cm in diameter), radical surgery was performed under the suspicion of craniopharyngioma or germ-cell tumor.
  • Pathologically, it was a unique pituitary adenoma composed of monotonous ACTH-producing cells, smaller folliculo-stellate cells (FSC), and mucin-producing cells.
  • The FSC, non-hormone-secreting pituitary cells of uncertain function, were confirmed by their S-100 protein, glial fibrillary acidic protein and cytokeratin expression immunoprofiles.
  • The abrupt transition between the prominent gland-forming mucin-producing epithelia and the FSC component suggested that the mucin-producing epithelia might be derived from the FSC.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / pathology. Mucins / secretion. Pituitary Neoplasms / pathology
  • [MeSH-minor] Biomarkers, Tumor / metabolism. Child, Preschool. Cytoplasm / ultrastructure. Disease Progression. Female. Glial Fibrillary Acidic Protein / metabolism. Humans. Keratins / metabolism. Magnetic Resonance Imaging. S100 Proteins / metabolism. Tomography, X-Ray Computed. Treatment Outcome

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  • (PMID = 17685932.001).
  • [ISSN] 1320-5463
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Glial Fibrillary Acidic Protein; 0 / Mucins; 0 / S100 Proteins; 68238-35-7 / Keratins
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98. Wan H, Chihiro O, Yuan S: MASEP gamma knife radiosurgery for secretory pituitary adenomas: experience in 347 consecutive cases. J Exp Clin Cancer Res; 2009;28:36
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  • [Title] MASEP gamma knife radiosurgery for secretory pituitary adenomas: experience in 347 consecutive cases.
  • BACKGROUND: Secretory pituitary adenomas are very common brain tumors.
  • Historically, the treatment armamentarium for secretory pituitary adenomas included neurosurgery, medical management, and fractionated radiotherapy.
  • In recent years, MASEP gamma knife radiosurgery (MASEP GKRS) has emerged as an important treatment modality in the management of secretory pituitary adenomas.
  • The goal of this research is to define accurately the efficacy, safety, complications, and role of MASEP GKRS for treatment of secretory pituitary adenomas.
  • METHODS: Between 1997 and 2007 a total of 347 patients with secretory pituitary adenomas treated with MASEP GKRS and with at least 60 months of follow-up data were identified.
  • Of the 68 patients with adrenocorticotropic hormone-secreting(ACTH) adenomas, 89.7% showed tumor volume decrease or remain unchanged and 27.9% experienced normalization of hormone level.
  • Of the 176 patients with prolactinomas, 23.3% had normalization of hormone level and 90.3% showed tumor volume decrease or remain unchanged.
  • Of the 103 patients with growth hormone-secreting(GH) adenomas, 95.1% experienced tumor volume decrease or remain unchanged and 36.9% showed normalization of hormone level.
  • CONCLUSION: MASEP GKRS is safe and effective in treating secretory pituitary adenomas.
  • However, treatment must be tailored to meet the patient's symptoms, tumor location, tumor morphometry, and overall health.
  • [MeSH-major] Adenoma / surgery. Pituitary Neoplasms / surgery. Radiosurgery / methods

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  • (PMID = 19284583.001).
  • [ISSN] 1756-9966
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Other-IDs] NLM/ PMC2660297
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99. Ruebel KH, Leontovich AA, Jin L, Stilling GA, Zhang H, Qian X, Nakamura N, Scheithauer BW, Kovacs K, Lloyd RV: Patterns of gene expression in pituitary carcinomas and adenomas analyzed by high-density oligonucleotide arrays, reverse transcriptase-quantitative PCR, and protein expression. Endocrine; 2006 Jun;29(3):435-44
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  • [Title] Patterns of gene expression in pituitary carcinomas and adenomas analyzed by high-density oligonucleotide arrays, reverse transcriptase-quantitative PCR, and protein expression.
  • Very few of the genes that are important in pituitary tumor initiation, progression, and metastasis have been identified to date.
  • To identify potential genes that may be important in pituitary tumor progression and carcinoma development, we used Affymetrix GeneChip HGU-133A-oligonucleotide arrays, which contain more than 15,000 characterized genes from the human genome to study gene expression in an ACTH pituitary carcinoma metastatic to the liver and four pituitary adenomas.
  • Reverse-transcriptase real-time quantitative- PCR (RT-qPCR) was then used to analyze 4 nonneoplastic pituitaries, 19 adenomas, and the ACTH carcinoma.
  • A larger series of pituitary adenomas and carcinomas were also analyzed for protein expression using tissue microarrays (TMA) (n = 233) and by Western blotting (n = 18).
  • Prolactin (PRL) and ACTH tumors had the highest levels of expression of galectin-3.
  • Prolactin and ACTH tumors had the highest levels of expression of hASH-1.
  • Transducin-like enhancer of split four/ Groucho (TLE-4) was over-expressed in adenomas compared to the ACTH carcinoma.
  • These results indicate that the LGALS3, hASH1, ID2, and TLE-4 genes may have important roles in the development of pituitary carcinomas.
  • [MeSH-major] Adenoma / genetics. Carcinoma / genetics. Gene Expression Profiling / methods. Oligonucleotide Array Sequence Analysis / methods. Pituitary Neoplasms / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / metabolism. Blotting, Western. DNA-Binding Proteins / metabolism. Follicle Stimulating Hormone / secretion. GRB2 Adaptor Protein / metabolism. Growth Hormone-Secreting Pituitary Adenoma / metabolism. Humans. Immunohistochemistry. Inhibitor of Differentiation Protein 2 / metabolism. Luteinizing Hormone / secretion. Nuclear Proteins / metabolism. Prolactinoma / metabolism. Repressor Proteins / metabolism

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  • (PMID = 16943582.001).
  • [ISSN] 1355-008X
  • [Journal-full-title] Endocrine
  • [ISO-abbreviation] Endocrine
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 90249
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Validation Studies
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / GRB2 Adaptor Protein; 0 / GRB2 protein, human; 0 / ID2 protein, human; 0 / Inhibitor of Differentiation Protein 2; 0 / Nuclear Proteins; 0 / Repressor Proteins; 0 / TLE4 protein, human; 9002-67-9 / Luteinizing Hormone; 9002-68-0 / Follicle Stimulating Hormone
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100. Ren SG, Melmed S: Pyridoxal phosphate inhibits pituitary cell proliferation and hormone secretion. Endocrinology; 2006 Aug;147(8):3936-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pyridoxal phosphate inhibits pituitary cell proliferation and hormone secretion.
  • Pyridoxal phosphate (PLP), a bioactive form of pyridoxine, dose-dependently (10-1000 microm) inhibited cell proliferation in rat pituitary MMQ and GH3 cells and in mouse AtT-20 cells.
  • PLP (400-1000 microm) reduced GH3 cell GH and prolactin secretion and AtT-20 cell ACTH secretion (adjusted for cell number) by approximately 70% after 2 d.
  • The 100 microm PLP also inhibited prolactin secretion (65%, P < 0.05) in primary rat pituitary cells treated for 2 d.
  • These results indicate that pharmacological doses of PLP inhibit pituitary cell proliferation and hormone secretion, in part mediated through PLP-induced cell-cycle arrest and apoptosis.
  • Pyridoxine may therefore be appropriate for testing as a relatively safe drug for adjuvant treatment of hormone-secreting pituitary adenomas.

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  • (PMID = 16690808.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA075979; United States / NCI NIH HHS / CA / CA 75979
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-bcl-2; 12001-76-2 / Vitamin B Complex; 5V5IOJ8338 / Pyridoxal Phosphate; 9002-62-4 / Prolactin; 9002-72-6 / Growth Hormone
  • [Other-IDs] NLM/ NIHMS10630; NLM/ PMC1513048
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