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1. Saveanu A, Gunz G, Guillen S, Dufour H, Culler MD, Jaquet P: Somatostatin and dopamine-somatostatin multiple ligands directed towards somatostatin and dopamine receptors in pituitary adenomas. Neuroendocrinology; 2006;83(3-4):258-63
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Somatostatin and dopamine-somatostatin multiple ligands directed towards somatostatin and dopamine receptors in pituitary adenomas.
  • AIM: We report the comparative efficacy of octreotide, cabergoline and multiple ligands directed towards the different somatostatin subtypes (ssts), such as BIM-23A779 and SOM-230, and of chimeric analogs which bind both somatostatin and the dopamine D2 receptors (D2R), such as BIM-23A760 and BIM-23A781, in cell cultures from human growth hormone (GH)-secreting pituitary adenomas.
  • PROCEDURES: RT-PCR analysis of the quantitative expression of the different ssts and D2R mRNAs was performed on tumor fragments of 22 GH-secreting adenomas collected after surgery.
  • Pharmacological studies, using the different ligands, were performed on cell cultures of such tumors.
  • The levels of expression of sst2 and D2R mRNAs were significantly correlated with the maximal GH suppression by either octreotide or cabergoline (p < 0.001).
  • In each tumor tested, 3 patterns of response, in terms of GH suppression, were observed.
  • GH secretion was preferentially inhibited by the sst2 preferential compound octreotide in 61% of the tumors.
  • In 19% of the tumors, the maximal inhibition of GH release was achieved with the sst5 preferential compound BIM-23268.
  • The dopamine analog cabergoline was the most effective inhibitor of GH secretion in 21% of cases.
  • Among the compounds tested, the most potent inhibitors of GH secretion were the sst2, sst5, D2R chimeric compound BIM-23A760, followed by the sst universal ligand SOM-230.
  • CONCLUSIONS: The variable patterns of response to sst2, sst5 and dopamine D2 analogs may explain the greater efficacy of drugs which bind to the 3 receptors in suppressing GH secretion.
  • The biological potency (EC50) and efficacy of the chimeric compound BIM-23A760 on GH secretion can be partly explained by its high affinity for sst2.
  • The effect of multiple receptor activation on the functions of other pituitary tumor types, such as prolactinomas and corticotropinomas, is not presently analyzed, and the efficacy of multireceptor ligands remains to be elucidated.
  • [MeSH-major] Adenoma / drug therapy. Antineoplastic Agents, Hormonal / therapeutic use. Dopamine / analogs & derivatives. Pituitary Neoplasms / drug therapy. Somatostatin / analogs & derivatives
  • [MeSH-minor] Adult. Drug Screening Assays, Antitumor. Ergolines / therapeutic use. Female. Human Growth Hormone / drug effects. Human Growth Hormone / metabolism. Humans. Ligands. Male. Octreotide / therapeutic use. RNA, Messenger / analysis. Receptors, Dopamine D2 / drug effects. Receptors, Dopamine D2 / genetics. Receptors, Dopamine D2 / metabolism. Receptors, Somatostatin / classification. Receptors, Somatostatin / drug effects. Receptors, Somatostatin / genetics. Receptors, Somatostatin / metabolism. Recombinant Fusion Proteins / therapeutic use. Tumor Cells, Cultured

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  • (PMID = 17047391.001).
  • [ISSN] 0028-3835
  • [Journal-full-title] Neuroendocrinology
  • [ISO-abbreviation] Neuroendocrinology
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / BIM 23268; 0 / Ergolines; 0 / Ligands; 0 / RNA, Messenger; 0 / Receptors, Dopamine D2; 0 / Receptors, Somatostatin; 0 / Recombinant Fusion Proteins; 12629-01-5 / Human Growth Hormone; 51110-01-1 / Somatostatin; LL60K9J05T / cabergoline; RWM8CCW8GP / Octreotide; VTD58H1Z2X / Dopamine
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2. Adamo MA, Drazin D, Popp AJ: Short-lasting, unilateral neuralgiform headache attacks with conjunctival injection and tearing syndrome treated successfully with transsphenoidal resection of a growth hormone-secreting pituitary adenoma. J Neurosurg; 2008 Jul;109(1):123-5
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  • [Title] Short-lasting, unilateral neuralgiform headache attacks with conjunctival injection and tearing syndrome treated successfully with transsphenoidal resection of a growth hormone-secreting pituitary adenoma.
  • In this paper the authors present a patient with a growth hormone-secreting pituitary adenoma who experienced resolution of SUNCT syndrome after transsphenoidal tumor resection.
  • [MeSH-major] Adenoma / surgery. Growth Hormone-Secreting Pituitary Adenoma / surgery. SUNCT Syndrome / surgery


3. Manahan MA, Dackiw AP, Ball DW, Zeiger MA: Unusual case of metastatic neuroendocrine tumor. Endocr Pract; 2007 Jan-Feb;13(1):72-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: To report a rare case of metastatic growth hormone (GH)-secreting pituitary carcinoma causing acromegaly.
  • RESULTS: A 68-year-old woman presented with persistent acromegaly after treatment for a GH-secreting pituitary adenoma.
  • After operative treatment including total thyroidectomy, subtotal parathyroidectomy, partial thymectomy, and right modified radical neck dissection, the patient's symptoms diminished, and her GH levels approached the normal range.
  • Surgical pathology findings were consistent with a GH-secreting pituitary carcinoma metastatic to the cervical lymph nodes, multinodular thyroid hyperplasia with a focus of papillary microcarcinoma, and parathyroid hyperplasia.
  • CONCLUSION: Overall, pituitary carcinomas are extremely rare.
  • To date, about 100 cases have been reported in the world's literature, and of these, only 19 cases originated from GH-secreting cells.
  • Our examination of the symptoms, signs, diagnosis, and treatment of our patient, in comparison with the previously reported cases, should enhance awareness of this unusual disease process.
  • [MeSH-major] Adenoma / pathology. Growth Hormone-Secreting Pituitary Adenoma / pathology. Parathyroid Neoplasms / secondary. Thymus Neoplasms / secondary. Thyroid Neoplasms / secondary
  • [MeSH-minor] Acromegaly / etiology. Aged. Female. Humans. Lymphatic Metastasis

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  • (PMID = 17360306.001).
  • [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
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 29
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4. Campbell PG, Kenning E, Andrews DW, Yadla S, Rosen M, Evans JJ: Outcomes after a purely endoscopic transsphenoidal resection of growth hormone-secreting pituitary adenomas. Neurosurg Focus; 2010 Oct;29(4):E5
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  • [Title] Outcomes after a purely endoscopic transsphenoidal resection of growth hormone-secreting pituitary adenomas.
  • OBJECT: Using strict biochemical remission criteria, the authors assessed surgical outcomes after endoscopic transsphenoidal resection of growth hormone (GH)-secreting pituitary adenomas and identified preoperative factors that significantly influence the rate of remission.
  • The authors reviewed cases in which an endoscopic resection of GH-secreting pituitary adenomas was performed.
  • The thresholds of an age-appropriate, normalized insulin-like growth factor-I concentration, a nadir GH level after oral glucose load of less than 1.0 μg/l, and a random GH value of less than 2.5 μg/l were required to establish biochemical cure postoperatively.
  • RESULTS: Overall, in 57.7% of patients undergoing a purely endoscopic transsphenoidal pituitary adenectomy for acromegaly, an endocrinological cure was achieved.
  • CONCLUSIONS: A purely endoscopic transsphenoidal approach to GH-secreting pituitary adenomas leads to similar outcome for noninvasive macroadenomas compared with traditional microsurgical techniques.
  • Furthermore, this approach may often provide maximal visualization of the tumor, the pituitary gland, and the surrounding neurovascular structures.
  • [MeSH-major] Acromegaly / surgery. Endoscopy / methods. Growth Hormone-Secreting Pituitary Adenoma / surgery. Human Growth Hormone / secretion
  • [MeSH-minor] Adenoma / surgery. Adult. Aged. Female. Humans. Insulin-Like Growth Factor I / analysis. Longitudinal Studies. Male. Microsurgery / methods. Middle Aged. Neoplasm Invasiveness. Neurosurgical Procedures / methods. Pituitary Neoplasms / surgery. Remission Induction. Sphenoid Bone. Treatment Outcome

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  • (PMID = 20887130.001).
  • [ISSN] 1092-0684
  • [Journal-full-title] Neurosurgical focus
  • [ISO-abbreviation] Neurosurg Focus
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I
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5. Melmed S, Sternberg R, Cook D, Klibanski A, Chanson P, Bonert V, Vance ML, Rhew D, Kleinberg D, Barkan A: A critical analysis of pituitary tumor shrinkage during primary medical therapy in acromegaly. J Clin Endocrinol Metab; 2005 Jul;90(7):4405-10
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  • [Title] A critical analysis of pituitary tumor shrinkage during primary medical therapy in acromegaly.
  • CONTEXT: Somatostatin analogs have been successfully used to treat patients with GH-secreting pituitary adenomas because they are safe, effective, and usually well tolerated.
  • The results of studies evaluating acromegaly treatment with the somatostatin receptor ligands (SRLs), octreotide and lanreotide, have supported the use of these agents for primary medical therapy before or as an alternative to traditional interventions of surgery and radiotherapy in selected cases.
  • EVIDENCE ACQUISITION: We therefore undertook a systematic literature overview to characterize the results of studies involving primary therapy with somatostatin analogs and their effects on pituitary tumor size.
  • Because most studies in which pituitary tumor shrinkage has been assessed involve uncontrolled, open-label, prospective trials or retrospective case series, the lack of a control arm does not permit pooling of data in a metaanalytic fashion to determine tumor size reduction.
  • EVIDENCE SYNTHESIS: Overall, for patients who experience significant shrinkage, an approximately 50% decrease in pituitary mass is achieved when a somatostatin analog is used exclusively or before surgery or radiotherapy.
  • Fourteen studies (n = 424) provided a definition of significant tumor shrinkage, and the results showed that 36.6% (weighted mean percentage) of patients receiving primary SRL therapy for acromegaly experienced a significant reduction in tumor size.
  • [MeSH-major] Acromegaly / drug therapy. Pituitary Neoplasms / drug therapy. Somatostatin / therapeutic use
  • [MeSH-minor] Clinical Trials as Topic. Dopamine Agonists / therapeutic use. Humans. Insulin-Like Growth Factor I / analysis

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  • (PMID = 15827109.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dopamine Agonists; 51110-01-1 / Somatostatin; 67763-96-6 / Insulin-Like Growth Factor I
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6. Okinaga H, Takano K, Hayashi S, Yasufuku-Takano J, Teramoto A, Fujita T: Mechanisms of TRH-induced GH release (paradoxical response) in human somatotroph adenoma cells. Endocr J; 2005 Dec;52(6):763-7
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  • [Title] Mechanisms of TRH-induced GH release (paradoxical response) in human somatotroph adenoma cells.
  • The mechanisms of paradoxical TRH response in human somatotroph adenoma cells were investigated using intracellular calcium measurement and static incubation assay.
  • These calcium responses, especially the second phase, was responsible for the TRH-induced GH release.
  • [MeSH-major] Adenoma / secretion. Growth Hormone-Secreting Pituitary Adenoma / secretion. Human Growth Hormone / secretion. Thyrotropin-Releasing Hormone / pharmacology

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  • (PMID = 16410670.001).
  • [ISSN] 0918-8959
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Calcium Channels; 12629-01-5 / Human Growth Hormone; 5Y5F15120W / Thyrotropin-Releasing Hormone; EC 2.7.11.13 / Protein Kinase C; SY7Q814VUP / Calcium
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7. Magri F, Villa C, Locatelli D, Scagnelli P, Lagonigro MS, Morbini P, Castellano M, Gabellieri E, Rotondi M, Solcia E, Daly AF, Chiovato L: Prevalence of double pituitary adenomas in a surgical series: Clinical, histological and genetic features. J Endocrinol Invest; 2010 May;33(5):325-31
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  • [Title] Prevalence of double pituitary adenomas in a surgical series: Clinical, histological and genetic features.
  • BACKGROUND: The term double pituitary adenomas (DPA) is usually referred to those rare lesions showing two distinct cellular components.
  • Genetic background may sustain the proliferation of more than one cell at the same time but no information is available on the presence of aip mutations in these patients.
  • The contribution of pituitary transcription factor immunostains in DPA was also evaluated.
  • RESULTS: One-hundred-seventeen patients out of 144 had a pituitary adenoma.
  • DPA was found in 3 (2.6%) out of 117 patients with pituitary adenoma.
  • The coexistence of somatotroph-lactotroph and silent mammosomatotroph histotype in 1 case and the coexistence of sparsely granulated lactotroph and null cell adenomas in the remaining two cases were first identified.
  • [MeSH-major] Adenoma / epidemiology. Pituitary Neoplasms / epidemiology

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  • [Cites] Arch Pathol Lab Med. 2008 Aug;132(8):1231-40 [18684022.001]
  • [Cites] Eur J Endocrinol. 2007 Jul;157(1):1-8 [17609395.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Mar 6;104(10):4101-5 [17360484.001]
  • [Cites] Endocr Pathol. 2005 Fall;16(3):187-94 [16299401.001]
  • [Cites] Pathology. 2002 Feb;34(1):57-60 [11902447.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Sep;91(9):3316-23 [16787992.001]
  • [Cites] Endocr Rev. 1998 Dec;19(6):798-827 [9861546.001]
  • [Cites] J Clin Endocrinol Metab. 2007 May;92(5):1934-7 [17341560.001]
  • [Cites] Pituitary. 2000 Nov;3(3):159-68 [11383480.001]
  • [Cites] Ann Intern Med. 1978 Sep;89(3):345-8 [686546.001]
  • [Cites] Reproduction. 2001 Mar;121(3):363-71 [11226062.001]
  • [Cites] Cancer. 2004 Aug 1;101(3):613-9 [15274075.001]
  • [Cites] J Endocrinol Invest. 2000 Jan;23(1):37-41 [10698050.001]
  • [Cites] Clin Endocrinol (Oxf). 2004 Jul;61(1):26-30 [15212641.001]
  • [Cites] Endocr Pathol. 2008 Spring;19(1):40-6 [18317953.001]
  • [Cites] J Neurosurg. 1991 Feb;74(2):243-7 [1988594.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Jun;93(6):2390-401 [18381572.001]
  • [Cites] Neuroendocrinology. 1991 Jun;53(6):562-72 [1715055.001]
  • [Cites] Endocr Pathol. 2007 Spring;18(1):37-41 [17652799.001]
  • [Cites] Pituitary. 1999 May;1(3-4):243-50 [11081204.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Apr;93(4):1324-30 [18230660.001]
  • [Cites] J Clin Endocrinol Metab. 2007 May;92(5):1952-5 [17299063.001]
  • [Cites] Radiographics. 1991 Sep;11(5):727-58 [1947311.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Dec;91(12):4769-75 [16968795.001]
  • [Cites] Am J Surg Pathol. 2008 Apr;32(4):534-43 [18300794.001]
  • [Cites] Science. 2006 May 26;312(5777):1228-30 [16728643.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Jan;84(1):249-56 [9920092.001]
  • [Cites] Horm Metab Res. 2005 Jun;37(6):347-54 [16001326.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Feb;85(2):707-14 [10690880.001]
  • [Cites] J Neurosurg. 2000 Nov;93(5):753-61 [11059654.001]
  • [Cites] J Clin Pathol. 2006 Dec;59(12):1245-53 [17142570.001]
  • [Cites] Am J Clin Pathol. 1999 Jun;111(6):817-25 [10361519.001]
  • [Cites] Neurosurgery. 1992 Nov;31(5):840-9; discussion 849 [1331847.001]
  • [Cites] Neurol Med Chir (Tokyo). 1996 Nov;36(11):818-21 [9420436.001]
  • [Cites] J Clin Endocrinol Metab. 2007 May;92(5):1891-6 [17244780.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Apr;93(4):1254-62 [18171702.001]
  • [Cites] Acta Neuropathol. 1981;54(2):161-4 [6264728.001]
  • [Cites] J Neurol Neurosurg Psychiatry. 2004 Jan;75(1):140 [14707324.001]
  • [Cites] Histochem Cell Biol. 2008 Sep;130(3):495-507 [18688636.001]
  • (PMID = 19955848.001).
  • [ISSN] 1720-8386
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / DNA, Neoplasm; 0 / MAGI2 protein, human; 0 / MEN1 protein, human; 0 / Proto-Oncogene Proteins; 0 / Transcription Factors
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8. Mercado M, Galeana M: [Pharmacological treatment of acromegaly]. Gac Med Mex; 2006 Jul-Aug;142(4):327-31
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  • [Title] [Pharmacological treatment of acromegaly].
  • [Transliterated title] Tratamiento farmacológico de la acromegalia.
  • Acromegaly is an endocrine disorder usually due to a growth hormone (GH)-secreting pituitary adenoma.
  • This deforming disease is associated with several metabolic abnormalities and results in an elevated cardiovascular mortality.
  • Pituitary transsesphenoidal surgery has been considered the treatment of choice, however, even in the most experienced hands this procedure succeeds in curing only 50 to 60% of the patients.
  • Therefore, close to 50% of patients require an adjunctive form of treatment such as radiation therapy or the use of diverse medications that modulate GH secretion (somatostatin analogues) or action (GH receptor antagonists).
  • [MeSH-major] Acromegaly / drug therapy
  • [MeSH-minor] Humans. Receptors, Somatotropin / antagonists & inhibitors. Somatostatin / analogs & derivatives. Somatostatin / therapeutic use

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  • (PMID = 17022308.001).
  • [ISSN] 0016-3813
  • [Journal-full-title] Gaceta médica de México
  • [ISO-abbreviation] Gac Med Mex
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Mexico
  • [Chemical-registry-number] 0 / Receptors, Somatotropin; 51110-01-1 / Somatostatin
  • [Number-of-references] 66
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9. Sekizawa N, Hayakawa E, Tsuchiya K, Yoshimoto T, Akashi T, Fujii T, Yamada S, Hirata Y: Acromegaly associated with multiple tumors. Intern Med; 2009;48(15):1273-8
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  • [Title] Acromegaly associated with multiple tumors.
  • A 56-year-old man was admitted to our hospital for the surgical removal of renal cell carcinoma (RCC).
  • He was diagnosed with acromegaly due to his characteristic clinical features, endocrine data, and the presence of pituitary tumor.
  • Pathological examination of the pituitary tumor after transsphenoidal surgery was compatible with growth hormone (GH)-secreting pituitary adenoma.
  • We also detected the transcripts and/or immunoreactivity of GH/insulin-like growth factor I components in the tumor specimen.
  • This is a rare case of acromegaly associated with multiple tumors, including RCC, colon cancer and thyroid tumor.
  • [MeSH-major] Acromegaly / etiology. Neoplasms, Multiple Primary / complications
  • [MeSH-minor] Base Sequence. Carcinoma, Renal Cell / complications. Carcinoma, Renal Cell / genetics. Carcinoma, Renal Cell / metabolism. Colonic Neoplasms / complications. Colonic Neoplasms / genetics. Colonic Neoplasms / metabolism. DNA Primers / genetics. Gene Expression. Humans. Immunohistochemistry. Insulin-Like Growth Factor I / genetics. Insulin-Like Growth Factor I / metabolism. Kidney Neoplasms / complications. Kidney Neoplasms / genetics. Kidney Neoplasms / metabolism. Male. Middle Aged. Pituitary Neoplasms / complications. Pituitary Neoplasms / genetics. Pituitary Neoplasms / metabolism. Receptor, IGF Type 1 / genetics. Receptor, IGF Type 1 / metabolism. Receptors, Somatotropin / genetics. Receptors, Somatotropin / metabolism. Thyroid Neoplasms / complications. Thyroid Neoplasms / genetics. Thyroid Neoplasms / metabolism

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  • (PMID = 19652429.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Receptors, Somatotropin; 67763-96-6 / Insulin-Like Growth Factor I; EC 2.7.10.1 / Receptor, IGF Type 1
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10. Isikay I, Berker M, Balci S, Cila A: Somatotroph adenoma cells may populate paranasal sinus mucosa. Acta Neurochir (Wien); 2010 Sep;152(9):1629-30; discussion 1630
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  • [Title] Somatotroph adenoma cells may populate paranasal sinus mucosa.
  • [MeSH-major] Growth Hormone-Secreting Pituitary Adenoma / secondary. Nasal Mucosa / pathology. Neoplasm Invasiveness / pathology. Paranasal Sinus Neoplasms / secondary. Pituitary Neoplasms / pathology. Sphenoid Sinus / pathology

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  • (PMID = 20446098.001).
  • [ISSN] 0942-0940
  • [Journal-full-title] Acta neurochirurgica
  • [ISO-abbreviation] Acta Neurochir (Wien)
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Austria
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11. Guerrero CA, Krayenbühl N, Husain M, Krisht AF: Ectopic suprasellar growth hormone-secreting pituitary adenoma: case report. Neurosurgery; 2007 Oct;61(4):E879; discussion E879
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ectopic suprasellar growth hormone-secreting pituitary adenoma: case report.
  • OBJECTIVE: Ectopic pituitary adenomas are rare.
  • We present an unusual case of an ectopic growth hormone-secreting pituitary adenoma in the suprasellar space.
  • CLINICAL PRESENTATION: A 31-year-old man presented with a history of chronic headache and typical clinical signs of acromegaly.
  • Magnetic resonance imaging scans revealed a suprasellar mass not arising from the normal looking pituitary gland.
  • Histological examination showed a growth hormone-secreting pituitary adenoma CONCLUSION: Although uncommon, growth hormone-secreting pituitary adenomas are encountered in the suprasellar region.
  • They should be added to the differential diagnosis of tumors in this location.
  • [MeSH-major] Adenoma / radiography. Choristoma. Growth Hormone-Secreting Pituitary Adenoma / radiography


12. Petersenn S, Schopohl J, Barkan A, Mohideen P, Colao A, Abs R, Buchelt A, Ho YY, Hu K, Farrall AJ, Melmed S, Biller BM, Pasireotide Acromegaly Study Group: Pasireotide (SOM230) demonstrates efficacy and safety in patients with acromegaly: a randomized, multicenter, phase II trial. J Clin Endocrinol Metab; 2010 Jun;95(6):2781-9
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  • [Title] Pasireotide (SOM230) demonstrates efficacy and safety in patients with acromegaly: a randomized, multicenter, phase II trial.
  • Because most GH-secreting pituitary adenomas express sst(2) and sst(5), pasireotide has the potential to be more effective than the sst(2)-preferential somatostatin analogs octreotide and lanreotide.
  • OBJECTIVE: Our objective was to evaluate the efficacy and safety of three different doses of pasireotide in patients with acromegaly.
  • PATIENTS: Sixty patients with acromegaly, defined by a 2-h five-point mean GH level higher than 5 microg/liter, lack of suppression of GH to less than 1 microg/liter after oral glucose tolerance test, and elevated IGF-I for age- and sex-matched controls.
  • MAIN OUTCOME MEASURE: A biochemical response was defined as a reduction in GH to no more than 2.5 microg/liter and normalization of IGF-I to age- and sex-matched controls.
  • After 4 wk of pasireotide 200-600 microg s.c. bid, 19% of patients achieved a biochemical response, which increased to 27% after 3 months of pasireotide; 39% of patients had a more than 20% reduction in pituitary tumor volume.
  • CONCLUSIONS: Pasireotide is a promising treatment for acromegaly.
  • Larger studies of longer duration evaluating the efficacy and safety of pasireotide in patients with acromegaly are ongoing.
  • [MeSH-major] Acromegaly / drug therapy. Somatostatin / analogs & derivatives
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Blood Glucose / metabolism. Cross-Over Studies. Dose-Response Relationship, Drug. Double-Blind Method. Endpoint Determination. Female. Human Growth Hormone / blood. Humans. Insulin-Like Growth Factor I / metabolism. Magnetic Resonance Imaging. Male. Middle Aged. Octreotide / adverse effects. Octreotide / therapeutic use. Pituitary Neoplasms / pathology. Young Adult

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  • [CommentIn] Nat Rev Endocrinol. 2010 Aug;6(8):417 [20681073.001]
  • (PMID = 20410233.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00088582
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Glucose; 12629-01-5 / Human Growth Hormone; 51110-01-1 / Somatostatin; 67763-96-6 / Insulin-Like Growth Factor I; 98H1T17066 / pasireotide; RWM8CCW8GP / Octreotide
  • [Investigator] Brue T; Caron P; Chanson P; Cuneo R; Díaz A; Ghigo E; Gaillard R; Halperin I; Kleinberg D; Rohmer V; Romijn JA; Schlienger JL; Stewart P; Tabarin A; Trainer PJ; van der Lely AJ; Vance ML
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13. Takano K, Yasufuku-Takano J, Morita K, Mori S, Takei M, Osamura RY, Teramoto A, Fujita T: Evidence that PKA activity is constitutively activated in human GH-secreting adenoma cells in a patient with Carney complex harbouring a PRKAR1A mutation. Clin Endocrinol (Oxf); 2009 May;70(5):769-75
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evidence that PKA activity is constitutively activated in human GH-secreting adenoma cells in a patient with Carney complex harbouring a PRKAR1A mutation.
  • CONTEXT: The GHRH-protein kinase A (PKA) signalling pathway is essential for cell proliferation and GH synthesis/secretion in somatotrophs.
  • The basal PKA activity of somatotroph adenoma cells from CNC has not been evaluated because of a limited amount of available tissue.
  • Primary cultured adenoma cells were subjected to electrophysiological experiments to evaluate PKA signalling in individual cells.
  • RESULTS: GHRH did not increase the nonselective cation current or the voltage-gated calcium current in these adenoma cells, in contrast to nonadenomatous somatotroph cells in which these currents increase through the PKA pathway.
  • Application of a PKA inhibitor inhibited the basal currents in these adenoma cells, results that were not observed in nonadenomatous somatotrophs.
  • CONCLUSIONS: The results demonstrate that PKA is activated at the basal state in these adenoma cells.
  • The data also show that both the nonselective cation current and the voltage-gated calcium current, vital regulators of GH secretion downstream of PKA, are maximally increased in these cells.
  • These maximally increased currents probably account for the excessive GH secretion.
  • [MeSH-major] Cyclic AMP-Dependent Protein Kinase RIalpha Subunit / genetics. Cyclic AMP-Dependent Protein Kinases / metabolism. Growth Hormone-Secreting Pituitary Adenoma / enzymology. Growth Hormone-Secreting Pituitary Adenoma / genetics. Lentigo / enzymology. Lentigo / genetics. Multiple Endocrine Neoplasia / enzymology. Multiple Endocrine Neoplasia / genetics. Mutation

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  • (PMID = 19178533.001).
  • [ISSN] 1365-2265
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Calcium Channels; 0 / Codon, Nonsense; 0 / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit; 0 / DNA, Neoplasm; 0 / PRKAR1A protein, human; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases
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14. Chahal HS, Chapple JP, Frohman LA, Grossman AB, Korbonits M: Clinical, genetic and molecular characterization of patients with familial isolated pituitary adenomas (FIPA). Trends Endocrinol Metab; 2010 Jul;21(7):419-27
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  • [Title] Clinical, genetic and molecular characterization of patients with familial isolated pituitary adenomas (FIPA).
  • Familial pituitary adenomas can occur in MEN1 and Carney complex, as well as in the recently characterized familial isolated pituitary adenoma (FIPA) syndrome.
  • FIPA is an autosomal dominant disease with incomplete penetrance, characterized by early-onset disease, often aggressive tumor growth and a predominance of somatotroph and lactotroph adenomas.
  • [MeSH-major] Pituitary Neoplasms / genetics. Pituitary Neoplasms / pathology


15. 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.
  • Up to 90% of cases show a strong decrease in hormone secretion and a distinct shrinkage of the adenomas based on strong decrease in adenoma cell volume.
  • Long-term medication with high doses of glucocorticoids induces Crooke's cells in the anterior pituitary.
  • [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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  • [Cites] Endocrine. 2004 Nov;25(2):141-5 [15711028.001]
  • [Cites] Endocr Pathol. 2000 Winter;11(4):341-352 [12114758.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Jul;87(7):3013-8 [12107192.001]
  • [Cites] Pathol Res Pract. 1986 Jun;181(3):280-90 [3748874.001]
  • [Cites] Histol Histopathol. 1987 Apr;2(2):135-42 [2980713.001]
  • [Cites] Ultrastruct Pathol. 2005 May-Aug;29(3-4):163-7 [16036872.001]
  • [Cites] Endocrine. 2001 Apr;14(3):329-36 [11444429.001]
  • [Cites] Pathol Res Pract. 1993 Nov;189(9):1044-51 [8302723.001]
  • [Cites] Exp Clin Endocrinol. 1992;100(3):106-11 [1305059.001]
  • [Cites] Acta Endocrinol (Copenh). 1991 Apr;124(4):487-91 [2031445.001]
  • [Cites] Mayo Clin Proc. 1997 Oct;72(10):893-900 [9379690.001]
  • [Cites] J Neurooncol. 2001 Sep;54(2):151-66 [11761432.001]
  • [Cites] Microsc Res Tech. 1992 Jan 15;20(2):162-76 [1547357.001]
  • [Cites] Exp Clin Endocrinol. 1988 Sep;92(1):59-68 [2906615.001]
  • (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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16. Lonser RR, Kindzelski BA, Mehta GU, Jane JA Jr, Oldfield EH: Acromegaly without imaging evidence of pituitary adenoma. J Clin Endocrinol Metab; 2010 Sep;95(9):4192-6
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  • [Title] Acromegaly without imaging evidence of pituitary adenoma.
  • CONTEXT: GH-secreting pituitary adenomas are nearly always visible on conventional magnetic resonance (MR) imaging.
  • However, management and outcome of acromegalic patients lacking imaging evidence of GH-secreting pituitary adenomas are undefined.
  • OBJECTIVE: The aim was to evaluate surgical exploration for MR-invisible GH-secreting pituitary adenomas.
  • PATIENTS OR OTHER PARTICIPANTS: Consecutive acromegalic patients without imaging evidence of a pituitary adenoma on pre- and postcontrast, spin echo T1-weighted MR imaging and who lacked evidence of an ectopic (nonpituitary) source causing GH excess were included.
  • INTERVENTIONS: Surgical exploration with identification and resection of a pituitary adenoma was performed.
  • MAIN OUTCOME MEASURES: Laboratory values (GH, IGF-I), surgical findings, and clinical outcome were analyzed.
  • RESULTS: Six patients (three males, three females; 3% of all patients) with suspected GH-secreting adenomas did not demonstrate imaging evidence of pituitary adenoma on conventional MR imaging.
  • Three patients underwent a postcontrast, volumetric interpolated breath-hold examination MR-imaging sequence (1.2-mm slice thickness), which revealed a 4-mm pituitary adenoma not seen on the spin echo T1-weighted MR imaging in one patient.
  • A pituitary adenoma was identified and removed in all patients (mean diameter, 5.6 mm; range, 5 to 6.7 mm).
  • Histological analysis confirmed that the lesions were GH-secreting adenomas.
  • CONCLUSION: Acromegaly can be caused by GH-secreting pituitary adenomas that are not evident on conventional MR imaging.
  • Adenomas in some of these patients become evident using volumetric interpolated breath-hold examination MR imaging.
  • Surgical exploration of the pituitary gland in acromegalic patients with endocrine findings consistent with a GH-secreting adenoma but negative MR imaging can lead to identification and removal of an adenoma.


17. Morita K, Takano K, Yasufuku-Takano J, Yamada S, Teramoto A, Takei M, Osamura RY, Sano T, Fujita T: Expression of pituitary tumour-derived, N-terminally truncated isoform of fibroblast growth factor receptor 4 (ptd-FGFR4) correlates with tumour invasiveness but not with G-protein alpha subunit (gsp) mutation in human GH-secreting pituitary adenomas. Clin Endocrinol (Oxf); 2008 Mar;68(3):435-41
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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 pituitary tumour-derived, N-terminally truncated isoform of fibroblast growth factor receptor 4 (ptd-FGFR4) correlates with tumour invasiveness but not with G-protein alpha subunit (gsp) mutation in human GH-secreting pituitary adenomas.
  • OBJECTIVE: Apart from the constitutively activating mutation of the G-protein alpha subunit (Gsalpha) (gsp mutation), factors involved in tumorigenesis or those in tumour behaviour remain elusive in sporadic GH-secreting pituitary adenomas.
  • Recently, the N-terminally truncated form of fibroblast growth factor receptor-4 (ptd-FGFR4) was identified in pituitary adenomas.
  • This aberrant receptor has transforming activity, and causes pituitary adenomas in transgenic mice.
  • MATERIALS AND METHODS: mRNA was extracted from excised adenomas of 45 Japanese acromegalic patients. ptd-FGFR4 expression and gsp mutations were determined by reverse transcription polymerase chain reaction (RT-PCR) and direct sequencing.
  • Preoperative clinical data were collected by reviewing medical charts and pituitary magnetic resonance imaging (MRI) scans.
  • The presence of ptd-FGFR4 did not correlate with age at operation, sex, preoperative serum GH or IGF-1 levels.
  • CONCLUSIONS: We found that ptd-FGFR4 expression and gsp mutations occur independently of each other, and that ptd-FGFR4 expression is associated with more invasive tumours in patients with GH-secreting pituitary adenomas.
  • [MeSH-major] GTP-Binding Protein alpha Subunits / genetics. Gene Expression. Growth Hormone-Secreting Pituitary Adenoma / genetics. Mutation. Neoplasm Invasiveness. Pituitary Neoplasms / genetics. Receptor, Fibroblast Growth Factor, Type 4 / genetics

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  • (PMID = 18070145.001).
  • [ISSN] 1365-2265
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / GTP-Binding Protein alpha Subunits; 0 / Protein Isoforms; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 4
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18. El-Bilbeisi H, Ghannam M, Nimri CF, Ahmad AT: Craniopharyngioma in a patient with acromegaly due to a pituitary macroadenoma. Ann Saudi Med; 2010 Nov-Dec;30(6):485-8
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  • [Title] Craniopharyngioma in a patient with acromegaly due to a pituitary macroadenoma.
  • We present the first reported case of a craniopharyngioma as a second primary tumor in a patient with acromegaly due to a growth hormone (GH)-secreting pituitary adenoma.
  • The patient was lost for follow-up for 18 years after trans-sphenoidal pituitary surgery for a GH-secreting pituitary adenoma.
  • She presented with headaches and decreased visual acuity, and showed unsuppressed GH in an oral glucose load test with high IGF-1 levels.
  • Biopsy of the mass confirmed the diagnosis of a craniopharyngioma.
  • We stress the need for close follow-up of patients with acromegaly with adequate control of GH and IGF-1 levels.
  • [MeSH-major] Acromegaly / etiology. Adenoma / pathology. Craniopharyngioma / pathology. Growth Hormone / secretion. Neoplasms, Second Primary / pathology. Pituitary Neoplasms / pathology

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  • [Cites] Am J Med. 1978 May;64(5):874-82 [206142.001]
  • [Cites] Pituitary. 2008;11(3):317-23 [17917812.001]
  • [Cites] J Clin Invest. 1980 Jan;65(1):43-54 [6243140.001]
  • [Cites] Clin Endocrinol (Oxf). 1980 Jan;12(1):71-9 [7379316.001]
  • [Cites] J Clin Invest. 1982 Nov;70(5):965-77 [6290540.001]
  • [Cites] Virchows Arch A Pathol Anat Histopathol. 1983;399(1):49-59 [6299000.001]
  • [Cites] Neurosurgery. 1986 Aug;19(2):267-70 [3748357.001]
  • [Cites] J Neurol Neurosurg Psychiatry. 1986 Nov;49(11):1305-7 [3794737.001]
  • [Cites] Neurosurgery. 1987 Sep;21(3):371-7 [3670583.001]
  • [Cites] Acta Med Scand. 1988;223(4):327-35 [3369313.001]
  • [Cites] Surg Neurol. 1989 May;31(5):381-6 [2711312.001]
  • [Cites] Ulster Med J. 1990 Apr;59(1):55-62 [2349750.001]
  • [Cites] Endocr Rev. 1995 Apr;16(2):143-63 [7540132.001]
  • [Cites] Nat Med. 1997 Oct;3(10):1141-4 [9334728.001]
  • [Cites] J Neurosurg. 1998 Oct;89(4):547-51 [9761047.001]
  • [Cites] J Pathol Bacteriol. 1955 Jan-Apr;69(1-2):141-5 [13243181.001]
  • [Cites] Arch Pathol. 1960 Sep;70:293-9 [13850582.001]
  • [Cites] Pituitary. 2004;7(1):39-44 [15638297.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Feb;90(2):800-4 [15562021.001]
  • [Cites] Clin Endocrinol (Oxf). 2005 Apr;62(4):397-409 [15807869.001]
  • [Cites] Clin Cancer Res. 2005 Jul 1;11(13):4674-80 [16000560.001]
  • [Cites] Rev Endocr Metab Disord. 2008 Mar;9(1):41-58 [18157698.001]
  • [Cites] Postgrad Med J. 2000 Aug;76(898):513, 519-21 [10908388.001]
  • [Cites] Growth Horm IGF Res. 2000 Apr;10 Suppl A:S12-3 [10984274.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Jul;86(7):2935-41 [11443146.001]
  • [Cites] Eur J Cancer. 2001 Oct;37(15):1886-94 [11576845.001]
  • [Cites] Br J Ophthalmol. 1975 Dec;59(12):689-95 [766825.001]
  • [Cites] Clin Endocrinol (Oxf). 1976 Sep;5(5):503-13 [991433.001]
  • [Cites] Clin Endocrinol (Oxf). 1979 Jan;10(1):61-7 [219974.001]
  • (PMID = 20864785.001).
  • [ISSN] 0975-4466
  • [Journal-full-title] Annals of Saudi medicine
  • [ISO-abbreviation] Ann Saudi Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Saudi Arabia
  • [Chemical-registry-number] 9002-72-6 / Growth Hormone
  • [Other-IDs] NLM/ PMC2994169
  •  go-up   go-down


19. Cañibano C, Rodriguez NL, Saez C, Tovar S, Garcia-Lavandeira M, Borrello MG, Vidal A, Costantini F, Japon M, Dieguez C, Alvarez CV: The dependence receptor Ret induces apoptosis in somatotrophs through a Pit-1/p53 pathway, preventing tumor growth. EMBO J; 2007 Apr 18;26(8):2015-28
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  • [Title] The dependence receptor Ret induces apoptosis in somatotrophs through a Pit-1/p53 pathway, preventing tumor growth.
  • Somatotrophs are the only pituitary cells that express Ret, GFRalpha1 and GDNF.
  • This study investigated the effects of Ret in a somatotroph cell line, in primary pituitary cultures and in Ret KO mice.
  • Ret regulates somatotroph numbers by inducing Pit-1 overexpression, leading to increased p53 expression and apoptosis, both of which can be prevented with Ret or Pit-1 siRNA.
  • The adenopituitary of Ret KO mice is larger than normal, showing Pit-1 and somatotroph hyperplasia.
  • In normal animals, activation of the Ret/Pit-1/p53 pathway by retroviral introduction of Ret blocked tumor growth in vivo.
  • Thus, somatotrophs have an intrinsic mechanism for controlling Pit-1/GH production through an apoptotic/survival pathway.
  • Ret might be of value for treatment of pituitary adenomas.
  • [MeSH-minor] Animals. Blotting, Northern. Cell Line. Chromatin Immunoprecipitation. Cyclic AMP Response Element-Binding Protein / metabolism. DNA Primers. Glial Cell Line-Derived Neurotrophic Factor / metabolism. Humans. Immunohistochemistry. MAP Kinase Kinase 4 / metabolism. Mice. Mice, Knockout. Protein Kinase C-delta / metabolism. RNA Interference. Rats

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  • [Cites] Endocrinology. 2000 Jun;141(6):2113-9 [10830298.001]
  • [Cites] Cancer Res. 2000 Jul 15;60(14):3727-31 [10919641.001]
  • [Cites] EMBO J. 2000 Aug 1;19(15):4056-63 [10921886.001]
  • [Cites] Oncogene. 2000 Sep 14;19(39):4469-75 [11002419.001]
  • [Cites] Pituitary. 1999 Jun;2(1):29-41 [11081170.001]
  • [Cites] J Biol Chem. 2000 Dec 15;275(50):39159-66 [10995764.001]
  • [Cites] Mol Endocrinol. 2001 Sep;15(9):1484-95 [11518797.001]
  • [Cites] J Neurosci Res. 2001 Nov 1;66(3):390-5 [11746356.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Apr;87(4):1879-84 [11932334.001]
  • [Cites] Nature. 2002 Apr 25;416(6883):860-5 [11976686.001]
  • [Cites] Nature. 2002 Apr 25;416(6883):865-9 [11976687.001]
  • [Cites] EMBO J. 2002 Nov 15;21(22):6050-60 [12426377.001]
  • [Cites] J Biol Chem. 2003 Feb 21;278(8):5597-604 [12493739.001]
  • [Cites] Oncogene. 1998 May 14;16(19):2435-45 [9627110.001]
  • [Cites] J Neuroendocrinol. 1999 May;11(5):351-60 [10320562.001]
  • [Cites] J Biol Chem. 1999 Jul 23;274(30):20885-94 [10409632.001]
  • [Cites] Neuroscience. 1999;93(1):265-73 [10430490.001]
  • [Cites] Endocrinology. 2004 Dec;145(12):5448-51 [15331579.001]
  • [Cites] EMBO J. 2005 Mar 23;24(6):1192-201 [15729359.001]
  • [Cites] J Biol Chem. 2005 Apr 29;280(17):17371-9 [15716280.001]
  • [Cites] J Clin Endocrinol Metab. 2005 May;90(5):3089-99 [15741248.001]
  • [Cites] Endocr Relat Cancer. 2005 Jun;12(2):423-33 [15947113.001]
  • [Cites] Cytokine Growth Factor Rev. 2005 Aug-Oct;16(4-5):441-67 [15982921.001]
  • [Cites] Mol Cell. 2006 Feb 17;21(4):467-80 [16483929.001]
  • [Cites] J Biol Chem. 2006 Apr 7;281(14):9728-37 [16452485.001]
  • [Cites] Nat Cell Biol. 2003 Mar;5(3):216-23 [12598906.001]
  • [Cites] Oncogene. 2003 Oct 30;22(49):7819-30 [14586408.001]
  • [Cites] J Clin Invest. 2003 Dec;112(11):1603-18 [14660734.001]
  • [Cites] Physiol Rev. 2004 Apr;84(2):411-30 [15044679.001]
  • [Cites] Genes Dev. 2004 Apr 15;18(8):912-25 [15107404.001]
  • [Cites] Bioessays. 2004 Jun;26(6):656-64 [15170863.001]
  • [Cites] J Biol Chem. 2004 Jul 16;279(29):30123-32 [15138267.001]
  • [Cites] Nature. 2004 Sep 2;431(7004):80-4 [15343335.001]
  • [Cites] Nature. 2004 Sep 23;431(7007):456-61 [15361883.001]
  • [Cites] Oncogene. 1990 Jan;5(1):97-102 [2181380.001]
  • [Cites] Science. 1991 Jul 12;253(5016):197-9 [1677216.001]
  • [Cites] Science. 1992 Aug 21;257(5073):1118-21 [1509263.001]
  • [Cites] J Mol Endocrinol. 1993 Oct;11(2):129-39 [8297469.001]
  • [Cites] Nature. 1994 Jan 27;367(6461):380-3 [8114940.001]
  • [Cites] J Mol Endocrinol. 1993 Dec;11(3):283-90 [8148036.001]
  • [Cites] J Clin Endocrinol Metab. 1994 Jul;79(1):189-96 [8027225.001]
  • [Cites] Endocr J. 1994 Oct;41(5):579-84 [7889120.001]
  • [Cites] Endocrinology. 1995 Sep;136(9):3863-70 [7649093.001]
  • [Cites] J Biol Chem. 1996 Aug 30;271(35):21484-9 [8702932.001]
  • [Cites] FASEB J. 1996 Dec;10(14):1569-77 [9002548.001]
  • [Cites] Oncogene. 1998 Mar;16(11):1455-65 [9525744.001]
  • [Cites] FEBS Lett. 1999 Dec 10;463(1-2):63-6 [10601639.001]
  • [Cites] Endocrinology. 2000 May;141(5):1893-6 [10803600.001]
  • (PMID = 17380130.001).
  • [ISSN] 0261-4189
  • [Journal-full-title] The EMBO journal
  • [ISO-abbreviation] EMBO J.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cyclic AMP Response Element-Binding Protein; 0 / DNA Primers; 0 / Glial Cell Line-Derived Neurotrophic Factor; 0 / Transcription Factor Pit-1; 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / Proto-Oncogene Proteins c-ret; EC 2.7.10.1 / Ret protein, rat; EC 2.7.11.13 / Protein Kinase C-delta; EC 2.7.12.2 / MAP Kinase Kinase 4
  • [Other-IDs] NLM/ PMC1852774
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20. Mao ZG, He DS, Zhou J, Yao B, Xiao WW, Chen CH, Zhu YH, Wang HJ: Differential expression of microRNAs in GH-secreting pituitary adenomas. Diagn Pathol; 2010 Dec 07;5:79
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  • [Title] Differential expression of microRNAs in GH-secreting pituitary adenomas.
  • BACKGROUND: The purpose of this study was to (1) identify specific miRNAs in growth hormones (GH)-secreting pituitary adenomas;.
  • METHODS: Fifteen GH-secreting adenomas patients were treated with lanreotide for 4 months before surgery.
  • Patients with 50% reduction of GH secretion by lanreotide were considered as SSA responders, while patients with less than 50% of GH reduction were considered as SSA nonresponders.
  • We analyzed the miRNAs in 21 GH-secreting pituitary adenomas and 6 normal pituitaries by miRCURY™ LNA array and some differentially expressed miRNAs were validated by quantitative real-time PCR.
  • RESULTS: Fifty-two miRNAs were differentially expressed between GH-secreting pituitary adenomas and normal pituitaries.
  • Differential expression of 9 miRNAs was observed between micro- and macro-adenomas.
  • Seven miRNAs were differentially expressed between SSA responders or GH nonresponders.
  • Several identified miRNAs may be involved in cell proliferation, apoptosis, cancer development and progression.
  • CONCLUSIONS: Our results indicate that altered miRNAs expression is involved in GH-secreting pituitary adenomas transformation, which will shed light on the mechanisms for the treatment of acromegaly by SSA.
  • Identification and characterization of the targets of altered miRNAs genes may elucidate molecular mechanisms involved in the pathogenesis of pituitary adenoma.
  • [MeSH-major] Adenoma / genetics. Gene Expression Profiling. Growth Hormone-Secreting Pituitary Adenoma / genetics. MicroRNAs / analysis


21. Stapleton CJ, Liu CY, Weiss MH: The role of stereotactic radiosurgery in the multimodal management of growth hormone-secreting pituitary adenomas. Neurosurg Focus; 2010 Oct;29(4):E11
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  • [Title] The role of stereotactic radiosurgery in the multimodal management of growth hormone-secreting pituitary adenomas.
  • Growth hormone (GH)-secreting pituitary adenomas represent a common source of GH excess in patients with acromegaly.
  • Whereas surgical extirpation of the culprit lesion is considered first-line treatment, as many as 19% of patients develop recurrent symptoms due to regrowth of previously resected adenomatous tissue or to continued growth of the surgically inaccessible tumor.
  • Although medical therapies that suppress GH production can be effective in the management of primary and recurrent acromegaly, these therapies are not curative, and lifelong treatment is required for hormonal control.
  • The authors reviewed the growing body of literature concerning the role of radiosurgical procedures in the treatment armamentarium of acromegaly, and identified more than 1350 patients across 45 case series.
  • In this review, the authors report that radiosurgery offers true hormonal normalization in 17% to 82% of patients and tumor growth control in 37% to 100% of cases across all series, while minimizing adverse complications.
  • As a result, stereotactic radiosurgery represents a safe and effective treatment option in the multimodal management of primary or recurrent acromegaly secondary to GH-secreting pituitary adenomas.
  • [MeSH-major] Acromegaly / surgery. Adenoma / surgery. Growth Hormone-Secreting Pituitary Adenoma / surgery. Radiosurgery / methods. Radiotherapy, Adjuvant / methods
  • [MeSH-minor] Combined Modality Therapy. Human Growth Hormone / antagonists & inhibitors. Human Growth Hormone / secretion. Humans. Pituitary Neoplasms / blood. Pituitary Neoplasms / radiotherapy. Pituitary Neoplasms / surgery. Treatment Outcome. Tumor Burden

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  • (PMID = 20887121.001).
  • [ISSN] 1092-0684
  • [Journal-full-title] Neurosurgical focus
  • [ISO-abbreviation] Neurosurg Focus
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 12629-01-5 / Human Growth Hormone
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22. Matsuno A: [Recent trends in the pathophysiology and treatment of pituitary adenomas]. Brain Nerve; 2009 Aug;61(8):957-62
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  • [Title] [Recent trends in the pathophysiology and treatment of pituitary adenomas].
  • Recent molecular pathological investigations have elucidated the cytodifferentiation of pituitary cells and identified several transcriptional factors that regulate this cytodifferentiation of pituitary cells.
  • The patterns of cytodifferentiation are closely related to the pathogenesis of pituitary adenomas.
  • Meanwhile, the role of hypothalamic hormones in the development of pituitary adenomas has recently attracted the attention of investigators.
  • The expression of growth hormone-releasing hormone and corticotrophin releasing hormone in corticotroph adenomas have been demonstrated in somatotroph adenomas and corticotropin adenomas, respectively.
  • This finding indicates that the endogenous expression of hypothalamic hormones and their receptors in human pituitary adenoma cells has ample significance in the autocrine or paracrine regulation of pituitary hormone production and tumor extension induced by hypothalamic hormones produced by adenoma cells.
  • The recent progress in surgical techniques for treatment of pituitary adenomas has provided several alternatives: transsphenoidal surgery vs. transcranial surgery, sublabial approach vs. endonasal approach, and microsurgery vs. endoscopic surgery.
  • There have also been developments in the medical treatment of pituitary adenomas.
  • The frequently used dopamine agonist, cabergoline, is very effective for treating prolactin-producing adenoma.
  • Long-acting octreotide and pegvisomant are now available for the treatment of growth hormone producing adenoma.
  • Cabergoline is also used for growth hormone producing adenoma.
  • Temozolomide has recently been used for atypical adenomas or pituitary carcinomas.
  • Adult growth hormone deficiency sometimes occurs in postoperative patients with pituitary adenomas.
  • Growth hormone replacement is recommended to maintain the quality of life of these patients.
  • [MeSH-major] Adenoma / etiology. Adenoma / therapy. Pituitary Neoplasms / etiology. Pituitary Neoplasms / therapy
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Corticotropin-Releasing Hormone. Dacarbazine / analogs & derivatives. Dacarbazine / therapeutic use. Ergolines / therapeutic use. Growth Hormone-Releasing Hormone. Human Growth Hormone / analogs & derivatives. Human Growth Hormone / therapeutic use. Humans. Hypothalamic Hormones. Incidental Findings. Neurosurgical Procedures / methods. Neurosurgical Procedures / trends. Octreotide / therapeutic use. Prolactinoma. Receptors, Neuropeptide. Receptors, Pituitary Hormone-Regulating Hormone

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  • (PMID = 19697885.001).
  • [ISSN] 1881-6096
  • [Journal-full-title] Brain and nerve = Shinkei kenkyū no shinpo
  • [ISO-abbreviation] Brain Nerve
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Ergolines; 0 / Hypothalamic Hormones; 0 / Receptors, Neuropeptide; 0 / Receptors, Pituitary Hormone-Regulating Hormone; 0 / pegvisomant; 0 / somatotropin releasing hormone receptor; 12629-01-5 / Human Growth Hormone; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; 9015-71-8 / Corticotropin-Releasing Hormone; 9034-39-3 / Growth Hormone-Releasing Hormone; LL60K9J05T / cabergoline; RWM8CCW8GP / Octreotide
  • [Number-of-references] 32
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23. Seda Jr L, Cukiert A, Nogueira KC, Huayllas MK, Liberman B: Intrasellar internal carotid aneurysm coexisting with GH-secreting pituitary adenoma in an acromegalic patient. Arq Neuropsiquiatr; 2008 Mar;66(1):99-100
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  • [Title] Intrasellar internal carotid aneurysm coexisting with GH-secreting pituitary adenoma in an acromegalic patient.
  • [MeSH-major] Acromegaly / complications. Carotid Artery Diseases / complications. Growth Hormone-Secreting Pituitary Adenoma / complications. Intracranial Aneurysm / complications

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  • (PMID = 18392428.001).
  • [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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24. Lee YH, Noh TW, Lee MK, Jameson JL, Lee EJ: Absence of activating mutations of CXCR4 in pituitary tumours. Clin Endocrinol (Oxf); 2010 Feb;72(2):209-13
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  • [Title] Absence of activating mutations of CXCR4 in pituitary tumours.
  • OBJECTIVE: Mutations of the gsp oncogene are responsible for 30-40% of GH-producing pituitary adenomas and 10% of nonfunctioning pituitary adenomas (NFPAs).
  • However, the pathogenetic mechanism of the remaining pituitary tumours still remains to be identified.
  • Recently, the interaction between the chemokine stromal cell-derived factor 1 and its receptor CXCR4 was found to play an important role in GH production and cell proliferation in various pituitary adenoma cell lines.
  • As CXCR4 is a Gi-coupled chemokine receptor, its constitutive activating mutations may be involved in pituitary tumour formation by cyclic adenosine monophosphate (cAMP)-independent, ERK-related pathways.
  • PATIENTS AND METHODS: We investigated whether somatic activating-mutations of CXCR4 might be a possible tumourigenic mechanism for gsp-negative GH-secreting pituitary adenomas and NFPAs.
  • Direct sequencing of polymerase chain reaction-amplified products for coding exons of CXCR4 were performed using genomic deoxyribonucleic acid samples from 37 GH-producing pituitary tumour tissues that were negative for the gsp mutation and 14 CXCR4 expressing NFPAs.
  • RESULTS: Immunohistochemical analyses and double immunofluorescent staining of sectioned paraffin-embedded pituitary tissues revealed that CXCR4 is highly expressed in GH-producing pituitary adenomas and NFPAs.
  • Direct sequencing showed that two synonymous mutations in exon 2 (87 C > T and 414 C > T) were detected in 4 out of 51 pituitary tumours.
  • CONCLUSION: Our results indicate that an activating mutation of the CXCR4 may not be a common pathogenetic mechanism in GH-producing pituitary tumours and NFPAs.
  • [MeSH-major] Pituitary Neoplasms / genetics. Pituitary Neoplasms / metabolism. Receptors, CXCR4 / genetics. Receptors, CXCR4 / metabolism
  • [MeSH-minor] Growth Hormone-Secreting Pituitary Adenoma / genetics. Growth Hormone-Secreting Pituitary Adenoma / metabolism. Humans. Immunohistochemistry. Mutation. Polymerase Chain Reaction

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  • (PMID = 19473177.001).
  • [ISSN] 1365-2265
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, CXCR4
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25. Jaquet P, Gunz G, Saveanu A, Barlier A, Dufour H, Taylor J, Dong J, Kim S, Moreau JP, Culler MD: BIM-23A760, a chimeric molecule directed towards somatostatin and dopamine receptors, vs universal somatostatin receptors ligands in GH-secreting pituitary adenomas partial responders to octreotide. J Endocrinol Invest; 2005;28(11 Suppl International):21-7
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  • [Title] BIM-23A760, a chimeric molecule directed towards somatostatin and dopamine receptors, vs universal somatostatin receptors ligands in GH-secreting pituitary adenomas partial responders to octreotide.
  • We report the comparative efficacy of a somatostatin receptor 1 and 5 subtypes (SSTR2 and SSTR5), and dopamine D2 (DAD2) compound, BIM-23A760, in suppressing GH secretion, in cell culture from human GH-secreting tumors, from patients partially responsive to long-term treatments with octreotide or lanreotide.
  • The SSTR2-selective analog, BIM-23197, the SSTR5-selective analog, BIM-23268, and the dopamine (DA) analog, BIM-53097, produced a mean maximal suppression of GH secretion (24 +/- 3, 20 +/- 3, and 20 +/- 3%, respectively) that was similar to that obtained with octreotide (23 +/- 3%).
  • Among a series of new chimeric compounds that bind the SSTR2, SSTR5, and DAD2 receptors with variable affinities, BIM-23A760 produced greater maximal suppression of GH secretion than octreotide (38 +/- 2 vs 24 +/- 2%; p<0.03).
  • In the presence of sulpride, the dose response inhibition of GH secretion by the trihybrid molecule, BIM-23A760, was partially reversed.
  • When SSTRs pan inhibitors such as BIM-23A779 (binding affinity for SSTR1, SSTR2, SSTR3, SSTR5, respectively: 2.5, 0.3, 0.6, 0.6 nmol/l) or SOM230 were tested for their suppressive effects on GH secretion, they were less potent than the previous dopastatin hybrid molecule.
  • After a brief exposure to a SSTR2-selective analog, BIM-23197, or to a DA analog, BIM-53097, the maximal GH suppression was achieved during 12 h.
  • Under exposure to BIM-23A760, in the same conditions, maximal suppression of GH secretion lasted for 24 h.
  • As compared to the dopastatin compound, the lower efficacy of the universal somatostatin ligands in the inhibition of GH secretion of GH-secreting tumors argues for the use of drugs targeted, according to specific receptors expression and functionality which may vary among the various classes of tumors.
  • [MeSH-major] Human Growth Hormone / secretion. Octreotide / therapeutic use. Pituitary Neoplasms / drug therapy. Pituitary Neoplasms / secretion. Receptors, Dopamine / metabolism. Receptors, Somatostatin / metabolism
  • [MeSH-minor] Acromegaly / drug therapy. Adult. Female. Gene Expression. Humans. Male. Oligopeptides / pharmacology. Piperazines / pharmacology. Prolactin / secretion. RNA, Messenger / analysis. Receptors, Dopamine D2 / genetics

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  • (PMID = 16625841.001).
  • [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 / BIM 23197; 0 / Oligopeptides; 0 / Piperazines; 0 / RNA, Messenger; 0 / Receptors, Dopamine; 0 / Receptors, Dopamine D2; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 0 / somatostatin receptor 5; 12629-01-5 / Human Growth Hormone; 9002-62-4 / Prolactin; RWM8CCW8GP / Octreotide
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26. Nakashima M, Takano K, Matsuno A: Analyses of factors influencing the acute effect of octreotide in growth hormone-secreting adenomas. Endocr J; 2009;56(2):295-304
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  • [Title] Analyses of factors influencing the acute effect of octreotide in growth hormone-secreting adenomas.
  • Somatostatin analogues such as octreotide are used to treat active acromegalic patients by reducing serum growth hormone (GH) levels.
  • However, the acute effect of octreotide on GH secretion differs among patients.
  • To elucidate factors influencing the acute effect of octreotide, we collected data from 56 patients with somatotroph adenoma from two institutions.
  • Monovariate analysis revealed a statistically significant inverse relation of Ki-67 SI with the reduction of GH by octreotide.
  • Post-test revealed that the plasma membrane-dominant staining pattern of SSTR 2A was significantly related to the reduction of GH by octreotide.
  • [MeSH-major] Growth Hormone-Secreting Pituitary Adenoma / secretion. Human Growth Hormone / secretion. Octreotide / therapeutic use. Pituitary Neoplasms / secretion
  • [MeSH-minor] Adult. Aged. Cell Membrane / metabolism. Female. Humans. Ki-67 Antigen / metabolism. Male. Middle Aged. Receptors, Somatostatin / metabolism. Regression Analysis

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  • (PMID = 19164866.001).
  • [ISSN] 1348-4540
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 12629-01-5 / Human Growth Hormone; RWM8CCW8GP / Octreotide
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27. Swords FM, Monson JP, Besser GM, Chew SL, Drake WM, Grossman AB, Plowman PN: Gamma knife radiosurgery: a safe and effective salvage treatment for pituitary tumours not controlled despite conventional radiotherapy. Eur J Endocrinol; 2009 Dec;161(6):819-28
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  • [Title] Gamma knife radiosurgery: a safe and effective salvage treatment for pituitary tumours not controlled despite conventional radiotherapy.
  • OBJECTIVE: We report the use of 'gamma knife' (GK) radiosurgery in 25 patients with pituitary adenomas not cured despite conventional therapy, including external beam radiotherapy.
  • PATIENTS AND METHODS: All patients had previously received conventional radiotherapy for a mean of 11.8 years prior to receiving GK; 23 out of 25 had also undergone pituitary surgery on at least one occasion.
  • Seventeen had hyperfunctioning adenomas that still required medical therapy without an adequate biochemical control--ten somatotroph adenomas, six corticotroph adenomas and one prolactinoma, while eight patients had non-functioning pituitary adenomas (NFPAs).
  • RESULTS: Following GK, mean GH fell by 49% at 1 year in patients with somatotroph tumours.
  • To date, 80% of the patients with acromegaly have achieved normalisation of IGF1, and 30% have also achieved a mean GH level of <1.8 ng/ml correlating with normalised mortality.
  • A total of 75% NFPAs showed disease stabilisation or shrinkage post GK.
  • The results in corticotroph adenomas were variable.
  • Prior to GK, 72% of the patients were panhypopituitary, and 42% of the remainder have developed new anterior pituitary hormone deficiencies to date.
  • CONCLUSIONS: These data indicate that GK is a safe and effective adjunctive treatment for patients with NFPAs and acromegaly not satisfactorily controlled with surgery and radiotherapy.

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  • (PMID = 19773368.001).
  • [ISSN] 1479-683X
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I
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28. Chanson P, Salenave S, Kamenicky P, Cazabat L, Young J: Pituitary tumours: acromegaly. Best Pract Res Clin Endocrinol Metab; 2009 Oct;23(5):555-74
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pituitary tumours: acromegaly.
  • Excessive production of the growth hormone (GH) is responsible for acromegaly.
  • It is related to a pituitary GH-secreting adenoma in most cases.
  • The diagnosis is confirmed by an increased serum GH concentration, unsuppressible by an oral glucose load and by detection of increased levels of insulin-like growth factor-I (IGF-I).
  • Treatment is aimed at correcting (or preventing) tumour compression by excising the disease-causing lesion, and at reducing GH and IGF-I levels to normal values.
  • When surgery, the usual first-line treatment, fails to correct GH/IGF-I hypersecretion, medical treatment with somatostatin analogues and/or radiotherapy can be used.
  • The GH-receptor antagonist (pegvisomant) is helpful in patients who are resistant to somatostatin analogues.
  • Thanks to this multistep therapeutic strategy, adequate hormonal disease control is achieved in most cases, allowing a normal life expectancy.
  • [MeSH-major] Acromegaly / etiology. Adenoma / complications. Growth Hormone-Secreting Pituitary Adenoma / complications
  • [MeSH-minor] Carcinoma / diagnosis. Carcinoma / secretion. Carcinoma / therapy. Humans. Models, Biological. Professional Practice

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  • (PMID = 19945023.001).
  • [ISSN] 1878-1594
  • [Journal-full-title] Best practice & research. Clinical endocrinology & metabolism
  • [ISO-abbreviation] Best Pract. Res. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 98
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29. Mantovani G, Lania AG, Spada A: GNAS imprinting and pituitary tumors. Mol Cell Endocrinol; 2010 Sep 15;326(1-2):15-8
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  • [Title] GNAS imprinting and pituitary tumors.
  • Evidence from in vitro studies and naturally occurring human diseases indicate that several endocrine cells, and particularly somatotrophs, recognize cAMP as a growth factor.
  • Accordingly, mutations of the alpha subunit of the stimulatory G protein gene (GNAS) leading to the constitutive activation of adenylyl cyclase (the so-called gsp oncogene) have been found in a significant proportion of GH-secreting pituitary adenomas.
  • This complex tissue-specific imprinting control results in a near-exclusive expression of Gsalpha from the maternal allele in specific endocrine tissues, including the pituitary.
  • Due to the monoallelic origin of Gsalpha in normal pituitary gsp mutations occur on a maternal allele in order to have a phenotypic effect in both sporadic GH-secreting adenomas and those associated with the McCune-Albright syndrome.
  • Therefore, genetic and epigenetic alterations of the GNAS gene, with subsequent dysregulation of the cAMP pathway, appear, to date, the only molecular hallmark of most GH-secreting adenomas.
  • [MeSH-major] GTP-Binding Protein alpha Subunits, Gs / genetics. Pituitary Neoplasms / genetics
  • [MeSH-minor] Animals. Cyclic AMP-Dependent Protein Kinases / metabolism. Fibrous Dysplasia, Polyostotic / genetics. Genomic Imprinting. Growth Hormone-Secreting Pituitary Adenoma / genetics. Humans. Mice. Pituitary Gland / pathology

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  • [Copyright] 2010 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 20398730.001).
  • [ISSN] 1872-8057
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; EC 3.6.1.- / GNAS protein, human; EC 3.6.1.- / Gnas protein, mouse; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs
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30. Kim MS, Jang HD, Kim OL: Surgical results of growth hormone-secreting pituitary adenoma. J Korean Neurosurg Soc; 2009 May;45(5):271-4
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  • [Title] Surgical results of growth hormone-secreting pituitary adenoma.
  • OBJECTIVE: We retrospectively analyzed the surgical outcomes of 42 patients with growth hormone (GH)-secreting pituitary adenoma to evaluate the clinical manifestations and to determine which preoperative factors that significantly influence the remission.
  • METHODS: Forty-two patients with GH-secreting pituitary adenoma underwent transsphenoidal surgery (TSS) between 1995 and 2007.
  • For comparable radiological criteria, we classified parasellar growth into five grades according to the Knosp classification.
  • There was a significant relationship between preoperative mean GH concentration and early postoperative outcome, with most patients in remission having a lower preoperative GH concentration.
  • CONCLUSION: TSS is thought to be an effective primary treatment for GH-secreting pituitary adenomas according to the most recent criteria of cure.
  • Because the remission rate in cases with cavernous sinus invasion is very low, early detection of the tumor before it extends into the cavernous sinus and a long-term endocrinological and radiological follow-up are necessary in order to improve the remission rate of acromegaly.

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  • [Cites] Rev Endocr Metab Disord. 2008 Mar;9(1):83-94 [18163213.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Feb;85(2):526-9 [10690849.001]
  • [Cites] Neuro Endocrinol Lett. 2006 Dec;27(6):828-32 [17187024.001]
  • [Cites] Neuroendocrinology. 2006;83(3-4):230-9 [17047388.001]
  • [Cites] Surg Neurol. 2006 Jul;66(1):26-31; discussion 31 [16793431.001]
  • [Cites] Eur J Endocrinol. 2005 Mar;152(3):379-87 [15757854.001]
  • [Cites] Endocrinol Metab Clin North Am. 1999 Mar;28(1):171-90 [10207690.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Oct;83(10):3419-26 [9768641.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Aug;83(8):2730-4 [9709939.001]
  • [Cites] J Neurosurg. 1998 Jun;88(6):1002-8 [9609294.001]
  • [Cites] Acta Neurochir (Wien). 1995;136(1-2):37-43 [8748825.001]
  • [Cites] Clin Endocrinol (Oxf). 1994 Jul;41(1):95-102 [8050136.001]
  • [Cites] Neurosurgery. 1993 Oct;33(4):610-7; discussion 617-8 [8232800.001]
  • [Cites] Endocrinol Metab Clin North Am. 1992 Sep;21(3):693-712 [1521519.001]
  • [Cites] Cancer. 1992 Jan 1;69(1):271-5 [1727672.001]
  • [Cites] Endocr Relat Cancer. 2003 Dec;10(4):611-9 [14713271.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Aug;88(8):3567-72 [12915637.001]
  • [Cites] Neurosurgery. 2003 Jul;53(1):51-9; discussion 59-61 [12823873.001]
  • [Cites] J Neurosurg. 2003 May;98(5):1084-93 [12744370.001]
  • [Cites] Clin Neurol Neurosurg. 2003 Apr;105(2):111-6 [12691803.001]
  • [Cites] Clin Endocrinol (Oxf). 2003 Jan;58(1):86-91 [12519417.001]
  • [Cites] Stereotact Funct Neurosurg. 2001;76(3-4):213-7 [12378100.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Jul;87(7):3142-7 [12107214.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Sep;86(9):4072-7 [11549628.001]
  • [Cites] Neurosurgery. 2001 Jun;48(6):1239-43; discussion 1244-5 [11383725.001]
  • [Cites] J Neurosurg. 2000 Dec;93 Suppl 3:6-9 [11143264.001]
  • [Cites] Rev Endocr Metab Disord. 2008 Mar;9(1):71-81 [18163211.001]
  • (PMID = 19516943.001).
  • [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/ PMC2693785
  • [Keywords] NOTNLM ; Cavernous sinus / Growth hormone-secreting pituitary adenoma / Remission induction
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31. Ferrer García JC, Sánchez Juan C, Herrera Ballester A: Contribution of positron emission tomography to the diagnosis of a case of acromegaly. Endocrinol Nutr; 2008 Apr;55(4):175-7
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  • [Title] Contribution of positron emission tomography to the diagnosis of a case of acromegaly.
  • Diagnosis of acromegaly is based on biochemical tests demonstrating increased growth hormone (GH) secretion.
  • More than 95% of patients with acromegaly harbor a GH-secreting pituitary adenoma.
  • The technique of choice in the diagnosis of an adenoma is magnetic resonance imaging (MRI).
  • We report the case of a woman with acromegaly.
  • The pituitary origin of the increased GH secretion was identified by PET.
  • In acromegaly, the absence of MRI findings and identification of location by means of PET are exceptional.

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  • [Copyright] Copyright © 2008 Sociedad Española de Endocrinología y Nutrición. Published by Elsevier Espana. All rights reserved.
  • (PMID = 22975454.001).
  • [ISSN] 1575-0922
  • [Journal-full-title] Endocrinología y nutrición : órgano de la Sociedad Española de Endocrinología y Nutrición
  • [ISO-abbreviation] Endocrinol Nutr
  • [Language] eng; spa
  • [Publication-type] Journal Article
  • [Publication-country] Spain
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32. Mohammed S, Syro L, Abad V, Salehi F, Horvath E, Scheithauer BW, Kovacs K, Cusimano M: Silent somatotroph adenoma of the pituitary in an adolescent. Can J Neurol Sci; 2009 Jan;36(1):123-5
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  • [Title] Silent somatotroph adenoma of the pituitary in an adolescent.
  • [MeSH-major] Adenoma / pathology. Growth Hormone / metabolism. Growth Hormone-Secreting Pituitary Adenoma / pathology. Pituitary Neoplasms / pathology
  • [MeSH-minor] Adolescent. Humans. Magnetic Resonance Imaging / methods. Male. Microscopy, Electron, Transmission / methods. Pituitary Gland / metabolism. Pituitary Gland / pathology. Pituitary Gland / ultrastructure

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  • (PMID = 19294904.001).
  • [ISSN] 0317-1671
  • [Journal-full-title] The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques
  • [ISO-abbreviation] Can J Neurol Sci
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Canada
  • [Chemical-registry-number] 9002-72-6 / Growth Hormone
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33. O'Toole D, Saveanu A, Couvelard A, Gunz G, Enjalbert A, Jaquet P, Ruszniewski P, Barlier A: The analysis of quantitative expression of somatostatin and dopamine receptors in gastro-entero-pancreatic tumours opens new therapeutic strategies. Eur J Endocrinol; 2006 Dec;155(6):849-57
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  • Cell lines derived from GEP express dopaminergic receptors D(2).
  • New chimeric analogues simultaneously recognising sst(2) and sst(5) or sst(2) and D(2) have additive effects in inhibition of GH and prolactin secretion in pituitary adenomas.
  • Levels of expression were compared with a group of 13 somatotroph adenomas.
  • Whereas sst(2) levels were similar between GEP and somatotroph tumours, levels of sst(5) and D(2) were higher in the former (394.9 +/- 156.1 x 10(-2) vs 69.7 +/- 19.5 x 10(-2) copy/copy beta-Gus (P < 0.0036) and 519.6 +/- 121.2 x 10(-2) vs 50.0 +/- 21.6 x 10(-2) copy/copy beta-Gus (P < 0.0001) respectively).
  • In pancreatic GEP, high-level sst(3) expression was found in tumours with more active angiogenesis (higher microvessel density and vascular endothelial growth factor expression (P < 0.03)).

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  • (PMID = 17132755.001).
  • [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 / Biomarkers, Tumor; 0 / Ki-67 Antigen; 0 / RNA, Messenger; 0 / Receptors, Dopamine D2; 0 / Receptors, Somatostatin; 0 / Vascular Endothelial Growth Factor A; 0 / somatostatin receptor 2; 0 / somatostatin receptor 3; 0 / somatostatin receptor 5
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34. Kawamata T, Kubo O, Hori T: Surgical removal of growth hormone-secreting pituitary adenomas with intensive microsurgical pseudocapsule resection results in complete remission of acromegaly. Neurosurg Rev; 2005 Jul;28(3):201-8
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  • [Title] Surgical removal of growth hormone-secreting pituitary adenomas with intensive microsurgical pseudocapsule resection results in complete remission of acromegaly.
  • Although some investigators recommended surgical removal of the borders between pituitary adenoma and the surrounding normal pituitary gland, there is so far little documentation of how intensive dissection of the border zone affects the actual clinical remission rate of pituitary adenomas.
  • We investigated the precise histological characteristics of the boundary, using surgical specimens from patients who underwent intensive resection of "microsurgical pseudocapsule" of growth hormone (GH)-secreting pituitary adenomas.
  • Furthermore, we compared the remission rate of acromegaly between subjects with (Group 1) and without (Group 2) intensive resection of microsurgical pseudocapsule in order to correlate the histological complete resection and endocrinological remission.
  • Histologically, most adenomas were in direct contact with normal pituitary gland that formed an increased fibrous component facing the adenoma, without a true histological pseudocapsule.
  • It was impossible to dissect the tumor at exactly the tumor--normal pituitary interface for the whole extent of the pituitary adenoma during surgery, and complete removal of the tumor inevitably included a portion of normal tissue (microsurgical pseudocapsule).
  • The biochemical remission rate was significantly higher in Group 1 than in Group 2 (90.0 vs 61.1%), and Group 1 showed no additional postoperative pituitary hypofunction.
  • The present results suggested that intensive resection of the microsurgical pseudocapsule is essential to accomplish histological and endocrinological total resection of the GH-secreting pituitary adenomas for remission of acromegaly.

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  • [Cites] Neurol Med Chir (Tokyo). 1996 Apr;36(4):211-4 [8741248.001]
  • [Cites] Pathol Res Pract. 1991 Jun;187(5):632-6 [1923959.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Sep;86(9):4072-7 [11549628.001]
  • [Cites] Neurosurgery. 1996 Jul;39(1):189-92; discussion 192-3 [8805160.001]
  • [Cites] J Neurosurg. 1986 Jan;64(1):16-20 [3941343.001]
  • [Cites] Neurosurgery. 2001 Jun;48(6):1239-43; discussion 1244-5 [11383725.001]
  • [Cites] Neurol Med Chir (Tokyo). 1979 Sep;19(9):895-902 [91994.001]
  • [Cites] J Neurosurg. 1987 Dec;67(6):803-6 [3681419.001]
  • [Cites] Neurosurgery. 1997 Sep;41(3):602-7 [9310977.001]
  • [Cites] Neurol Res. 2002 Apr;24(3):259-65 [11958419.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Feb;85(2):526-9 [10690849.001]
  • [Cites] No To Shinkei. 1982 Sep;34(9):887-94 [7138702.001]
  • [Cites] J Neurosurg. 1986 Mar;64(3):402-7 [3950720.001]
  • [Cites] J Neurosurg. 1997 Jul;87(1):44-51 [9202264.001]
  • [Cites] J Neurosurg. 2003 Feb;98(2):350-8 [12593622.001]
  • [Cites] J Neurol Neurosurg Psychiatry. 1978 Mar;41(3):283-9 [632827.001]
  • [Cites] J Neurosurg. 1986 Dec;65(6):733-44 [3095506.001]
  • [Cites] Laryngoscope. 1999 Nov;109(11):1838-40 [10569418.001]
  • [Cites] Neurosurgery. 1993 Oct;33(4):610-7; discussion 617-8 [8232800.001]
  • [Cites] Minim Invasive Neurosurg. 2002 Dec;45(4):208-10 [12494355.001]
  • [Cites] J Neurosurg. 2002 Feb;96(2):195-208 [11838791.001]
  • [Cites] Neurosurgery. 2002 Jun;50(6):1393-7 [12015864.001]
  • [Cites] Virchows Arch. 1994;424(1):75-82 [7981907.001]
  • [Cites] Clin Endocrinol (Oxf). 1999 Jan;50(1):27-35 [10341853.001]
  • (PMID = 15765245.001).
  • [ISSN] 0344-5607
  • [Journal-full-title] Neurosurgical review
  • [ISO-abbreviation] Neurosurg Rev
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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35. Levy MJ, Classey JD, Maneesri S, Meeran K, Powell M, Goadsby PJ: The relationship between neuropeptide Y expression and headache in pituitary tumours. Eur J Neurol; 2006 Feb;13(2):125-9
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  • [Title] The relationship between neuropeptide Y expression and headache in pituitary tumours.
  • Patients with pituitary tumours often present with disabling headache but there is no clear relationship between tumour size and headache.
  • Neuropeptide Y (NPY) has been identified in pituitary tumours and may serve as a biochemical marker of the propensity for headache.
  • Using immunohistochemical techniques we examined 27 consecutive pituitary adenoma specimens for NPY (including one normal postmortem control anterior pituitary specimen).
  • NPY positive immunoreactivity was seen in 13 tumour specimens (50%, 13 of 26 pituitary tumour specimens), characterized by cytoplasmic and nuclear staining patterns.
  • We did not observe NPY in the normal anterior pituitary control specimen.
  • NPY was present in four of five (80%) growth hormone-secreting tumours and two of two (100%) prolactinomas, compared with four of 11 (36%) non-functioning adenomas.
  • The mechanism of many pituitary tumour-associated headaches remains undetermined.
  • The significance of NPY positivity in pituitary tumours is unknown, although the results of this study may implicate this peptide in the control of somatotroph and lactotroph activity.
  • Our data do not support a clear role for NPY pituitary tumour-associated headache.
  • [MeSH-major] Headache / etiology. Headache / metabolism. Neuropeptide Y / metabolism. Pituitary Neoplasms / complications. Pituitary Neoplasms / metabolism

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  • (PMID = 16490041.001).
  • [ISSN] 1351-5101
  • [Journal-full-title] European journal of neurology
  • [ISO-abbreviation] Eur. J. Neurol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Neuropeptide Y
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36. Buchfelder M, Weigel D, Droste M, Mann K, Saller B, Brübach K, Stalla GK, Bidlingmaier M, Strasburger CJ, Investigators of German Pegvisomant Observational Study: Pituitary tumor size in acromegaly during pegvisomant treatment: experience from MR re-evaluations of the German Pegvisomant Observational Study. Eur J Endocrinol; 2009 Jul;161(1):27-35
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  • [Title] Pituitary tumor size in acromegaly during pegvisomant treatment: experience from MR re-evaluations of the German Pegvisomant Observational Study.
  • In treatment-resistant patients with acromegaly, pharmacotherapy with pegvisomant (Somavert) is a highly effective option.
  • All three patients had undergone pituitary surgery as primary treatment, but had not been pre-treated with radiotherapy.
  • It was reported in between 2 and 3% of patients treated, and did not exceed the expected rate in patients with acromegaly not treated with pegvisomant.
  • As from this presently largest database of acromegalic patients treated with pegvisomant, tumor-growth rate appears not to be different from patients on other treatment modalities.
  • Although these data are reassuring with regard to the concern of somatotroph adenoma growth under peripheral GH receptor blockade, further study is required.

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  • (PMID = 19411302.001).
  • [ISSN] 1479-683X
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / pegvisomant; 12629-01-5 / Human Growth Hormone
  • [Investigator] Droste M; Stalla GK; Allolio B; Faust M; Brendel M; Finke R; Tuchelt H; Bidlingmaier M; Engelbach M; Santen R; Hampel R; Mann K; Kann H; Boehm B; Kasperk C; Kerber C; Wallaschofski H; Moenig H; Stumvoll M; Schopohl J; Völz B; Würl K; Ittner J; Reschke K; Jacobeit J; Ramadori G; Schindler A; Zeuzem S; Badenhoop K; Beil FU; Pfeiffer AF; Vogel C; Hofbauer LC; Strasburger CJ; Tuschy U; Plöckinger U; Seidlitz B; Demtröder F; Gellner R; Gräf KJ; Schröder U; Ball P; Ventzke K; Hensen J; Lux H; Etzrodt H; Alexopoulos A; Spitzweg C; Schnabel D; Dost A; Weber MM; Wiemer K; Omran W; Keuser R; Salzgeber K; Gutekunst R; Terkamp C; Gaissmaier S; Eversmann T; Seufert J; Jaursch-Hancke C; Ritter M; Undeutsch C; Jochum E; Schleiffer T; Karges W; Meuser J; Wildbrett J; Krug J; Buchfelder M; Klingmüller D; Schmitz U; Perras B; Zick R; Leicht E; Manfras B; Schuppert F; Müller OA; Stahmer E; Kajdan U; Gallwitz; Rochlitz H; Heckmann C; Haak E; Weber R; Herrmann BL; Schneider S; Scherbaum WA; Deuss U; Jacobs B; Gerbert B; Wolf M; West T; Lippe J; Biering H
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37. Koutourousiou M, Seretis A, Kontogeorgos G: Intra-sellar schwannoma co-existing with GH-secreting pituitary adenoma. Acta Neurochir (Wien); 2009 Dec;151(12):1693-7
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  • [Title] Intra-sellar schwannoma co-existing with GH-secreting pituitary adenoma.
  • BACKGROUND: We present a unique example of an intra-sellar schwannoma co-existing with a growth hormone (GH)-secreting pituitary adenoma.
  • METHOD AND FINDINGS: The patient presented with acromegaly and magnetic resonance imaging (MRI) revealed an intra-sellar mass.
  • Histopathology demonstrated the presence of a GH-secreting adenoma as well as a schwannoma at the periphery of the adenoma.
  • After surgical excision, remission of the acromegaly occurred.
  • Follow-up monitoring showed no evidence of recurrence of the adenoma two years after surgery.
  • CONCLUSION: To the best of our knowledge, this is the first example of an intra-sellar schwannoma co-existing with a GH-secreting pituitary adenoma.
  • [MeSH-major] Adenoma / pathology. Neoplasms, Multiple Primary / pathology. Neurilemmoma / pathology. Pituitary Neoplasms / pathology. Sella Turcica / pathology
  • [MeSH-minor] Adult. Humans. Neoplasm Recurrence, Local / diagnosis. Neoplasm Recurrence, Local / pathology. Neoplasm Recurrence, Local / surgery

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  • (PMID = 19350200.001).
  • [ISSN] 0942-0940
  • [Journal-full-title] Acta neurochirurgica
  • [ISO-abbreviation] Acta Neurochir (Wien)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Austria
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38. Saveanu A, Jaquet P, Brue T, Barlier A: Relevance of coexpression of somatostatin and dopamine D2 receptors in pituitary adenomas. Mol Cell Endocrinol; 2008 May 14;286(1-2):206-13
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  • [Title] Relevance of coexpression of somatostatin and dopamine D2 receptors in pituitary adenomas.
  • Dopamine and somatostatin are both involved in the negative control of normal pituitary cells.
  • Dopamine subtype 2 receptor (D2DR) and somatostatin receptor (sst) agonists, mainly directed to sst2, are used in the treatment of pituitary adenomas.
  • Nevertheless, a majority of corticotroph and gonadotroph adenomas and a third of somatotroph adenomas are still not sufficiently controlled by these treatments.
  • D2DR and sst1, 2, 3 and 5 are present in most pituitary adenomas.
  • D2DR and sst2 agonist cotreatment showed limited additivity on GH secretion in acromegaly.
  • Moreover, new chimeric compounds with sst2, D2DR and sst5 affinity have shown an increased control of secretion and/or proliferation of different types of pituitary adenomas in cell culture.
  • Together with the multi-sst ligand drugs recently developed, these dopamine-somatostatin ligands represent a new opportunity in the combinatory treatment of pituitary adenomas.
  • [MeSH-major] Adenoma / drug therapy. Pituitary Neoplasms / drug therapy. Receptors, Dopamine D2 / metabolism. Receptors, Somatostatin / metabolism. Somatostatin / metabolism
  • [MeSH-minor] Antineoplastic Agents, Hormonal / therapeutic use. Cell Proliferation / drug effects. Dopamine / analogs & derivatives. Dopamine / therapeutic use. Ergolines / therapeutic use. Growth Hormone-Secreting Pituitary Adenoma / drug therapy. Growth Hormone-Secreting Pituitary Adenoma / metabolism. Human Growth Hormone / metabolism. Humans. Octreotide / therapeutic use. Protein Multimerization. Tumor Cells, Cultured

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  • (PMID = 18241980.001).
  • [ISSN] 1872-8057
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Ergolines; 0 / Receptors, Dopamine D2; 0 / Receptors, Somatostatin; 12629-01-5 / Human Growth Hormone; 51110-01-1 / Somatostatin; LL60K9J05T / cabergoline; RWM8CCW8GP / Octreotide; VTD58H1Z2X / Dopamine
  • [Number-of-references] 90
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39. Yamada S, Fukuhara N, Oyama K, Takeshita A, Takeuchi Y: Repeat transsphenoidal surgery for the treatment of remaining or recurring pituitary tumors in acromegaly. Neurosurgery; 2010 Oct;67(4):949-56
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  • [Title] Repeat transsphenoidal surgery for the treatment of remaining or recurring pituitary tumors in acromegaly.
  • BACKGROUND: Acromegaly is a disorder characterized by hypersecretion of growth hormone caused by a growth hormone-secreting pituitary adenoma.
  • OBJECTIVE: To evaluate the long-term efficacy and safety of repeat transsphenoidal surgery for persistent or recurrent acromegaly.
  • METHODS: We retrospectively reviewed records for 53 acromegalic patients who underwent repeat transsphenoidal surgery for persistent or progressive acromegaly at Toranomon Hospital between 1987 and 2006.
  • Furthermore, 17 patients were well controlled with normal insulin-like growth factor I levels without (2 patients) or with medication (15 patients), whereas insulin-like growth factor I levels were still above normal in 5 patients after postoperative adjuvant therapy.
  • Only 1 patient was undergoing additional hormonal replacement after surgery, although transient cerebrospinal fluid leak, transient abducens nerve palsy, severe nasal bleeding, and pituitary abscess occurred in each patient, respectively.
  • Reoperation should therefore be considered for persistent or recurrent disease in acromegalic patients in whom adjuvant therapy is not effective enough or cannot be accepted.
  • [MeSH-major] Acromegaly / etiology. Acromegaly / surgery. Growth Hormone / secretion. Hypophysectomy / adverse effects. Pituitary Neoplasms / complications
  • [MeSH-minor] Adult. Chi-Square Distribution. Female. Humans. Longitudinal Studies. Magnetic Resonance Imaging / methods. Male. Middle Aged. Pituitary Gland / surgery. Postoperative Complications. Predictive Value of Tests. Reoperation / methods. Retrospective Studies. Secondary Prevention. Statistics, Nonparametric. Treatment Outcome


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

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  • [Copyright] J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart. New York.
  • (PMID = 19373754.001).
  • [ISSN] 1439-3646
  • [Journal-full-title] Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association
  • [ISO-abbreviation] Exp. Clin. Endocrinol. Diabetes
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Platelet-Derived Growth Factor; 0 / RNA, Messenger; 0 / Vascular Endothelial Growth Factor A; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Receptors, Platelet-Derived Growth Factor
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41. Petrossians P, Borges-Martins L, Espinoza C, Daly A, Betea D, Valdes-Socin H, Stevenaert A, Chanson P, Beckers A: Gross total resection or debulking of pituitary adenomas improves hormonal control of acromegaly by somatostatin analogs. Eur J Endocrinol; 2005 Jan;152(1):61-6
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  • [Title] Gross total resection or debulking of pituitary adenomas improves hormonal control of acromegaly by somatostatin analogs.
  • INTRODUCTION: Invasive GH-secreting pituitary adenomas are rarely cured by surgery and although long-term therapy with somatostatin analogs (SSAs) may be employed, hormonal control is achieved in only 60% of cases.
  • The impact of tumor debulking on subsequent control of acromegaly with SSAs has not been studied previously.
  • A case review identified 24 acromegalic patients who had received SSA therapy for > or = 1 month before and after gross total resection or debulking of adenomas.
  • GH and IGV-I responses to SSAs were recorded pre- and postoperatively.
  • RESULTS: Before preoperative SSA treatment, 24/24 (100%) patients had elevated GH levels and IGF-I levels were elevated in 19/21 (90.5%) patients with recorded values.
  • During preoperative SSA treatment, GH and IGF-I levels were normalized in 7/24 (29.2%) and 11/24 (45.8%) patients respectively.
  • Following postoperative washout, GH was controlled in only 3/24 (12.5%) patients, while IGF-I was controlled in 8/19 (42.1%) patients with available data.
  • During the second SSA treatment period, normal GH levels were seen in 13/24 (54.2%) patients, while IGF-I control was noted in 18/23 (78.3%).
  • CONCLUSION: Gross total tumor resection or debulking increases the likelihood of achieving biochemical disease control with SSAs in acromegalic patients with adenomas that were not amenable to complete surgical resection and in whom primary SSA therapy was unable to achieve good biochemical control.

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  • [CommentIn] Eur J Endocrinol. 2005 May;152(5):693-4 [15879353.001]
  • (PMID = 15762188.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 12629-01-5 / Human Growth Hormone; 51110-01-1 / Somatostatin; 67763-96-6 / Insulin-Like Growth Factor I; RWM8CCW8GP / Octreotide
  • [Number-of-references] 18
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42. Mohammed S, Cusimano MD, Scheithauer BW, Rotondo F, Horvath E, Kovacs K: O-methylguanine-DNA methyltransferase immunoexpression in a double pituitary adenoma: case report. Neurosurgery; 2010 Feb;66(2):E421-2; discussion E422
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] O-methylguanine-DNA methyltransferase immunoexpression in a double pituitary adenoma: case report.
  • OBJECTIVE: Double pituitary adenomas in surgical cases are rarely reported.
  • We present a treatment dilemma of a double adenoma that had differential O-methylguanine-DNA methyltransferase (MGMT) reactivity.
  • CLINICAL PRESENTATION: A 48-year-old man presented with acromegaly and a recurrent pituitary adenoma.
  • He had elevated growth hormone (GH) and elevated insulin-like growth factor blood levels and hyperprolactinemia.
  • Morphologic examination disclosed 2 histologically distinct tumors, including a GH adenoma and a prolactin adenoma.
  • Of significant note was MGMT immunopositivity in the GH adenoma and lack of staining in the prolactin adenoma.
  • CONCLUSION: This is the first clinical instance in which MGMT was assessed in double adenomas of the pituitary.
  • The adenomas underwent recurrence, a feature that reflects their invasive nature and the possibility that chemotherapeutic intervention may be required in the future.
  • Response to temozolomide use is anticipated with respect to the prolactin adenoma but would likely not benefit the GH cell adenoma of our patient.
  • [MeSH-major] Adenoma / enzymology. DNA Modification Methylases / metabolism. DNA Repair Enzymes / metabolism. Pituitary Neoplasms / enzymology. Tumor Suppressor Proteins / metabolism
  • [MeSH-minor] Growth Hormone / blood. Humans. Hyperprolactinemia / etiology. Insulin-Like Growth Factor Binding Proteins / blood. Ki-67 Antigen / metabolism. Male. Middle Aged

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  • (PMID = 20087113.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Insulin-Like Growth Factor Binding Proteins; 0 / Ki-67 Antigen; 0 / Tumor Suppressor Proteins; 9002-72-6 / Growth Hormone; 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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43. Bhatoe HS, Kotwal N, Badwal S: Clival pituitary adenoma with acromegaly: case report and review of literature. Skull Base; 2007 Jul;17(4):265-8
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  • [Title] Clival pituitary adenoma with acromegaly: case report and review of literature.
  • The pituitary develops as a result of complex, intricate, and precise neuro-embryological events in the sixth to eighth weeks of gestation.
  • Some ectopic cell rests can become adenomatous.
  • Rarely, these cell rests in the clivus can be the site of formation of adenoma.
  • Our patient, a 35-year-old parous woman, was being treated for acromegaly, and imaging studies revealed a clival mass lesion.
  • Trans-sphenoidal excision was done and immunohistochemistry revealed the tumor to be a growth hormone-secreting tumor.

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  • [Cites] Acta Neurochir (Wien). 2002 Nov;144(11):1221-4 [12434179.001]
  • [Cites] Acta Neuropathol. 1999 Sep;98(3):262-72 [10483784.001]
  • [Cites] Neurosurgery. 1989 Feb;24(2):279-82 [2918981.001]
  • [Cites] J Clin Endocrinol Metab. 1986 May;62(5):1065-9 [3958123.001]
  • [Cites] Australas Radiol. 1970 Aug;14(3):241-7 [5477195.001]
  • [Cites] Am J Surg Pathol. 1995 Aug;19(8):900-3 [7611536.001]
  • [Cites] Ultrastruct Pathol. 1993 Nov-Dec;17(6):637-42 [8122329.001]
  • [Cites] Otolaryngol Head Neck Surg. 1993 Feb;108(2):178-83 [8441545.001]
  • [Cites] Radiat Med. 1996 Jul-Aug;14(4):189-91 [8916261.001]
  • [Cites] Acta Chir Belg. 1998 Jan-Feb;98(1):10-3 [9538914.001]
  • (PMID = 18174927.001).
  • [ISSN] 1531-5010
  • [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/ PMC2039716
  • [Keywords] NOTNLM ; Acromegaly / clivus / pituitary tumor
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44. Segal-Lieberman G, Rubinfeld H, Glick M, Kronfeld-Schor N, Shimon I: Melanin-concentrating hormone stimulates human growth hormone secretion: a novel effect of MCH on the hypothalamic-pituitary axis. Am J Physiol Endocrinol Metab; 2006 May;290(5):E982-8
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  • [Title] Melanin-concentrating hormone stimulates human growth hormone secretion: a novel effect of MCH on the hypothalamic-pituitary axis.
  • Melanin-concentrating hormone (MCH), a 19-amino acid orexigenic (appetite-stimulating) hypothalamic peptide, is an important regulator of energy homeostasis.
  • Because pituitary hormones such as growth hormone (GH), ACTH, and thyroid-stimulating hormone affect body weight and composition, appetite, insulin sensitivity, and lipoprotein metabolism, we investigated whether MCH exerts direct effects on the human pituitary to regulate energy balance using dispersed human fetal pituitaries (21-22 wk gestation) and cultured GH-secreting adenomas.
  • We found that MCH receptor-1 (MCH-R1), but not MCH receptor-2, is expressed in both normal (fetal and adult) human pituitary tissues and in GH cell adenomas.
  • MCH (10 nM) stimulated GH release from human fetal pituitary cultures by up to 62% during a 4-h incubation (P < 0.05).
  • Interestingly, neuropeptide EI (10 nM), which is also cleaved from ppMCH, increased human GH secretion by up to 124% in fetal pituitaries.
  • A milder, albeit significant, induction of GH secretion by MCH (20%) was seen in cultured GH-secreting pituitary adenomas.
  • A comparable stimulation of GH secretion was seen when cultured mouse pituitary cells were treated with MCH.
  • Treatment of cultured GH adenoma cells with MCH (100 nM) induced extracellular signal-regulated kinases 1 and 2 phosphorylation, suggesting activation of MCH-R1.
  • In aggregate, these data suggest that MCH may regulate pituitary GH secretion and imply a potential cross-talk mechanism between appetite-regulating neuropeptides and pituitary hormones.
  • [MeSH-major] Human Growth Hormone / secretion. Hypothalamic Hormones / pharmacology. Hypothalamo-Hypophyseal System / drug effects. Melanins / pharmacology. Pituitary Hormones / pharmacology
  • [MeSH-minor] Animals. Cells, Cultured. Fetus. Gene Expression / genetics. Growth Hormone-Releasing Hormone / pharmacology. Humans. Mice. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. Oligopeptides / pharmacology. Phosphorylation / drug effects. Pituitary Gland / cytology. Pituitary Gland / metabolism. Pituitary Neoplasms / metabolism. Pituitary Neoplasms / pathology. Receptors, Somatostatin / genetics. Tumor Cells, Cultured

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  • (PMID = 16603725.001).
  • [ISSN] 0193-1849
  • [Journal-full-title] American journal of physiology. Endocrinology and metabolism
  • [ISO-abbreviation] Am. J. Physiol. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hypothalamic Hormones; 0 / MCHR1 protein, human; 0 / Melanins; 0 / Oligopeptides; 0 / Pituitary Hormones; 0 / Receptors, Somatostatin; 0 / neuropeptide EI; 12629-01-5 / Human Growth Hormone; 67382-96-1 / melanin-concentrating hormone; 9034-39-3 / Growth Hormone-Releasing Hormone; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3
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45. Mantovani G, Bondioni S, Ferrero S, Gamba B, Ferrante E, Peverelli E, Corbetta S, Locatelli M, Rampini P, Beck-Peccoz P, Spada A, Lania AG: Effect of cyclic adenosine 3',5'-monophosphate/protein kinase a pathway on markers of cell proliferation in nonfunctioning pituitary adenomas. J Clin Endocrinol Metab; 2005 Dec;90(12):6721-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of cyclic adenosine 3',5'-monophosphate/protein kinase a pathway on markers of cell proliferation in nonfunctioning pituitary adenomas.
  • In particular, activating mutations of the G(s)alpha gene and protein kinase A (PKA) overactivity due to low expression of PKA regulatory subunit 1A (R1A) have been implicated in somatotroph proliferation.
  • OBJECTIVE: The objective of this study was to evaluate the effects of cAMP-PKA cascade activation in nonfunctioning pituitary adenomas (NFPA).
  • CONCLUSIONS: These data show that in contrast with what was previously observed in transformed somatotrophs, activation of the cAMP-PKA pathway did not generate proliferative signals in tumoral cells of the gonadotroph lineage, and in a subset of tumors even exerted a tonic inhibitory effect, thus confirming a different role for the cAMP-mediated pathway in promoting proliferation in the pituitary.
  • [MeSH-major] Adenoma / metabolism. Adenoma / pathology. Biomarkers, Tumor / metabolism. Cyclic AMP / metabolism. Cyclic AMP-Dependent Protein Kinases / metabolism. Pituitary Neoplasms / metabolism. Pituitary Neoplasms / pathology
  • [MeSH-minor] Base Sequence. Cell Proliferation. Cyclic AMP-Dependent Protein Kinase RIalpha Subunit. Cyclin D1 / metabolism. Enzyme Activation. Humans. In Vitro Techniques. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. Proteins / genetics. Proteins / metabolism. Receptors, Cell Surface / metabolism

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  • (PMID = 16204369.001).
  • [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 / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit; 0 / PRKAR1A protein, human; 0 / Proteins; 0 / Receptors, Cell Surface; 136601-57-5 / Cyclin D1; E0399OZS9N / Cyclic AMP; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3
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46. Burdman JA, Pauni M, Heredia Sereno GM, Bordón AE: Estrogen receptors in human pituitary tumors. Horm Metab Res; 2008 Aug;40(8):524-7
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  • [Title] Estrogen receptors in human pituitary tumors.
  • The relationship between the presence of estrogen receptors in pituitary adenomas and the post surgical evolution of the patients in order to find another prognostic parameter for these tumors have been studied to improve the treatment selection.
  • Estrogen receptors were studied by immunocytochemistry in histological sections of paraffin embedded 42 pituitary adenomas.
  • As expected, the higher concentration (60%) was found in prolactin secreting adenomas, although we found estrogen receptors in one somatotroph and in one nonsecreting.
  • The results of this work suggest that the determination of estrogen receptors in pituitary tumors might help as a prognostic factor in these adenomas.
  • [MeSH-major] Adenoma / metabolism. Pituitary Neoplasms / metabolism. Receptors, Estrogen / metabolism
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / metabolism. Adult. Female. Growth Hormone-Secreting Pituitary Adenoma / metabolism. Humans. Immunohistochemistry. Male. Middle Aged. Prognosis. Prolactinoma / metabolism

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  • (PMID = 18398784.001).
  • [ISSN] 0018-5043
  • [Journal-full-title] Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et métabolisme
  • [ISO-abbreviation] Horm. Metab. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Receptors, Estrogen
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47. Zatelli MC, Minoia M, Filieri C, Tagliati F, Buratto M, Ambrosio MR, Lapparelli M, Scanarini M, Degli Uberti EC: Effect of everolimus on cell viability in nonfunctioning pituitary adenomas. J Clin Endocrinol Metab; 2010 Feb;95(2):968-76
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of everolimus on cell viability in nonfunctioning pituitary adenomas.
  • CONTEXT: Pituitary adenomas can cause specific syndromes due to hormone excess and/or determine sellar mass symptoms.
  • Pituitary cell growth can sometimes be influenced by medical therapy, such as for somatotroph adenomas treated with somatostatin analogs or prolactinomas treated with dopaminergic drugs.
  • However, nonfunctioning pituitary adenomas (NFAs) are still orphans of medical therapy.
  • Cell viability and apoptosis were evaluated after 48 h, and vascular endothelial growth factor (VEGF) secretion was assessed after an 8-h incubation.
  • RESULTS: In 28 cultures (70%), Everolimus significantly reduced cell viability (by approximately 40%; P < 0.05 vs. control), promoted apoptosis (+30%; P < 0.05 vs. control), inhibited p70S6K activity (-20%), and blocked IGF-I proliferative and antiapoptotic effects.
  • CONCLUSIONS: Everolimus reduced NFA cell viability by inducing apoptosis, with a mechanism likely involving IGF-I signaling but not VEGF secretion, suggesting that it might represent a possible medical treatment of invasive/recurrent NFAs.
  • [MeSH-major] Adenoma / drug therapy. Immunosuppressive Agents / pharmacology. Pituitary Neoplasms / drug therapy. Sirolimus / analogs & derivatives
  • [MeSH-minor] Aged. Apoptosis / drug effects. Cell Line, Tumor. Cell Survival / drug effects. Ergolines / pharmacology. Everolimus. Female. Humans. Male. Middle Aged. Receptors, Somatostatin / physiology. Ribosomal Protein S6 Kinases, 70-kDa / metabolism. Somatostatin / analogs & derivatives. Somatostatin / pharmacology. Vascular Endothelial Growth Factor A / secretion

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  • (PMID = 19965918.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ergolines; 0 / Immunosuppressive Agents; 0 / Receptors, Somatostatin; 0 / Vascular Endothelial Growth Factor A; 0 / somatostatin receptor 2; 51110-01-1 / Somatostatin; 98H1T17066 / pasireotide; 9HW64Q8G6G / Everolimus; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa; LL60K9J05T / cabergoline; W36ZG6FT64 / Sirolimus
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48. Bondanelli M, Bonadonna S, Ambrosio MR, Doga M, Gola M, Onofri A, Zatelli MC, Giustina A, degli Uberti EC: Cardiac and metabolic effects of chronic growth hormone and insulin-like growth factor I excess in young adults with pituitary gigantism. Metabolism; 2005 Sep;54(9):1174-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cardiac and metabolic effects of chronic growth hormone and insulin-like growth factor I excess in young adults with pituitary gigantism.
  • Chronic growth hormone (GH)/insulin-like growth factor I (IGF-I) excess is associated with considerable mortality in acromegaly, but no data are available in pituitary gigantism.
  • The aim of the study was to evaluate the long-term effects of early exposure to GH and IGF-I excess on cardiovascular and metabolic parameters in adult patients with pituitary gigantism.
  • Six adult male patients with newly diagnosed gigantism due to GH secreting pituitary adenoma were studied and compared with 6 age- and sex-matched patients with acromegaly and 10 healthy subjects.
  • Disease duration was significantly longer (P<.05) in patients with gigantism than in patients with acromegaly, whereas GH and IGF-I concentrations were comparable.
  • Left ventricular mass was increased both in patients with gigantism and in patients with acromegaly, as compared with controls.
  • Left ventricular hypertrophy was detected in 2 of 6 of both patients with gigantism and patients with acromegaly, and isolated intraventricular septum thickening in 1 patient with gigantism.
  • Inadequate diastolic filling (ratio between early and late transmitral flow velocity<1) was detected in 2 of 6 patients with gigantism and 1 of 6 patients with acromegaly.
  • Impaired glucose metabolism occurrence was higher in patients with acromegaly (66%) compared with patients with gigantism (16%).
  • In conclusion, our data suggest that GH/IGF-I excess in young adult patients is associated with morphologic and functional cardiac abnormalities that are similar in patients with gigantism and in patients with acromegaly, whereas occurrence of impaired glucose metabolism appears to be higher in patients with acromegaly, although patients with gigantism are exposed to GH excess for a longer period.
  • [MeSH-major] Gigantism / complications. Gigantism / metabolism. Human Growth Hormone / blood. Hypertrophy, Left Ventricular / etiology. Hypertrophy, Left Ventricular / metabolism. Insulin-Like Growth Factor I / metabolism
  • [MeSH-minor] Acromegaly / complications. Acromegaly / metabolism. Adult. Blood Pressure. Echocardiography, Doppler. Electrocardiography. Glucose / metabolism. Glucose Intolerance / etiology. Glucose Intolerance / metabolism. Humans. Male. Ventricular Dysfunction, Left / etiology. Ventricular Dysfunction, Left / metabolism. Ventricular Dysfunction, Left / ultrasonography

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  • (PMID = 16125529.001).
  • [ISSN] 0026-0495
  • [Journal-full-title] Metabolism: clinical and experimental
  • [ISO-abbreviation] Metab. Clin. Exp.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I; IY9XDZ35W2 / Glucose
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49. Johnson MD, Fan X, Bourne P, Walters D: Neuronal differentiation and expression of neural epitopes in pituitary adenomas. J Histochem Cytochem; 2007 Dec;55(12):1265-71
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  • [Title] Neuronal differentiation and expression of neural epitopes in pituitary adenomas.
  • Neural transdifferentiation is increasingly recognized in neural crest and neural stem cell tumors.
  • Neuronal differentiation has been anecdotally described primarily in somatotroph cell adenomas associated with acromegaly, but its prevalence in adenomas and relationship to adenoma type has not been completely established.
  • In this study we performed a retrospective morphological and immunohistochemical analysis of neurofilament, phosphoneurofilament, Neu-N, class III tubulin, and Hu in WHO grade I pituitary adenomas.
  • Limited numbers of cells with neuronal features and neuron-associated epitopes may be more common in pituitary adenomas than previously recognized.
  • These may occur in many forms of adenomas including somatotroph, lactotroph, mixed somatotroph and lactotroph, null cell/gonadotroph cell and, rarely, corticotroph cell adenomas.
  • [MeSH-major] Adenoma / metabolism. Biomarkers, Tumor / biosynthesis. Epitopes. Neurons / metabolism. Pituitary Neoplasms / metabolism
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / metabolism. ACTH-Secreting Pituitary Adenoma / pathology. Adult. Aged. Aged, 80 and over. Antibodies. Cell Differentiation. Female. Gonadotrophs / metabolism. Gonadotrophs / pathology. Human Growth Hormone / metabolism. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Staging. Prolactin / metabolism. Prolactinoma / metabolism. Prolactinoma / pathology. Retrospective Studies

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  • (PMID = 17875653.001).
  • [ISSN] 0022-1554
  • [Journal-full-title] The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society
  • [ISO-abbreviation] J. Histochem. Cytochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Biomarkers, Tumor; 0 / Epitopes; 12629-01-5 / Human Growth Hormone; 9002-62-4 / Prolactin
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50. Jaquet P, Gunz G, Saveanu A, Dufour H, Taylor J, Dong J, Kim S, Moreau JP, Enjalbert A, Culler MD: Efficacy of chimeric molecules directed towards multiple somatostatin and dopamine receptors on inhibition of GH and prolactin secretion from GH-secreting pituitary adenomas classified as partially responsive to somatostatin analog therapy. Eur J Endocrinol; 2005 Jul;153(1):135-41
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  • [Title] Efficacy of chimeric molecules directed towards multiple somatostatin and dopamine receptors on inhibition of GH and prolactin secretion from GH-secreting pituitary adenomas classified as partially responsive to somatostatin analog therapy.
  • OBJECTIVE: This study compared the potency of a somatostatin receptor (sstr)2-sstr5 analog, BIM-23244, of an sstr2-dopamine D2 receptor (sstr2-DAD2) molecule, BIM-23A387 and of new somatostatin-dopamine chimeric molecules with differing, enhanced affinities for sstr2, sstr5 and DAD2, BIM-23A758, BIM-23A760 and BIM-23A761, to suppress GH and prolactin (PRL) from 18 human GH adenomas that are partially responsive to octreotide or lanreotide.
  • The effect of drugs was tested in cell cultures at various concentrations.
  • In 13 tumors, the maximal suppression of GH secretion produced by BIM-23A387 (30+/-3%) and BIM-23244 (28+/-3%) was greater than that produced by octreotide (23+/-3%).
  • In six out of 13 tumors, BIM-23A758, BIM-23A760 and BIM- 23A761 produced greater maximal suppression of GH secretion than octreotide (33+/-5, 38+/-2 and 41+/-2 vs 24+/-2%).
  • BIM-23A761 was more effective than BIM-23A387 in GH suppression (41+/-2 vs 32+/-4%).
  • CONCLUSIONS: Novel dopamine-somatostatin chimeric molecules with differing, enhanced activity at sstr2, sstr5 and DAD2, consistently produced significatly greater suppression of GH and PRL than either octreotide or single-receptor-interacting ligands in tumors from patients classified as only partially responsive to octreotide therapy.
  • The other mechanisms by which such molecules produce an enhanced inhibition of GH remain to be elucidated.

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  • (PMID = 15994755.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / BIM 23A760; 0 / BIM-23244; 0 / BIM-23A761; 0 / RNA, Messenger; 0 / Receptors, Dopamine D2; 0 / Receptors, Somatostatin; 0 / Recombinant Fusion Proteins; 0 / somatostatin receptor 2; 0 / somatostatin receptor 5; 12629-01-5 / Human Growth Hormone; 51110-01-1 / Somatostatin; 9002-62-4 / Prolactin; RWM8CCW8GP / Octreotide; VTD58H1Z2X / Dopamine
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51. Manavela MP, Juri A, Danilowicz K, Bruno OD: [Therapeutic management in 154 acromegalic patients]. Medicina (B Aires); 2010;70(4):328-32
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  • Acromegaly is a chronic, invalidating disease due in over 95% of cases to a growth hormone (GH) secreting pituitary adenoma.
  • Its clinical manifestations are associated to local complications related to the tumor growth and/or to the metabolic consequences of GH excess.
  • In only 14.0% of acromegalics drug therapy with dopaminergic agents was effective in controlling the disease.
  • In summary, multimodal therapy of acromegaly can lead to a global safe control of the disease in 55.2% of the cases.
  • [MeSH-major] Acromegaly / therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Female. Human Growth Hormone / metabolism. Humans. Male. Middle Aged. Retrospective Studies. Young Adult

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  • (PMID = 20679052.001).
  • [ISSN] 0025-7680
  • [Journal-full-title] Medicina
  • [ISO-abbreviation] Medicina (B Aires)
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Argentina
  • [Chemical-registry-number] 12629-01-5 / Human Growth Hormone
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52. Melmed S: Acromegaly pathogenesis and treatment. J Clin Invest; 2009 Nov;119(11):3189-202
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  • [Title] Acromegaly pathogenesis and treatment.
  • Dysregulated growth hormone (GH) hypersecretion is usually caused by a GH-secreting pituitary adenoma and leads to acromegaly - a disorder of disproportionate skeletal, tissue, and organ growth.
  • High GH and IGF1 levels lead to comorbidities including arthritis, facial changes, prognathism, and glucose intolerance.
  • This Review discusses acromegaly pathogenesis and management options.
  • Somatostatin receptor (SSTR) ligands inhibit GH release, control tumor growth, and attenuate peripheral GH action, while GH receptor antagonists block GH action and effectively lower IGF1 levels.
  • Effective control of GH and IGF1 hypersecretion and ablation or stabilization of the pituitary tumor mass lead to improved comorbidities and lowering of mortality rates for this hormonal disorder.

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  • [Cites] J Clin Endocrinol Metab. 2009 Apr;94(4):1255-63 [19158203.001]
  • [Cites] Annu Rev Pathol. 2009;4:97-126 [19400692.001]
  • [Cites] J Clin Endocrinol Metab. 2009 May;94(5):1500-8 [19208728.001]
  • [Cites] J Clin Endocrinol Metab. 2009 May;94(5):1509-17 [19208732.001]
  • [Cites] J Biol Chem. 2009 Jul 24;284(30):19937-44 [19460757.001]
  • [Cites] Science. 2000 Apr 7;288(5463):154-7 [10753124.001]
  • [Cites] N Engl J Med. 2000 Apr 20;342(16):1171-7 [10770982.001]
  • [Cites] Recent Prog Horm Res. 2000;55:237-66; discussion 266-7 [11036940.001]
  • [Cites] Dev Biol. 2001 Jan 1;229(1):141-62 [11133160.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Jan;86(1):140-5 [11231991.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Apr;86(4):1716-23 [11297608.001]
  • [Cites] Neurosurgery. 2001 Jun;48(6):1239-43; discussion 1244-5 [11383725.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Sep;86(9):4072-7 [11549628.001]
  • [Cites] Endocr Rev. 2001 Dec;22(6):800-17 [11739334.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Mar;87(3):1262-7 [11889197.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Jul;87(7):3013-8 [12107192.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Sep;87(9):4142-6 [12213862.001]
  • [Cites] Nat Genet. 2002 Oct;32(2):306-11 [12355087.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Oct;87(10):4554-63 [12364434.001]
  • [Cites] Endocrinology. 2003 Mar;144(3):967-74 [12586774.001]
  • [Cites] Horm Res. 2003;60(2):53-60 [12876414.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Sep;88(9):4239-45 [12970293.001]
  • [Cites] N Engl J Med. 2003 Sep 18;349(12):1139-47 [13679528.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Nov;88(11):5414-21 [14602782.001]
  • [Cites] Nat Rev Drug Discov. 2003 Dec;2(12):999-1017 [14654798.001]
  • [Cites] J Clin Invest. 2003 Dec;112(11):1603-18 [14660734.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Feb;89(2):638-45 [14764775.001]
  • [Cites] Endocr Rev. 2004 Feb;25(1):102-52 [14769829.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Apr;89(4):1613-7 [15070920.001]
  • [Cites] Nat Genet. 2004 Jul;36(7):720-4 [15208626.001]
  • [Cites] J Clin Invest. 2004 Aug;114(3):349-56 [15286801.001]
  • [Cites] N Engl J Med. 1979 Nov 22;301(21):1138-42 [492275.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Apr;91(4):1239-45 [16403824.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Apr;91(4):1397-403 [16449332.001]
  • [Cites] Cancer Cell. 2006 Jun;9(6):459-71 [16766265.001]
  • [Cites] Clin Chim Acta. 2006 Nov;373(1-2):176-9 [16815351.001]
  • [Cites] Endocr Relat Cancer. 2006 Sep;13(3):707-16 [16954426.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Oct 17;103(42):15558-63 [17030811.001]
  • [Cites] Curr Opin Oncol. 2007 Jan;19(1):24-9 [17133108.001]
  • [Cites] N Engl J Med. 2006 Dec 14;355(24):2558-73 [17167139.001]
  • [Cites] Eur J Endocrinol. 2007 Jan;156(1):75-82 [17218728.001]
  • [Cites] Mol Cell Biol. 2007 Feb;27(4):1495-504 [17145768.001]
  • [Cites] Nat Clin Pract Endocrinol Metab. 2007 Mar;3(3):302-10 [17315038.001]
  • [Cites] Rev Endocr Metab Disord. 2006 Dec;7(4):225-35 [17308965.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Mar 6;104(10):4101-5 [17360484.001]
  • [Cites] Carcinogenesis. 2007 Mar;28(3):749-59 [17071631.001]
  • [Cites] Endocr Rev. 2007 Apr;28(2):165-86 [17325339.001]
  • [Cites] Pituitary. 2007;10(2):165-72 [17458702.001]
  • [Cites] Clin Endocrinol (Oxf). 2007 Jun;66(6):859-68 [17465997.001]
  • [Cites] Clin Endocrinol (Oxf). 2007 Jul;67(1):65-70 [17437512.001]
  • [Cites] Clin Endocrinol (Oxf). 2007 Aug;67(2):282-9 [17524029.001]
  • [Cites] Clin Endocrinol (Oxf). 2007 Aug;67(2):310-5 [17555503.001]
  • [Cites] Eur J Endocrinol. 2007 Oct;157(4):371-82 [17893250.001]
  • [Cites] IDrugs. 2007 Dec;10(12):885-95 [18041687.001]
  • [Cites] Cell Death Differ. 2008 Jan;15(1):202-12 [17962814.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Jan;93(1):61-7 [17971431.001]
  • [Cites] Rev Endocr Metab Disord. 2008 Mar;9(1):33-9 [18075787.001]
  • [Cites] Clin Cancer Res. 2008 Apr 1;14(7):1984-96 [18381936.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Apr;93(4):1412-7 [18211974.001]
  • [Cites] Nat Med. 1999 Nov;5(11):1317-21 [10546001.001]
  • [Cites] Recent Prog Horm Res. 1999;54:397-438; discussion 438-9 [10548885.001]
  • [Cites] Nature. 1999 Dec 9;402(6762):656-60 [10604470.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Feb;85(2):707-14 [10690880.001]
  • [Cites] J Clin Invest. 1982 Nov;70(5):965-77 [6290540.001]
  • [Cites] Endocrinology. 1983 Apr;112(4):1553-5 [6131812.001]
  • [Cites] Endocr Rev. 1983 Spring;4(2):97-130 [6345149.001]
  • [Cites] Endocrinology. 1984 Nov;115(5):1952-7 [6149116.001]
  • [Cites] Nature. 1987 Dec 10-16;330(6148):566-8 [2825031.001]
  • [Cites] J Clin Invest. 1988 Apr;81(4):968-75 [3127426.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Jul;87(13):5061-5 [2367524.001]
  • [Cites] Endocrinology. 1990 Sep;127(3):1033-40 [2387246.001]
  • [Cites] Ann Intern Med. 1990 Dec 15;113(12):921-5 [2240917.001]
  • [Cites] Endocrinology. 1990 Dec;127(6):3187-95 [2123448.001]
  • [Cites] N Engl J Med. 1991 Dec 12;325(24):1688-95 [1944469.001]
  • [Cites] J Clin Endocrinol Metab. 1992 Apr;74(4):914-9 [1312542.001]
  • [Cites] Mol Endocrinol. 1992 Apr;6(4):598-606 [1584223.001]
  • [Cites] Endocrinol Metab Clin North Am. 1992 Sep;21(3):597-614 [1521514.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Oct 15;89(20):9826-30 [1409707.001]
  • [Cites] J Clin Endocrinol Metab. 1994 Sep;79(3):724-9 [7521350.001]
  • [Cites] Mol Endocrinol. 1995 Jul;9(7):777-83 [7476961.001]
  • [Cites] Recent Prog Horm Res. 1996;51:189-215; discussion 215-6 [8701079.001]
  • [Cites] J Clin Invest. 1997 Feb 15;99(4):789-98 [9045884.001]
  • [Cites] Mol Endocrinol. 1997 Apr;11(4):433-41 [9092795.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Jul 8;94(14):7239-44 [9207075.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Oct 14;94(21):11381-6 [9326618.001]
  • [Cites] J Clin Invest. 1997 Nov 1;100(9):2386-92 [9410919.001]
  • [Cites] Nat Genet. 1998 Apr;18(4):360-4 [9537419.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Nov;83(11):3808-16 [9814451.001]
  • [Cites] J Clin Endocrinol Metab. 1999 May;84(5):1518-23 [10323372.001]
  • [Cites] Science. 1999 Jul 16;285(5426):418-22 [10411507.001]
  • [Cites] Clin Endocrinol (Oxf). 1999 May;50(5):561-7 [10468920.001]
  • [Cites] J Biol Chem. 2004 Dec 3;279(49):51100-6 [15456744.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Feb;90(2):800-4 [15562021.001]
  • [Cites] Endocrinology. 2005 Apr;146(4):1772-9 [15618350.001]
  • [Cites] Mol Endocrinol. 2005 May;19(5):1383-91 [15677710.001]
  • [Cites] Curr Opin Genet Dev. 2005 Jun;15(3):332-40 [15917210.001]
  • [Cites] J Biol Chem. 2005 Jun 24;280(25):24011-21 [15857828.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Jul;90(7):4405-10 [15827109.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Aug;90(8):4483-8 [15899958.001]
  • [Cites] Nat Struct Mol Biol. 2005 Sep;12(9):814-21 [16116438.001]
  • [Cites] Clin Endocrinol (Oxf). 2008 Jun;68(6):970-5 [18031313.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Jun;93(6):2390-401 [18381572.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Jun;93(6):2035-41 [18381584.001]
  • [Cites] Cell. 2008 Jun 13;133(6):1019-31 [18555778.001]
  • [Cites] Endocrinology. 2008 Jul;149(7):3294-305 [18388193.001]
  • [Cites] Int J Biochem Cell Biol. 2008;40(10):1984-9 [17888716.001]
  • [Cites] Clin Chem. 2008 Aug;54(8):1268-76 [18567697.001]
  • [Cites] Eur J Endocrinol. 2008 Aug;159(2):89-95 [18524797.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Aug;93(8):2957-68 [18477663.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Aug;93(8):2984-90 [18492760.001]
  • [Cites] Mol Endocrinol. 2008 Sep;22(9):2190-202 [18635665.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Sep;93(9):3411-5 [18611972.001]
  • [Cites] Mol Endocrinol. 2008 Oct;22(10):2278-92 [18653781.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Oct;93(10):4119-25 [18628527.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Nov 11;105(45):17498-503 [18981426.001]
  • [Cites] Cancer Res. 2008 Dec 15;68(24):10163-70 [19074883.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Dec 23;105(51):20452-7 [19088192.001]
  • [Cites] J Clin Endocrinol Metab. 2009 Jan;94(1):218-22 [18957501.001]
  • [Cites] J Clin Endocrinol Metab. 2009 Feb;94(2):523-7 [19033371.001]
  • [Cites] Mol Endocrinol. 2009 Mar;23(3):337-48 [19131507.001]
  • [Cites] Cancer Res. 2009 Mar 1;69(5):1844-50 [19223528.001]
  • [Cites] Eur J Endocrinol. 2009 Apr;160(4):543-8 [19141605.001]
  • [Cites] Clin Endocrinol (Oxf). 2009 May;70(5):757-68 [19178516.001]
  • (PMID = 19884662.001).
  • [ISSN] 1558-8238
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA075979; United States / NCI NIH HHS / CA / CA 075979
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 67763-96-6 / Insulin-Like Growth Factor I; 9002-72-6 / Growth Hormone
  • [Number-of-references] 125
  • [Other-IDs] NLM/ PMC2769196
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53. Chesnokova V, Melmed S: Pituitary senescence: the evolving role of Pttg. Mol Cell Endocrinol; 2010 Sep 15;326(1-2):55-9
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  • [Title] Pituitary senescence: the evolving role of Pttg.
  • Despite the high prevalence of pituitary adenomas they are invariably benign, indicative of unique intrinsic mechanisms controlling pituitary cell proliferation.
  • Cellular senescence is characterized by a largely irreversible cell cycle arrest and constitutes a strong anti-proliferative response, which can be triggered by DNA damage, chromosomal instability and aneuploidy, loss of tumor suppressive signaling or oncogene activation.
  • Here we discuss prospective mechanisms underlying senescence-associated molecular pathways activated in benign pituitary adenomas.
  • Both deletion and over-expression of pituitary tumor transforming gene (Pttg) promote chromosomal instability and aneuploidy.
  • Abundant PTTG in GH-secreting pituitary adenomas also triggers p21-dependent senescence.
  • Pituitary p21 may therefore safeguard against further chromosomal instability by constraining pituitary tumor growth.
  • These observations point to senescence as a target for effective therapy for both tumor silencing and growth restraint towards development of pituitary malignancy.

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  • [Copyright] 2010 Elsevier Ireland Ltd. All rights reserved.
  • [Cites] Mol Endocrinol. 2001 Nov;15(11):1870-9 [11682618.001]
  • [Cites] Trends Cell Biol. 2001 Nov;11(11):S27-31 [11684439.001]
  • [Cites] J Clin Invest. 2001 Dec;108(12):1729-33 [11748253.001]
  • [Cites] Oncogene. 2002 Jan 21;21(4):503-11 [11850775.001]
  • [Cites] Cell. 2002 May 3;109(3):335-46 [12015983.001]
  • [Cites] Nat Genet. 2003 Jan;33(1):49-54 [12469122.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Mar 18;100(6):3428-32 [12626748.001]
  • [Cites] Front Neuroendocrinol. 2003 Apr;24(2):94-127 [12763000.001]
  • [Cites] Endocr Relat Cancer. 2003 Jun;10(2):323-30 [12790793.001]
  • [Cites] Cell. 2003 Jun 13;113(6):703-16 [12809602.001]
  • [Cites] Endocrinology. 2003 Nov;144(11):4991-8 [12960092.001]
  • [Cites] J Clin Invest. 2003 Dec;112(11):1603-18 [14660734.001]
  • [Cites] J Clin Invest. 2004 Jan;113(2):160-8 [14722605.001]
  • [Cites] Nature. 1989 Aug 31;340(6236):692-6 [2549426.001]
  • [Cites] Nature. 1990 May 31;345(6274):458-60 [2342578.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Sep 26;92(20):9363-7 [7568133.001]
  • [Cites] Cell. 1997 Mar 7;88(5):593-602 [9054499.001]
  • [Cites] Mol Endocrinol. 1997 Apr;11(4):433-41 [9092795.001]
  • [Cites] Mol Endocrinol. 1999 Jan;13(1):156-66 [9892021.001]
  • [Cites] Prog Mol Subcell Biol. 1998;20:43-71 [9928526.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Feb 2;96(3):1002-7 [9927683.001]
  • [Cites] Nat Med. 1999 Nov;5(11):1317-21 [10546001.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Feb;84(2):761-7 [10022450.001]
  • [Cites] Science. 1999 Jul 16;285(5426):418-22 [10411507.001]
  • [Cites] Exp Cell Res. 1961 Dec;25:585-621 [13905658.001]
  • [Cites] Ann Diagn Pathol. 2005 Feb;9(1):6-10 [15692944.001]
  • [Cites] Mol Endocrinol. 2005 May;19(5):1383-91 [15677710.001]
  • [Cites] Oncogene. 2005 Jul 14;24(30):4861-6 [15897900.001]
  • [Cites] Nature. 2005 Aug 4;436(7051):642 [16079833.001]
  • [Cites] Nature. 2005 Aug 4;436(7051):660-5 [16079837.001]
  • [Cites] Nature. 2005 Aug 4;436(7051):720-4 [16079850.001]
  • [Cites] Science. 2005 Aug 5;309(5736):886-7 [16081723.001]
  • [Cites] Mol Endocrinol. 2005 Sep;19(9):2371-9 [15919720.001]
  • [Cites] Cancer Res. 2005 Oct 1;65(19):8747-53 [16204044.001]
  • [Cites] Anal Quant Cytol Histol. 2005 Oct;27(5):241-52 [16447816.001]
  • [Cites] Endocr Relat Cancer. 2006 Sep;13(3):707-16 [16954426.001]
  • [Cites] N Engl J Med. 2006 Sep 7;355(10):1037-46 [16957149.001]
  • [Cites] Nature. 2006 Nov 30;444(7119):633-7 [17136093.001]
  • [Cites] Am J Physiol Cell Physiol. 2007 Sep;293(3):C1082-92 [17626243.001]
  • [Cites] Cancer Res. 2007 Nov 1;67(21):10564-72 [17975001.001]
  • [Cites] Endocrinology. 2007 Dec;148(12):6019-25 [17872367.001]
  • [Cites] Cell Death Differ. 2008 Jan;15(1):202-12 [17962814.001]
  • [Cites] Trends Genet. 2008 Feb;24(2):77-85 [18192065.001]
  • [Cites] Science. 2008 Mar 7;319(5868):1352-5 [18323444.001]
  • [Cites] Cell. 2008 Jun 13;133(6):958-61 [18555773.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Nov 11;105(45):17498-503 [18981426.001]
  • [Cites] Pituitary. 2009;12(1):40-50 [18270844.001]
  • [Cites] Nat Rev Cancer. 2009 Feb;9(2):81-94 [19132009.001]
  • [Cites] Cell Cycle. 2009 Mar 1;8(5):677-8 [19223763.001]
  • [Cites] Clin Endocrinol (Oxf). 2010 Mar;72(3):377-82 [19650784.001]
  • [Cites] Nat Clin Pract Endocrinol Metab. 2006 Dec;2(12):681-93 [17143315.001]
  • [Cites] Nature. 2006 Dec 21;444(7122):1038-43 [17183314.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Dec 26;103(52):19842-7 [17170138.001]
  • [Cites] Carcinogenesis. 2007 Mar;28(3):749-59 [17071631.001]
  • [Cites] Endocr Rev. 2007 Apr;28(2):165-86 [17325339.001]
  • [Cites] Cell. 2007 Jul 27;130(2):223-33 [17662938.001]
  • [Cites] J Biol Chem. 2000 Nov 24;275(47):36502-5 [11013229.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Feb;86(2):867-74 [11158059.001]
  • (PMID = 20153804.001).
  • [ISSN] 1872-8057
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA075979-11A1; United States / NCI NIH HHS / CA / R01 CA075979; United States / NCI NIH HHS / CA / R01 CA075979-11A1
  • [Publication-type] Journal Article; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Securin; 0 / pituitary tumor-transforming protein 1, human
  • [Other-IDs] NLM/ NIHMS185500; NLM/ PMC2906651
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54. Lau SL, McGrath S, Evain-Brion D, Smith R: Clinical and biochemical improvement in acromegaly during pregnancy. J Endocrinol Invest; 2008 Mar;31(3):255-61
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  • [Title] Clinical and biochemical improvement in acromegaly during pregnancy.
  • Numerous case reports of pregnancy in acromegaly exist, however detailed descriptions of changes in placental and pituitary GH and IGF-I throughout gestation are rare.
  • A 19-yr-old female presented to this institution with signs and symptoms of a GH-secreting pituitary adenoma.
  • Following transphenoidal hypophysectomy, she had 3 unplanned pregnancies, despite ongoing active disease.
  • This was despite increasing placental GH levels, and was not consistent with previous reports in the literature.
  • Further surgical and medical therapies for acromegaly failed to normalize nonpregnant GH or IGF-I levels in this woman.
  • Estrogen is known to alter GH signaling via its interaction with Janus kinase/signal transducers and activators of transcription (JAK-STAT) pathways.
  • [MeSH-major] Acromegaly / physiopathology. Pregnancy Complications / physiopathology
  • [MeSH-minor] Adult. Female. Human Growth Hormone / analysis. Human Growth Hormone / blood. Human Growth Hormone / secretion. Humans. Hypophysectomy. Insulin-Like Growth Factor I / analysis. Magnetic Resonance Imaging. Pituitary Neoplasms / secretion. Pituitary Neoplasms / surgery. Placenta / chemistry. Pregnancy. Pregnancy Complications, Neoplastic / physiopathology. Pregnancy Outcome. Reoperation

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  • [Cites] J Clin Endocrinol Metab. 1990 Sep;71(3):725-31 [2118540.001]
  • [Cites] N Engl J Med. 1989 Mar 9;320(10):671-2 [2918882.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Jun;86(6):2456-8 [11397839.001]
  • [Cites] J Clin Endocrinol Metab. 1992 Jan;74(1):177-83 [1370163.001]
  • [Cites] Clin Endocrinol (Oxf). 2000 Nov;53(5):645-7 [11106927.001]
  • [Cites] J Endocrinol Invest. 2003 Apr;26(4):347-52 [12841543.001]
  • [Cites] J Clin Endocrinol Metab. 1967 Nov;27(11):1633-6 [6075592.001]
  • [Cites] Am J Med. 1980 Oct;69(4):571-5 [7424946.001]
  • [Cites] Am J Obstet Gynecol. 2003 Jan;188(1):247-51 [12548225.001]
  • [Cites] Endocr Rev. 2004 Oct;25(5):693-721 [15466938.001]
  • [Cites] J Clin Endocrinol Metab. 1996 Jun;81(6):2250-6 [8964860.001]
  • [Cites] Mayo Clin Proc. 2002 Mar;77(3):297-8 [11888040.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Jan;89(1):384-91 [14715876.001]
  • [Cites] Pituitary. 2002;5(2):99-107 [12675507.001]
  • [Cites] Endocrinology. 2005 May;146(5):2434-44 [15718272.001]
  • [Cites] Clin Endocrinol (Oxf). 2000 Aug;53(2):262-3 [10931109.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Mar;83(3):727-31 [9506716.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Nov;86(11):5240-4 [11701684.001]
  • [Cites] J Clin Endocrinol Metab. 1987 Jan;64(1):51-8 [3782436.001]
  • [Cites] Clin Endocrinol (Oxf). 1995 Apr;42(4):417-23 [7750196.001]
  • [Cites] Obstet Gynecol. 1999 May;93(5 Pt 2):848 [10912424.001]
  • [Cites] J Clin Endocrinol Metab. 1996 Jul;81(7):2460-7 [8675561.001]
  • [Cites] J Clin Endocrinol Metab. 1991 Feb;72(2):374-81 [1991807.001]
  • [Cites] Br J Obstet Gynaecol. 1989 Aug;96(8):949-53 [2775694.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Sep;82(9):2777-81 [9284694.001]
  • [Cites] Endocr J. 1997 Feb;44(1):117-20 [9152623.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Apr;84(4):1489 [10199803.001]
  • [Cites] J Clin Endocrinol Metab. 1970 May;30(5):646-52 [5462817.001]
  • [Cites] Clin Endocrinol (Oxf). 2003 Dec;59(6):690-8 [14974909.001]
  • [Cites] Clin Endocrinol (Oxf). 2001 Sep;55(3):411-5 [11589686.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Dec;82(12):4208-13 [9398741.001]
  • [Cites] J Clin Endocrinol Metab. 1988 Jun;66(6):1171-80 [3372680.001]
  • (PMID = 18401209.001).
  • [ISSN] 1720-8386
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I
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55. Yasufuku-Takano J, Takano K, Morita K, Takakura K, Teramoto A, Fujita T: Does the prevalence of gsp mutations in GH-secreting pituitary adenomas differ geographically or racially? Prevalence of gsp mutations in Japanese patients revisited. Clin Endocrinol (Oxf); 2006 Jan;64(1):91-6
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  • [Title] Does the prevalence of gsp mutations in GH-secreting pituitary adenomas differ geographically or racially? Prevalence of gsp mutations in Japanese patients revisited.
  • OBJECTIVE: The prevalence of gsp mutations in GH-secreting pituitary adenomas was thought to differ geographically or racially, given its exceptionally lower incidence among Japanese patients (4.4-9.3%) compared to other regions (30-50%).
  • However, this notion is now being challenged after a recent paper reported a 53.3% incidence among Japanese with acromegaly.
  • PATIENTS: One hundred Japanese acromegaly patients with surgically confirmed GH-secreting pituitary adenomas were enrolled.
  • METHODS: mRNAs from primary cultured adenomas were used for reverse transcriptase-polymerase chain reaction and direct sequencing of the Gsalpha subunit.
  • Age at operation, sex ratio, basal serum GH and IGF-I levels were no different with or without the mutations.
  • In contrast, patients responded differently to most dynamic tests with statistical significance: serum GH levels in gsp-positive patients had blunted response to GHRH, were well suppressed by bromocriptine, and had higher rates of paradoxical response to TRH.
  • Octreotide suppressed GH levels strongly regardless of gsp status.
  • CONCLUSION: We conclude that the prevalence of gsp mutations in Japanese acromegaly patients is comparable to those of other reports from various regions.
  • Therefore, Japanese patients do not stand as an example for geographical or racial difference in the prevalence of gsp mutations in GH-secreting pituitary adenomas.
  • [MeSH-major] Adenoma / genetics. GTP-Binding Protein alpha Subunits, Gs / genetics. Pituitary Neoplasms / genetics. Point Mutation
  • [MeSH-minor] Acromegaly / ethnology. Acromegaly / metabolism. Adult. Asian Continental Ancestry Group. DNA Mutational Analysis. Female. Growth Hormone / blood. Growth Hormone / secretion. Growth Hormone-Releasing Hormone. Humans. Insulin-Like Growth Factor I / analysis. Japan. Male. Middle Aged. Prevalence. Reverse Transcriptase Polymerase Chain Reaction. Sequence Analysis, DNA. Statistics, Nonparametric

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  • (PMID = 16402935.001).
  • [ISSN] 0300-0664
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 67763-96-6 / Insulin-Like Growth Factor I; 9002-72-6 / Growth Hormone; 9034-39-3 / Growth Hormone-Releasing Hormone; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs
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56. Oshino S, Saitoh Y, Kasayama S, Arita N, Ohnishi T, Kohara H, Izumoto S, Yoshimine T: Short-term preoperative octreotide treatment of GH-secreting pituitary adenoma: predictors of tumor shrinkage. Endocr J; 2006 Feb;53(1):125-32
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  • [Title] Short-term preoperative octreotide treatment of GH-secreting pituitary adenoma: predictors of tumor shrinkage.
  • We reviewed the cases of 32 patients with growth hormone (GH)-secreting macroadenoma who underwent short-term octreotide treatment before transsphenoidal surgery to determine which types of adenoma the preoperative treatment were sensitive and whether predictors of tumor shrinkage could be identified.
  • At a daily dose of 300 microg for 2-3 weeks, octreotide reduced serum GH and insulin-like growth factor-1 (IGF-1) levels to 31.9 % and 51.6% of pretreatment values, respectively, and led to a mean tumor volume of 68% of pretreatment volume in 52% of the patients.
  • Preoperative short-term octreotide treatment is effective for GH-secreting macroadeomas of Knosp grades 1-2 and a good response to both octreotide and bromocriptine challenge tests is a predictor of subsequent tumor shrinkage.
  • [MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Growth Hormone-Secreting Pituitary Adenoma / drug therapy. Growth Hormone-Secreting Pituitary Adenoma / pathology. Octreotide / therapeutic use. Pituitary Neoplasms / drug therapy. Pituitary Neoplasms / pathology
  • [MeSH-minor] Acromegaly / etiology. Adult. Aged. Combined Modality Therapy. Dose-Response Relationship, Drug. Female. Growth Hormone / blood. Humans. Insulin-Like Growth Factor I / analysis. Magnetic Resonance Imaging. Male. Middle Aged. Patient Selection. Predictive Value of Tests. Preoperative Care / methods. Time Factors. Tumor Burden / drug effects

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  • (PMID = 16543682.001).
  • [ISSN] 0918-8959
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 67763-96-6 / Insulin-Like Growth Factor I; 9002-72-6 / Growth Hormone; RWM8CCW8GP / Octreotide
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57. Uccella S, Tibiletti MG, Bernasconi B, Finzi G, Oldrini R, Capella C: Aneuploidy, centrosome alteration and securin overexpression as features of pituitary somatotroph and lactotroph adenomas. Anal Quant Cytol Histol; 2005 Oct;27(5):241-52
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  • [Title] Aneuploidy, centrosome alteration and securin overexpression as features of pituitary somatotroph and lactotroph adenomas.
  • OBJECTIVE: To verify the presence of numerical chromosomal aberrations (NCAs) in different types of pituitary adenomas (PAs) and to investigate 2 of the mechanisms that are possibly related to aneuploidies in PAs: securin overexpression and centrosome alterations.
  • RESULTS: At interphase FISH analysis, growth hormone (GH)-cell and prolactin (PRL)-cell PAs showed multiple chromosome gains and a low frequency of chromosome losses, suggesting a hyperdiploid chromosome assessment.
  • In addition, when compared to other types of PAs, GH-cell and PRL-cell adenomas showed overexpression of securin and a higher number of both cells with abnormal nuclear shape and cells with centrosomes.
  • CONCLUSION: Somatotroph and lactotroph adenomas are characterized by aneuploidy, abnormal nuclear shape and centrosome amplification, which are possibly related to securin overexpression.

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  • (PMID = 16447816.001).
  • [ISSN] 0884-6812
  • [Journal-full-title] Analytical and quantitative cytology and histology
  • [ISO-abbreviation] Anal. Quant. Cytol. Histol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Securin; 0 / pituitary tumor-transforming protein 1, human
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58. Zatelli MC, Piccin D, Tagliati F, Bottoni A, Ambrosio MR, Margutti A, Scanarini M, Bondanelli M, Culler MD, degli Uberti EC: Dopamine receptor subtype 2 and somatostatin receptor subtype 5 expression influences somatostatin analogs effects on human somatotroph pituitary adenomas in vitro. J Mol Endocrinol; 2005 Oct;35(2):333-41
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  • [Title] Dopamine receptor subtype 2 and somatostatin receptor subtype 5 expression influences somatostatin analogs effects on human somatotroph pituitary adenomas in vitro.
  • Dopamine (DA) and somatostatin (SRIF) receptor agonists inhibit growth hormone (GH) secretion by pituitary adenomas.
  • We investigated DA subtype 2 receptor (DR2) and SRIF receptor (sst) subtypes 2 and 5 expression in 25 GH-secreting pituitary adenomas and tested in primary culture the effects on GH and prolactin (PRL) secretion of sst agonists selectively interacting with sst2 (BIM-23120), sst5 (BIM-23206), and sst2 and sst5 (BIM-23244).
  • All adenomas expressed sst2; eight adenomas expressed both sst5 and DR2, eight sst5 but not DR2, and eight DR2 but not sst5.
  • GH secretion was inhibited by BIM-23120 in all samples, while it was reduced by BIM-23206 only in adenomas not expressing DR2.
  • BIM-23120's inhibitory effects correlated with sst2 and DR2 expression, whereas DR2 expression correlated inversely with BIM-23206 inhibitory effects on GH secretion.
  • In seven mixed GH-/PRL-secreting pituitary adenomas, PRL secretion was inhibited in sst5-expressing tumors by BIM-23206, but not by BIM-23120.
  • BIM-23244 reduced PRL secretion only in adenomas expressing sst2, sst5 and DR2. sst5 and DR2 expression correlated directly with BIM23206 inhibitory effects on PRL secretion.
  • Our results suggest that adenomas expressing DR2 are less likely to respond to clinically available SRIF analogs in terms of GH secretion inhibition.
  • Therefore, drugs interacting also with DR2 might better control secretion of pituitary adenomas.
  • [MeSH-major] Growth Hormone-Secreting Pituitary Adenoma / metabolism. Protein Isoforms / metabolism. Receptors, Dopamine / metabolism. Receptors, Somatostatin / metabolism. Somatostatin / analogs & derivatives
  • [MeSH-minor] Acromegaly / metabolism. Adult. Aged, 80 and over. Dopamine Agonists. Female. Human Growth Hormone / secretion. Humans. Male. Middle Aged. Prolactin / secretion. RNA, Messenger / metabolism

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  • (PMID = 16216913.001).
  • [ISSN] 0952-5041
  • [Journal-full-title] Journal of molecular endocrinology
  • [ISO-abbreviation] J. Mol. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Dopamine Agonists; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / Receptors, Dopamine; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 0 / somatostatin receptor 5; 12629-01-5 / Human Growth Hormone; 51110-01-1 / Somatostatin; 9002-62-4 / Prolactin
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59. Acunzo J, Thirion S, Roche C, Saveanu A, Gunz G, Germanetti AL, Couderc B, Cohen R, Figarella-Branger D, Dufour H, Brue T, Enjalbert A, Barlier A: Somatostatin receptor sst2 decreases cell viability and hormonal hypersecretion and reverses octreotide resistance of human pituitary adenomas. Cancer Res; 2008 Dec 15;68(24):10163-70
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  • [Title] Somatostatin receptor sst2 decreases cell viability and hormonal hypersecretion and reverses octreotide resistance of human pituitary adenomas.
  • In human somatotroph adenomas, growth hormone (GH) hypersecretion can be inhibited by somatostatin analogues such as octreotide.
  • Unfortunately, serum GH levels reach normal values in only 60% of treated patients.
  • In this present study, the sst2 gene was transferred by an adenoviral vector (Ad-sst2) in human somatotroph (n = 7) and lactotroph (n = 2) adenomas in vitro.
  • Ten days after infection at 20 multiplicity of infection (MOI), sst2 gene transfer decreased cell viability from 19% to 90% by caspase-dependent apoptosis.
  • At low viral doses (5 MOI), Ad-sst2 decreased GH or prolactin (PRL) basal secretion and mRNA expression.
  • Somatotroph tumors were classified in three groups according to their octreotide sensitivity.
  • Four days after infection by 5 MOI Ad-sst2, the maximal GH suppression by octreotide increased from 31% to 57% in the octreotide partially resistant group and from 0% to 27% in the resistant ones.
  • In the octreotide-sensitive group, EC(50) values significantly decreased from 1.3 x 10(-11) to 6.6 x 10(-13) mol/L without improving maximal GH suppression.
  • [MeSH-major] Antineoplastic Agents, Hormonal / pharmacology. Growth Hormone-Secreting Pituitary Adenoma / drug therapy. Human Growth Hormone / secretion. Octreotide / pharmacology. Pituitary Neoplasms / drug therapy. Prolactin / secretion. Prolactinoma / drug therapy
  • [MeSH-minor] Adenoviridae / genetics. Cell Survival / physiology. Drug Resistance, Neoplasm. Humans. Immunohistochemistry. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Receptors, Somatostatin / biosynthesis. Receptors, Somatostatin / genetics. Transduction, Genetic. Transgenes


60. Kurosaki M, Saegert W, Abe T, Lüdecke DK: Expression of vascular endothelial growth factor in growth hormone-secreting pituitary adenomas: special reference to the octreotide treatment. Neurol Res; 2008 Jun;30(5):518-22
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  • [Title] Expression of vascular endothelial growth factor in growth hormone-secreting pituitary adenomas: special reference to the octreotide treatment.
  • OBJECTIVE: The present study was designed to investigate the localization of VEGF in GH-secreting pituitary adenomas and to evaluate the characteristic differences of VEGF expression in relation to the clinical effect of preoperative treatment with octreotide.
  • METHODS: Fifty-six cases of GH-secreting adenomas, which were divided into three groups and three normal pituitary glands, were studied using immunohistochemistry for expression of VEGF.
  • VEGF staining was strongly seen in the cytoplasm in normal pituitary glands.
  • The staining pattern differs statistically between the octreotide and control group, typically in densely granulated GH cell adenomas.
  • Age, gender, tumor size, tumor invasiveness and adenoma type did not influence VEGF expression.
  • [MeSH-major] Adenoma / drug therapy. Antineoplastic Agents, Hormonal / therapeutic use. Octreotide / therapeutic use. Pituitary Neoplasms / drug therapy. Vascular Endothelial Growth Factor A / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Female. Humans. Male. Middle Aged. Pituitary Gland / drug effects. Pituitary Gland / metabolism. Pituitary Gland / pathology. Retrospective Studies. Statistics, Nonparametric. Technology, Radiologic / methods

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  • (PMID = 18953743.001).
  • [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] 0 / Antineoplastic Agents, Hormonal; 0 / Vascular Endothelial Growth Factor A; RWM8CCW8GP / Octreotide
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61. Watanabe M, Hirokawa Y, Tsuji M, Yanagawa M, Murata T, Suzuki H, Ichikawa T, Katoh T, Sugimura Y, Shiraishi T: Lack of involvement of the GNAS1 T393C polymorphism in prostate cancer risk in a Japanese population. Anticancer Res; 2008 Nov-Dec;28(6A):3711-6
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  • Activating mutations lead to somatotroph, thyroid, adrenal and gonadal adenomas or the McCune-Albright syndrome and recently the T399C polymorphism in GNAS1 has been reported to be associated with malignancies.
  • The C/C genotype was more frequent among the prostate cancer patients (22.9%) than the controls (20.7%), although without significance (OR, 1.30; 95% CI, 0.80-2.12; p=0.29).
  • [MeSH-minor] Aged. Case-Control Studies. Genetic Predisposition to Disease. Humans. Male. Polymorphism, Single Nucleotide. Prostatic Hyperplasia / genetics

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  • (PMID = 19189654.001).
  • [ISSN] 0250-7005
  • [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] EC 3.6.1.- / GNAS protein, human; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs
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62. Onofri C, Theodoropoulou M, Losa M, Uhl E, Lange M, Arzt E, Stalla GK, Renner U: Localization of vascular endothelial growth factor (VEGF) receptors in normal and adenomatous pituitaries: detection of a non-endothelial function of VEGF in pituitary tumours. J Endocrinol; 2006 Oct;191(1):249-61
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  • [Title] Localization of vascular endothelial growth factor (VEGF) receptors in normal and adenomatous pituitaries: detection of a non-endothelial function of VEGF in pituitary tumours.
  • As for any solid tumour, pituitary adenoma expansion is dependent on neovascularization through angiogenesis.
  • In this process, vascular endothelial growth factor (VEGF) and its receptors VEGFR-1, VEGFR-2 and neuropilin-1 (NRP-1) may play an outstanding role.
  • The intention of this work was to study the expression/localization and possible function of VEGF receptors in pituitary adenomas.
  • VEGF receptor mRNA and protein expression was studied by in situ hybridization, immunohistochemistry and RT-PCR in 6 normal human pituitaries, 39 human pituitary adenomas and 4 rodent pituitary adenoma cell lines.
  • VEGFR-1 expressing somatotroph MtT-S cells were used as a model to study the role of VEGF on cell proliferation and to elucidate the underlying mechanism of action.
  • In pituitary tumours, a heterogeneous VEGFR expression pattern was observed by IHC.
  • VEGFR-1, VEGFR-2 and NRP-1 were detected in 24, 18 and 17 adenomas respectively.
  • In the adenomas, VEGFR-1 was expressed in epithelial tumour cells and VEGFR-2/NRP-1 in vessel endothelial cells.
  • Functional studies in VEGFR-1-positive MtT-S cells showed that the ligands of VEGFR-1 significantly stimulated cell proliferation.
  • Based on our results, we speculate that the ligands of VEGF receptors, such as VEGF-A and placenta growth factor, not only play a role in angiogenesis in pituitary adenomas, but also affect the growth of pituitary tumour cells through VEGFR-1.
  • [MeSH-major] Adenoma / chemistry. Pituitary Gland / chemistry. Pituitary Neoplasms / chemistry. Receptors, Vascular Endothelial Growth Factor / analysis. Vascular Endothelial Growth Factor A / metabolism
  • [MeSH-minor] Adult. Aged. Animals. Antibodies, Monoclonal / pharmacology. Blotting, Western / methods. Cell Line, Tumor. Cell Proliferation / drug effects. Chromones / pharmacology. Endothelial Cells / chemistry. Female. Humans. Immunohistochemistry / methods. In Situ Hybridization / methods. Ligands. Male. Middle Aged. Morpholines / pharmacology. Neuropilin-1 / genetics. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Rats. Reverse Transcriptase Polymerase Chain Reaction. Somatotrophs / cytology. Somatotrophs / drug effects. Stimulation, Chemical. Vascular Endothelial Growth Factor Receptor-1 / analysis. Vascular Endothelial Growth Factor Receptor-1 / genetics. Vascular Endothelial Growth Factor Receptor-2 / analysis. Vascular Endothelial Growth Factor Receptor-2 / genetics

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  • (PMID = 17065408.001).
  • [ISSN] 0022-0795
  • [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 / Antibodies, Monoclonal; 0 / Chromones; 0 / Ligands; 0 / Morpholines; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 144713-63-3 / Neuropilin-1; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
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63. Horvath E, Kovacs K: Pathology of acromegaly. Neuroendocrinology; 2006;83(3-4):161-5
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  • [Title] Pathology of acromegaly.
  • This review summarizes current knowledge on pituitary changes in patients with acromegaly.
  • The histologic, immunohistochemical and electron microscopic study provided conclusive evidence that a marked diversity exists between the tumors which secrete growth hormone (GH) in excess, such as densely and sparsely granulated GH cell adenoma, the mixed GH prolactin cell adenoma and the mammosomatotrope adenoma.
  • The latter two tumors produce GH and prolactin simultaneously.
  • Densely granulated GH cell tumors may produce thyrotropin and alpha subunit as well.
  • Somatotrope carcinomas are extremely rare.
  • GH cell hyperplasia can also be associated with acromegaly in patients with extrapituitary GH-releasing hormone secreting tumors.
  • The medical therapy of acromegaly is reviewed briefly, including long-acting somatostatin analogs and pegvisomant, a GH receptor blocker.
  • [MeSH-major] Acromegaly / pathology. Human Growth Hormone / metabolism. Pituitary Gland / pathology. Pituitary Neoplasms / pathology
  • [MeSH-minor] Adenoma / metabolism. Adenoma / pathology. Adenoma / therapy. Adenoma / ultrastructure. Carcinoma / metabolism. Carcinoma / pathology. Carcinoma / therapy. Carcinoma / ultrastructure. Humans. Immunohistochemistry

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  • (PMID = 17047379.001).
  • [ISSN] 0028-3835
  • [Journal-full-title] Neuroendocrinology
  • [ISO-abbreviation] Neuroendocrinology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 12629-01-5 / Human Growth Hormone
  • [Number-of-references] 22
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64. Thodou E, Kontogeorgos G, Theodossiou D, Pateraki M: Mapping of somatostatin receptor types in GH or/and PRL producing pituitary adenomas. J Clin Pathol; 2006 Mar;59(3):274-9
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  • [Title] Mapping of somatostatin receptor types in GH or/and PRL producing pituitary adenomas.
  • BACKGROUND: Somatostatin is a tetradecapeptide exerting inhibitory action on endocrine and exocrine cell secretion and proliferation.
  • Using immunohistochemistry, the expression of SST(1), SST(2A), SST(2B), SST(3), SST(4), and SST(5) was studied in tissue microarrays (TMAs), using a series of 90 human pituitary adenomas producing growth hormone and/or prolactin, including 30 of each somatotroph, lactotroph, and mixed somatotroph/lactotroph adenoma type.
  • SST(5) and SST(2A) were the predominant receptors, showing strong expression in high frequency in all three adenoma types.
  • Strong expression of SST(1) was higher in lactotroph adenomas than in other tumour types.
  • [MeSH-major] Adenoma / chemistry. Biomarkers, Tumor / analysis. Pituitary Neoplasms / chemistry. Receptors, Somatostatin / analysis
  • [MeSH-minor] Case-Control Studies. Female. Growth Hormone / secretion. Humans. Immunohistochemistry / methods. Membrane Proteins / analysis. Prolactinoma / chemistry

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  • [Cites] J Clin Endocrinol Metab. 1987 Dec;65(6):1127-34 [2824549.001]
  • [Cites] Front Horm Res. 2004;32:235-52 [15281350.001]
  • [Cites] J Clin Endocrinol Metab. 1994 Feb;78(2):398-403 [8106629.001]
  • [Cites] Cancer Res. 1994 Jul 1;54(13):3455-9 [8012966.001]
  • [Cites] J Clin Endocrinol Metab. 1994 Sep;79(3):724-9 [7521350.001]
  • [Cites] Life Sci. 1995;56(5):333-42 [7530798.001]
  • [Cites] J Clin Endocrinol Metab. 1995 Apr;80(4):1386-92 [7714115.001]
  • [Cites] Endocr Rev. 1995 Aug;16(4):427-42 [8521788.001]
  • [Cites] J Neuroendocrinol. 1996 Aug;8(8):605-10 [8866248.001]
  • [Cites] J Clin Invest. 1997 Feb 15;99(4):789-98 [9045884.001]
  • [Cites] Int J Cancer. 1997 Mar 4;70(5):530-7 [9052751.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Sep;82(9):3011-8 [9284735.001]
  • [Cites] J Endocrinol Invest. 1997 Jun;20(6):348-67 [9294784.001]
  • [Cites] J Clin Invest. 1997 Nov 1;100(9):2386-92 [9410919.001]
  • [Cites] Nat Med. 1998 Jul;4(7):844-7 [9662379.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Jul;83(7):2417-20 [9661621.001]
  • [Cites] Am J Pathol. 1998 Jul;153(1):233-45 [9665484.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Aug;83(8):2997-3000 [9709982.001]
  • [Cites] Clin Cancer Res. 1998 Sep;4(9):2047-52 [9748118.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Feb;84(2):775-80 [10022452.001]
  • [Cites] Front Neuroendocrinol. 1999 Jul;20(3):157-98 [10433861.001]
  • [Cites] Clin Cancer Res. 1999 Aug;5(8):1966-75 [10473073.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Sep;84(9):3268-76 [10487698.001]
  • [Cites] Virchows Arch. 2001 Dec;439(6):787-97 [11787852.001]
  • [Cites] Virchows Arch. 2002 May;440(5):461-75 [12021920.001]
  • [Cites] Surg Today. 2002;32(8):690-4 [12181718.001]
  • [Cites] Endocr Rev. 2003 Feb;24(1):28-47 [12588807.001]
  • [Cites] Endocr Rev. 2003 Aug;24(4):389-427 [12920149.001]
  • [Cites] Clin Cancer Res. 1999 Nov;5(11):3483-7 [10589762.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Feb;85(2):781-92 [10690891.001]
  • [Cites] J Biol Chem. 2000 Mar 17;275(11):7862-9 [10713101.001]
  • [Cites] Diagn Mol Pathol. 2000 Mar;9(1):47-57 [10718213.001]
  • [Cites] Lab Invest. 2000 Dec;80(12):1943-9 [11140706.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Jan;86(1):140-5 [11231991.001]
  • [Cites] Eur J Clin Invest. 2001 Mar;31(3):208-14 [11264647.001]
  • [Cites] Clin Endocrinol (Oxf). 2001 May;54(5):641-9 [11380495.001]
  • [Cites] J Natl Cancer Inst. 2001 Aug 1;93(15):1141-6 [11481385.001]
  • [Cites] Gut. 2002 Jan;50(1):52-60 [11772967.001]
  • [Cites] N Engl J Med. 1983 Dec 15;309(24):1495-501 [6139753.001]
  • [Cites] Clin Endocrinol (Oxf). 1986 Aug;25(2):201-12 [2878748.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Apr;89(4):1577-85 [15070915.001]
  • [Cites] Neuroendocrinology. 2004 Mar;79(3):142-8 [15103227.001]
  • [Cites] Cancer Res. 1990 Sep 15;50(18):5969-77 [2168286.001]
  • (PMID = 16505278.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Membrane Proteins; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 0 / somatostatin receptor 3; 0 / somatostatin receptor 5; 0 / somatostatin receptor subtype-4; 9002-72-6 / Growth Hormone
  • [Other-IDs] NLM/ PMC1860351
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65. Donangelo I, Marcos HP, Araújo PB, Marcondes J, Filho PN, Gadelha M, Chimelli L: Expression of retinoblastoma protein in human growth hormone-secreting pituitary adenomas. Endocr Pathol; 2005;16(1):53-62
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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 retinoblastoma protein in human growth hormone-secreting pituitary adenomas.
  • Its role in the pathogenesis of pituitary tumors has not been fully clarified.
  • Conversely, lack of expression of pRB was observed in one fourth of GH-secreting pituitary adenomas (GH-tumors).
  • In order to further study the expression of pRB in GH-tumors, we evaluated this protein in 49 tumors from patients with acromegaly (20 noninvasive, 25 invasive, and 4 with no information) and 8 normal pituitaries using immunohistochemistry (IHC).
  • In conclusion, pRB is underexpressed in a subgroup of GH-tumors, and this may represent an early event in the pathogenesis of this tumor subtype.
  • [MeSH-major] Adenoma / secretion. Human Growth Hormone / secretion. Pituitary Gland, Anterior / secretion. Pituitary Neoplasms / secretion. Retinoblastoma Protein / metabolism
  • [MeSH-minor] Acromegaly / etiology. Acromegaly / metabolism. Acromegaly / pathology. Adult. Aged. Cell Count. Child. Female. Fluorescent Antibody Technique, Indirect. Humans. Male. Middle Aged

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  • [Cites] J Endocrinol. 1998 May;157(2):337-41 [9659297.001]
  • [Cites] Hum Genet. 1994 Nov;94(5):491-6 [7959682.001]
  • [Cites] Hum Mol Genet. 2001 Jun 1;10(12):1275-85 [11406609.001]
  • [Cites] Pituitary. 2003 Sep;6(2):75-80 [14703016.001]
  • [Cites] Oncogene. 2003 Sep 11;22(39):7942-9 [12970742.001]
  • [Cites] Cancer Lett. 1998 Apr 24;126(2):209-14 [9585068.001]
  • [Cites] Am J Pathol. 2001 Dec;159(6):2239-48 [11733373.001]
  • [Cites] Eur J Endocrinol. 1999 Jun;140(6):573-6 [10366412.001]
  • [Cites] Cancer. 1993 Aug 15;72(4):1386-93 [8339229.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Apr;83(4):1388-91 [9543172.001]
  • [Cites] J Clin Endocrinol Metab. 1994 Feb;78(2):387-92 [8106627.001]
  • [Cites] J Biol Chem. 2003 Mar 21;278(12):10824-30 [12531887.001]
  • [Cites] Am J Pathol. 1997 Feb;150(2):401-7 [9033255.001]
  • [Cites] Oncogene. 1994 Apr;9(4):1021-7 [8134105.001]
  • [Cites] J Clin Endocrinol Metab. 1993 Sep;77(3):644-6 [7690360.001]
  • [Cites] FEBS Lett. 1998 Apr 17;426(2):266-70 [9599022.001]
  • [Cites] J Endocrinol Invest. 2000 May;23(5):304-9 [10882148.001]
  • [Cites] J Pediatr Endocrinol Metab. 1999 May-Jun;12(3):381-7 [10821217.001]
  • [Cites] J Clin Endocrinol Metab. 1994 Apr;78(4):922-7 [8157722.001]
  • [Cites] Br J Cancer. 1999 Apr;80(1-2):44-50 [10389976.001]
  • [Cites] Endocr Pathol. 1995 Autumn;6(3):189-196 [12114739.001]
  • [Cites] Cancer Res. 1997 Dec 15;57(24):5446-51 [9407947.001]
  • [Cites] Cancer. 1994 Jul 15;74(2):693-6 [8033049.001]
  • [Cites] Genomics. 2002 Jul;80(1):5-7 [12079276.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Feb;84(2):761-7 [10022450.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Aug;83(8):2631-4 [9709923.001]
  • [Cites] Eur J Endocrinol. 1996 Jun;134(6):720-6 [8766942.001]
  • [Cites] Cancer Res. 1999 Apr 1;59(7):1562-6 [10197629.001]
  • [Cites] Oncogene. 1997 Nov 13;15(20):2463-73 [9395242.001]
  • [Cites] Eur J Endocrinol. 1999 Mar;140(3):250-5 [10216521.001]
  • [Cites] Cancer Res. 1995 Apr 15;55(8):1613-6 [7712461.001]
  • [Cites] Oncogene. 1993 Apr;8(4):1063-7 [8455933.001]
  • [Cites] J Clin Invest. 1993 Jun;91(6):2815-21 [8514889.001]
  • [Cites] Oncol Res. 2001;12(11-12):491-500 [11939413.001]
  • [Cites] Science. 1990 Aug 10;249(4969):655-9 [2116665.001]
  • [Cites] Oncogene. 2003 Jul 10;22(28):4398-405 [12853976.001]
  • [Cites] J Pathol. 1999 Jun;188(2):168-73 [10398160.001]
  • [Cites] Am J Pathol. 1997 Aug;151(2):509-19 [9250163.001]
  • [Cites] Cancer Res. 2000 Mar 1;60(5):1211-6 [10728677.001]
  • [Cites] Oncogene. 2002 Sep 26;21(43):6567-72 [12242654.001]
  • [Cites] J Clin Endocrinol Metab. 1990 Dec;71(6):1421-6 [1977758.001]
  • [Cites] Nature. 1992 Sep 24;359(6393):295-300 [1406933.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Mar;82(3):818-24 [9062489.001]
  • [Cites] Am J Hum Genet. 1991 May;48(5):880-8 [1673287.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Sep;83(9):3210-2 [9745428.001]
  • [Cites] Microsc Res Tech. 2002 Oct 1;59(1):68-83 [12242698.001]
  • [Cites] Clin Endocrinol (Oxf). 2003 Feb;58(2):141-50 [12580928.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Sep;82(9):3141-7 [9284759.001]
  • [Cites] Eur J Biochem. 1997 Jun 15;246(3):581-601 [9219514.001]
  • [Cites] Cancer Lett. 1999 Sep 20;144(1):85-92 [10503881.001]
  • [Cites] Acta Endocrinol (Copenh). 1993 Oct;129(4):301-6 [8237246.001]
  • (PMID = 16000847.001).
  • [ISSN] 1046-3976
  • [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 / Retinoblastoma Protein; 12629-01-5 / Human Growth Hormone
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66. Vlotides G, Cooper O, Chen YH, Ren SG, Greenman Y, Melmed S: Heregulin regulates prolactinoma gene expression. Cancer Res; 2009 May 15;69(10):4209-16
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  • To investigate the role of p185(her2/neu)/ErbB3 signaling in pituitary tumor function, we examined these receptors in human prolactinomas.
  • Immunofluorescent p185(her2/neu) was detected in almost all (seven of eight), and ErbB3 expression in a subset (four of eight) of tumors (seven adenomas and one carcinoma).
  • Quantitative PCR also showed abundant ErbB3 mRNA in tumor specimens derived from a rarely encountered prolactin-cell carcinoma.
  • Activation of p185(c-neu)/ErbB3 signaling with heregulin, the ErbB3 ligand, in rat lacto-somatotroph (GH4C1) tumor cells specifically induced prolactin (PRL) mRNA expression approximately 5-fold and PRL secretion approximately 4-fold, whereas growth hormone expression was unchanged.
  • The Akt signal was specific to ErbB3 activation by heregulin, and was not observed in response to epidermal growth factor activation of epidermal growth factor receptor.

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  • [Cites] Eur J Endocrinol. 2006 Oct;155(4):523-34 [16990651.001]
  • [Cites] Nat Clin Pract Endocrinol Metab. 2006 Oct;2(10):552-61 [17024154.001]
  • [Cites] Nat Clin Pract Endocrinol Metab. 2006 Oct;2(10):571-81 [17024156.001]
  • [Cites] Hum Pathol. 2007 Jan;38(1):185-9 [17056093.001]
  • [Cites] Cell Signal. 2007 Mar;19(3):466-71 [16978839.001]
  • [Cites] Nature. 2007 Jan 25;445(7126):437-41 [17206155.001]
  • [Cites] Pituitary. 2007;10(1):81-6 [17285366.001]
  • [Cites] Science. 2007 May 18;316(5827):1039-43 [17463250.001]
  • [Cites] J Clin Invest. 2007 Aug;117(8):2051-8 [17671639.001]
  • [Cites] Cancer Res. 2008 Aug 1;68(15):6377-86 [18676863.001]
  • [Cites] Endocrinology. 2009 Feb;150(2):795-802 [18832099.001]
  • [Cites] Clin Cancer Res. 2003 Apr;9(4):1274-83 [12684395.001]
  • [Cites] J Neurosurg. 2003 Aug;99(2):402-8 [12924717.001]
  • [Cites] J Clin Invest. 2003 Dec;112(11):1603-18 [14660734.001]
  • [Cites] Mod Pathol. 2004 Jul;17(7):772-80 [15098012.001]
  • [Cites] Endocrinology. 1980 Mar;106(3):718-23 [7353539.001]
  • [Cites] J Neurosci. 1984 Jan;4(1):75-83 [6693948.001]
  • [Cites] Nature. 1984 Dec 6-12;312(5994):545-8 [6504162.001]
  • [Cites] J Clin Endocrinol Metab. 1987 Aug;65(2):275-81 [3597708.001]
  • [Cites] Mol Endocrinol. 2000 Sep;14(9):1328-37 [10976912.001]
  • [Cites] Pituitary. 1999 May;1(3-4):213-20 [11081200.001]
  • [Cites] Endocrinology. 2002 Jan;143(1):11-2 [11751585.001]
  • [Cites] Horm Res. 1989;31(1-2):13-8 [2566572.001]
  • [Cites] DNA. 1989 Dec;8(10):723-32 [2575488.001]
  • [Cites] Lab Invest. 1992 May;66(5):639-45 [1573857.001]
  • [Cites] Endocrinology. 1992 Jun;130(6):3453-8 [1534540.001]
  • [Cites] Mol Cell Biol. 1994 Mar;14(3):1553-65 [8114693.001]
  • [Cites] Endocrinology. 1994 Nov;135(5):2012-21 [7956924.001]
  • [Cites] Endocrinology. 1995 Oct;136(10):4479-88 [7664668.001]
  • [Cites] Mol Cell Biol. 1995 Dec;15(12):6777-84 [8524243.001]
  • [Cites] J Clin Endocrinol Metab. 1996 Feb;81(2):656-62 [8636285.001]
  • [Cites] Mol Cell Biol. 1996 Oct;16(10):5276-87 [8816440.001]
  • [Cites] Clin Endocrinol (Oxf). 1997 May;46(5):599-606 [9231056.001]
  • [Cites] J Endocrinol. 1998 Sep;158(3):425-33 [9846172.001]
  • [Cites] J Endocrinol. 2004 Nov;183(2):385-94 [15531726.001]
  • [Cites] Neurosurgery. 2005 May;56(5):1066-74; discussion 1066-74 [15854256.001]
  • [Cites] J Clin Endocrinol Metab. 2005 May;90(5):3089-99 [15741248.001]
  • [Cites] Cancer Res. 2005 May 15;65(10):4253-60 [15899817.001]
  • [Cites] Endocr Relat Cancer. 2005 Jun;12(2):423-33 [15947113.001]
  • [Cites] Arq Neuropsiquiatr. 2006 Mar;64(1):60-6 [16622555.001]
  • [Cites] Nat Rev Mol Cell Biol. 2006 Jul;7(7):505-16 [16829981.001]
  • [Cites] Eur J Endocrinol. 2006 Aug;155(2):371-9 [16868153.001]
  • [Cites] Clin Endocrinol (Oxf). 2006 Aug;65(2):265-73 [16886971.001]
  • [Cites] Endocr Rev. 2006 Aug;27(5):485-534 [16705142.001]
  • (PMID = 19401448.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA075979-09; United States / NCI NIH HHS / CA / CA 075979; United States / NCI NIH HHS / CA / R01 CA075979-09; United States / NCI NIH HHS / CA / R01 CA075979; United States / NIDDK NIH HHS / DK / K23 DK085148
  • [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 / Actins; 0 / Neuregulin-1; 0 / RNA, Small Interfering; 0 / beta 2-Microglobulin; 9002-62-4 / Prolactin; 9002-72-6 / Growth Hormone; EC 1.2.1.- / Glyceraldehyde-3-Phosphate Dehydrogenases; EC 3.2.1.31 / Glucuronidase
  • [Other-IDs] NLM/ NIHMS112443; NLM/ PMC2688701
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67. Gondim JA, Ferraz T, Mota I, Studart D, Almeida JP, Gomes E, Schops M: Outcome of surgical intrasellar growth hormone tumor performed by a pituitary specialist surgeon in a developing country. Surg Neurol; 2009 Jul;72(1):15-9; discussion 19
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  • [Title] Outcome of surgical intrasellar growth hormone tumor performed by a pituitary specialist surgeon in a developing country.
  • BACKGROUND: Acromegaly is an excessive GH secretion, which in most cases, is caused by a pituitary GH-secreting adenoma.
  • Traditional treatment of acromegaly consists of surgery, drug therapy, and eventually radiotherapy.
  • The aim of this retrospective study is to evaluate the results of transsphenoidal endoscopic surgery in a group of patients with intrasellar GH adenoma who were operated by a pituitary specialist surgeon.
  • METHODS: We have analyzed data from 33 patients with intrasellar GH tumor who had been referred to the neuroendocrine department of the HGF, Brazil.
  • The patients underwent a transsphenoidal endoscopic adenomectomy for acromegaly between 2000 and 2005.
  • RESULTS: All 33 patients had intrasellar adenoma, 84.84% of patients achieved remission by surgery.
  • Five patients still had the disease and refused a second surgery.
  • A treatment with octreotide was started for these 5 patients and resulted in an adequate control of GH and IGF-1 levels.
  • CONCLUSION: Our patients, with intrasellar GH tumor, operated by a pituitary specialist neurosurgeon had remission rates approaching those obtained by most specialized neurosurgical centers worldwide.
  • [MeSH-major] Adenoma / surgery. Endoscopy / statistics & numerical data. Growth Hormone-Secreting Pituitary Adenoma / surgery. Neurosurgical Procedures / statistics & numerical data. Sella Turcica / surgery. Sphenoid Bone / surgery

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  • (PMID = 18440607.001).
  • [ISSN] 1879-3339
  • [Journal-full-title] Surgical neurology
  • [ISO-abbreviation] Surg Neurol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; RWM8CCW8GP / Octreotide
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68. Theodoropoulou M, Labeur M, Paez Pereda M, Haedo M, Perone MJ, Renner U, Arzt E, Stalla GK: Novel medical therapies for pituitary tumors. Front Horm Res; 2010;38:158-64
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Novel medical therapies for pituitary tumors.
  • Despite considerable progress, there is still no medical treatment available for some kinds of pituitary tumors, in particular hormone inactive adenomas and corticotroph pituitary tumors.
  • Moreover, treatment resistance is present in a considerable proportion of patients bearing pituitary tumors, for which medical treatment regimens are already available (prolactinomas, somatotroph adenomas).
  • Here, we summarize preclinical and clinical findings about the hormone and growth-suppressive action of various drugs, which will probably lead to novel future medical treatment concepts for pituitary tumors.
  • [MeSH-major] Pituitary Neoplasms / drug therapy

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  • [Copyright] Copyright (c) 2010 S. Karger AG, Basel.
  • (PMID = 20616507.001).
  • [ISSN] 0301-3073
  • [Journal-full-title] Frontiers of hormone research
  • [ISO-abbreviation] Front Horm Res
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / BIM 23A760; 0 / Dopamine Agonists; 51110-01-1 / Somatostatin; 5688UTC01R / Tretinoin; 82115-62-6 / Interferon-gamma; 98H1T17066 / pasireotide; VTD58H1Z2X / Dopamine
  • [Number-of-references] 32
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69. Georgitsi M, Raitila A, Karhu A, van der Luijt RB, Aalfs CM, Sane T, Vierimaa O, Mäkinen MJ, Tuppurainen K, Paschke R, Gimm O, Koch CA, Gündogdu S, Lucassen A, Tischkowitz M, Izatt L, Aylwin S, Bano G, Hodgson S, De Menis E, Launonen V, Vahteristo P, Aaltonen LA: Germline CDKN1B/p27Kip1 mutation in multiple endocrine neoplasia. J Clin Endocrinol Metab; 2007 Aug;92(8):3321-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: Our objective was to evaluate the role of CDKN1B/p27(Kip1) in human tumor predisposition in patients clinically suspected of MEN1 but testing negative for MEN1 germline mutation as well as in familial and sporadic acromegaly/pituitary adenoma patients.
  • In addition, 19 familial and 50 sporadic acromegaly/pituitary adenoma patients from Europe and the United States were included in the study.
  • MAIN OUTCOME MEASURES: We analyzed germline CDKN1B/p27(Kip1) mutations in individuals with pituitary adenoma and MEN1-like features.
  • RESULTS: A heterozygous 19-bp duplication (c.59_77dup19) leading to a truncated protein product was identified in one Dutch patient with suspected MEN1 phenotype, pituitary adenoma, carcinoid tumor, and hyperparathyroidism (one of 36, 2.8%).
  • No mutations were detected in either familial or sporadic acromegaly/pituitary adenoma patients.
  • CONCLUSIONS: Our results support the previous finding that germline CDKN1B/p27(Kip1) mutations predispose to a human MEN1-like condition.
  • However, such mutations appear uncommon in suspected MEN1 cases and rare or nonexistent in familial or sporadic acromegaly/pituitary adenoma patients.

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  • (PMID = 17519308.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ EF474465
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CDKN1B protein, human; 0 / Intracellular Signaling Peptides and Proteins; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 9007-49-2 / DNA
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70. Kobayashi T, Mori Y, Uchiyama Y, Kida Y, Fujitani S: Long-term results of gamma knife surgery for growth hormone-producing pituitary adenoma: is the disease difficult to cure? J Neurosurg; 2005 Jan;102 Suppl:119-23
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term results of gamma knife surgery for growth hormone-producing pituitary adenoma: is the disease difficult to cure?
  • OBJECT: The authors conducted a study to determine the long-term results of gamma knife surgery for residual or recurrent growth hormine (GH)-producing pituitary adenomas and to compare the results with those after treatment of other pituitary adenomas.
  • Growth hormone normalization (GH < 1.0 ng/ml) was found in 4.8%, nearly normal (< 2.0 ng/ml) in 11.9%, significantly decreased (< 5.0 ng/ml) in 23.8%, decreased in 21.4%, unchanged in 21.4%, and increased in 16.7%.
  • Serum insulin-like growth factor (IGF)-1 was significantly decreased (IGF-1 < 400 ng/ml) in 40.7%, decreased in 29.6%, unchanged in 18.5%, and increased in 11.1%, which was almost parallel to the GH changes.
  • CONCLUSIONS: Gamma knife surgery was effective and safe for the control of tumors; however, normalization of GH and IGF-1 secretion was difficult to achieve in cases with large tumors and low-dose radiation.
  • [MeSH-major] Adenoma / secretion. Adenoma / surgery. Human Growth Hormone / secretion. Pituitary Neoplasms / secretion. Pituitary Neoplasms / surgery. Radiosurgery / instrumentation
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Follow-Up Studies. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Neoplasm Recurrence, Local. Outcome Assessment (Health Care). Pituitary ACTH Hypersecretion / pathology. Pituitary ACTH Hypersecretion / surgery. Prolactinoma / pathology. Prolactinoma / surgery

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  • (PMID = 15662793.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 12629-01-5 / Human Growth Hormone
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71. Maiza JC, Vezzosi D, Matta M, Donadille F, Loubes-Lacroix F, Cournot M, Bennet A, Caron P: Long-term (up to 18 years) effects on GH/IGF-1 hypersecretion and tumour size of primary somatostatin analogue (SSTa) therapy in patients with GH-secreting pituitary adenoma responsive to SSTa. Clin Endocrinol (Oxf); 2007 Aug;67(2):282-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term (up to 18 years) effects on GH/IGF-1 hypersecretion and tumour size of primary somatostatin analogue (SSTa) therapy in patients with GH-secreting pituitary adenoma responsive to SSTa.
  • CONTEXT: The role of somatostatin analogues (SSTa) in the treatment of acromegaly.
  • OBJECTIVE: To evaluate the antihormonal and antitumour efficacy of long-term (up to 18 years) primary treatment with SSTa in patients with GH-secreting pituitary adenoma responsive to SSTa.
  • PATIENTS: Thirty-six acromegalic patients, aged 17-75 years (postoral glucose tolerance test GH > 1 microg/l, increased IGF-1 for age and sex), were monitored in a single centre and treated with SSTa as first-line therapy.
  • The mean pretreatment GH level was 13.5 +/- 3.1 microg/l, and IGF-1 (as a percentage of the value over the normal range) was 302 +/- 26%.
  • RESULTS: After 1 year, the mean GH and IGF-1 levels had reduced considerably (GH: 2.4 +/- 0.3 microg/l; IGF-1; 174 +/- 14%, P < 0.01), and they continued to decrease over 10 years, with a mean GH level of 1.6 +/- 0.1 microg/l and IGF-1 of 123 +/- 18% (P = 0.02).
  • GH < 2 microg/l, normal IGF-1, or both were observed in 25 (70%), 24 (67%) and 21 (58%) patients, respectively.
  • [MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Growth Hormone / blood. Growth Hormone-Secreting Pituitary Adenoma / drug therapy. Insulin-Like Growth Factor I / analysis. Pituitary Neoplasms / drug therapy. Somatostatin / analogs & derivatives

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  • [Cites] J Clin Endocrinol Metab. 2005 Oct;90(10):5627-31 [16046586.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Aug;90(8):4483-8 [15899958.001]
  • [Cites] Trends Endocrinol Metab. 2005 Nov;16(9):407-13 [16213744.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Jan;91(1):85-92 [16263832.001]
  • [Cites] Clin Endocrinol (Oxf). 2006 Feb;64(2):209-14 [16430722.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Apr;91(4):1397-403 [16449332.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Oct;85(10):3779-85 [11061538.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Nov;85(11):4099-103 [11095439.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Dec;85(12):4596-602 [11134114.001]
  • [Cites] Lancet. 2001 Feb 10;357(9254):425-31 [11273062.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Jun;86(6):2779-86 [11397887.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Sep;86(9):4072-7 [11549628.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Jan;87(1):99-104 [11788630.001]
  • [Cites] Clin Endocrinol (Oxf). 2002 Jan;56(1):65-71 [11849248.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Sep;87(9):4054-8 [12213843.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Sep;87(9):4142-6 [12213862.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Oct;87(10):4554-63 [12364434.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Jul;88(7):3090-8 [12843148.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Jul;88(7):3105-12 [12843150.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Oct;88(10):4709-19 [14557445.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Nov;88(11):5258-65 [14602759.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Nov;88(11):5414-21 [14602782.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Feb;89(2):667-74 [14764779.001]
  • [Cites] Endocr Rev. 2004 Feb;25(1):102-52 [14769829.001]
  • [Cites] Growth Horm IGF Res. 2004 Jun;14 Suppl A:S101-6 [15135788.001]
  • [Cites] Clin Endocrinol (Oxf). 2004 Aug;61(2):209-15 [15272916.001]
  • [Cites] J Clin Endocrinol Metab. 1994 Jul;79(1):113-8 [8027215.001]
  • [Cites] AJNR Am J Neuroradiol. 1997 Apr;18(4):765-72 [9127047.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Feb;83(2):374-8 [9467544.001]
  • [Cites] Clin Endocrinol (Oxf). 1998 Mar;48(3):311-6 [9578821.001]
  • [Cites] Am J Roentgenol Radium Ther Nucl Med. 1962 Jun;87:989-1008 [13885978.001]
  • [Cites] Eur J Endocrinol. 2005 Mar;152(3):379-87 [15757854.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Mar;90(3):1856-63 [15613435.001]
  • [Cites] Eur J Endocrinol. 2005 Jan;152(1):61-6 [15762188.001]
  • [Cites] Eur J Endocrinol. 2005 Apr;152(4):569-74 [15817912.001]
  • [Cites] Lancet. 2005 May 7-13;365(9471):1644-6 [15885297.001]
  • [Cites] Eur J Endocrinol. 2005 Jul;153(1):135-41 [15994755.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Jul;90(7):4405-10 [15827109.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Aug;90(8):4465-73 [15886238.001]
  • (PMID = 17524029.001).
  • [ISSN] 0300-0664
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Dopamine Agonists; 0 / Peptides, Cyclic; 118992-92-0 / lanreotide; 51110-01-1 / Somatostatin; 67763-96-6 / Insulin-Like Growth Factor I; 9002-72-6 / Growth Hormone; RWM8CCW8GP / Octreotide
  • [Other-IDs] NLM/ PMC1974833
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72. Hubina E, Ruscica M, Nanzer AM, Czirják S, Góth MI, Grossman AB, Korbonits M: Novel molecular aspects of pituitary adenomas. J Endocrinol Invest; 2005;28(11 Suppl International):87-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Novel molecular aspects of pituitary adenomas.
  • Ghrelin stimulates while somatostatin inhibits GH release and they thus serve as functional antagonists.
  • We have compared their effects on cell proliferation.
  • Ghrelin stimulates while somatostatin inhibits cell proliferation in most tissues and cell lines.
  • Here we show that ghrelin and desoctanoyl ghrelin stimulate cell proliferation in rat pituitary cell line (GH3), and these effects could be inhibited with mitogen-activated protein kinase (MAPK), tyrosine kinase and protein kinase C inhibitors.
  • Somatostatin and its analogs negatively regulate the growth of pituitary cells, and we now show that they inhibit MAPK activation.
  • We hypothesised that one of the mechanisms involved in the somatostatin effect is a stimulation of cell cycle inhibitor p27, as pituitary adenomas have decreased p27 peptide content.
  • In summary, we suggest that ghrelin and somatostatin have opposite effects on somatotroph cells not just at the level of GH release but also in terms of cell proliferation.
  • Ghrelin may play a role in pituitary tumorigenesis via an autocrine/paracrine pathway.
  • [MeSH-major] Adenoma / pathology. Adenoma / physiopathology. Peptide Hormones / physiology. Pituitary Neoplasms / pathology. Pituitary Neoplasms / physiopathology. Somatostatin / physiology
  • [MeSH-minor] Cell Division / drug effects. Cell Line, Tumor. Cyclin-Dependent Kinase Inhibitor p27 / metabolism. Enzyme Activation. Ghrelin. Human Growth Hormone / secretion. Humans. Mitogen-Activated Protein Kinases / metabolism. Octreotide / pharmacology. Receptors, Somatostatin / physiology

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  • (PMID = 16625855.001).
  • [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 / Ghrelin; 0 / Peptide Hormones; 0 / Receptors, Somatostatin; 12629-01-5 / Human Growth Hormone; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 51110-01-1 / Somatostatin; 98H1T17066 / pasireotide; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; RWM8CCW8GP / Octreotide
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73. Pertuit M, Barlier A, Enjalbert A, Gérard C: Signalling pathway alterations in pituitary adenomas: involvement of Gsalpha, cAMP and mitogen-activated protein kinases. J Neuroendocrinol; 2009 Nov;21(11):869-77
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Signalling pathway alterations in pituitary adenomas: involvement of Gsalpha, cAMP and mitogen-activated protein kinases.
  • Despite extensive research on sporadic pituitary adenomas, it is not yet possible to assign one protein alteration to one specific type of pituitary adenomas.
  • Nevertheless, alterations of the cAMP pathway appear to be molecular hallmarks of most growth hormone (GH)-secreting adenomas.
  • In this review, we summarise the literature regarding signalling alterations observed in GH-secreting adenomas.
  • In the light of results obtained on human somatotroph adenoma cells in primary culture and on models of murine somatotroph cell lines, we postulate a crucial role for ERK1/2 in GH-secreting adenomas downstream of cAMP pathway alterations that might impact the tumoural phenotype.
  • [MeSH-major] Adenoma / metabolism. Cyclic AMP / metabolism. GTP-Binding Protein alpha Subunits, Gs / metabolism. Mitogen-Activated Protein Kinases / metabolism. Pituitary Neoplasms / metabolism. Signal Transduction
  • [MeSH-minor] Growth Hormone / secretion. Humans

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  • (PMID = 19732293.001).
  • [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; Review
  • [Publication-country] England
  • [Chemical-registry-number] 9002-72-6 / Growth Hormone; E0399OZS9N / Cyclic AMP; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs
  • [Number-of-references] 95
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74. Kobayashi T, Mori Y, Uchiyama Y, Kida Y, Fujitani S: Long-term results of gamma knife surgery for growth hormone-producing pituitary adenoma: is the disease difficult to cure? J Neurosurg; 2005 Jan;102(s_supplement):119-123
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term results of gamma knife surgery for growth hormone-producing pituitary adenoma: is the disease difficult to cure?
  • OBJECT: The authors conducted a study to determine the long-term results of gamma knife surgery for residual or recurrent growth hormine (GH)-producing pituitary adenomas and to compare the results with those after treatment of other pituitary adenomas.
  • Growth hormone normalization (GH < 1.0 ng/ml) was found in 4.8%, nearly normal (< 2.0 ng/ml) in 11.9%, significantly decreased (< 5.0 ng/ml) in 23.8%, decreased in 21.4%, unchanged in 21.4%, and increased in 16.7%.
  • Serum insulin-like growth factor (IGF)-1 was significantly decreased (IGF-1 < 400 ng/ml) in 40.7%, decreased in 29.6%, unchanged in 18.5%, and increased in 11.1%, which was almost parallel to the GH changes.
  • CONCLUSIONS: Gamma knife surgery was effective and safe for the control of tumors; however, normalization of GH and IGF-1 secretion was difficult to achieve in cases with large tumors and low-dose radiation.

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  • (PMID = 28306435.001).
  • [ISSN] 1933-0693
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Keywords] NOTNLM ; gamma knife surgery / growth hormone—producing pituitary adenoma / insulin-like growth factor
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75. Zieliński G, Hendzel P, Szałański P, Gołowicz J, Gryszko L, Podgórski JK: [Severe cardiovascular complications due to the pituitary adenoma with acromegaly. An interdisciplinary approach to the treatment. A case report]. Neurol Neurochir Pol; 2006 Jul-Aug;40(4):354-60
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Severe cardiovascular complications due to the pituitary adenoma with acromegaly. An interdisciplinary approach to the treatment. A case report].
  • [Transliterated title] Ciezkie powikłania sercowo-naczyniowe w przebiegu guza przysadki powodujacego akromegalie. Propozycja równoczesnego wielospecjalistycznego leczenia. Opis przypadku.
  • Acromegaly reduces life expectancy and leads to 3-5-fold increase in mortality.
  • Successful therapy ought to normalize GH, IGF-I secretion, remove the adenoma mass and its local pressure effects and preserve pituitary functions intact to improve systemic morbidity and normalize mortality.
  • The primary therapy for most patients with acromegaly is still transsphenoidal adenomectomy.
  • The authors present a 64-year-old woman with diagnosed GH-secreting pituitary macroadenoma suffering from severe coronary heart disease and diabetes mellitus.
  • [MeSH-major] Acromegaly / surgery. Adenoma / surgery. Coronary Artery Disease / surgery. Growth Hormone-Secreting Pituitary Adenoma / surgery. Pituitary Neoplasms / surgery

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  • (PMID = 16967359.001).
  • [ISSN] 0028-3843
  • [Journal-full-title] Neurologia i neurochirurgia polska
  • [ISO-abbreviation] Neurol. Neurochir. Pol.
  • [Language] pol
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Poland
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76. Romano D, Magalon K, Pertuit M, Rasolonjanahary R, Barlier A, Enjalbert A, Gerard C: Conditional overexpression of the wild-type Gs alpha as the gsp oncogene initiates chronic extracellularly regulated kinase 1/2 activation and hormone hypersecretion in pituitary cell lines. Endocrinology; 2007 Jun;148(6):2973-83
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Conditional overexpression of the wild-type Gs alpha as the gsp oncogene initiates chronic extracellularly regulated kinase 1/2 activation and hormone hypersecretion in pituitary cell lines.
  • In pituitary cells, activation of the cAMP pathway by specific G protein-coupled receptors controls differentiative functions and proliferation.
  • Constitutively active forms of the alpha subunit of the heterotrimeric G(s) protein resulting from mutations at codon 201 or 227 (gsp oncogene) were first identified in 30-40% of human GH-secreting pituitary adenomas.
  • To explore the role of G(s)alpha in GH-secreting adenomas, we obtained somatolactotroph GH4C1 cell lines by performing doxycycline-dependent conditional overexpression of the wild-type G(s)alpha protein and expression of the gsp oncogene.
  • Although the resulting adenylyl cyclase and cAMP levels were 10-fold lower in the wild-type G(s)alpha-overexpressing cell line, a sustained MAPK ERK1/2 activation was observed in both cell lines.
  • Overexpression of the wild-type G(s)alpha protein as the gsp oncogene initiated chronic activation of endogenous prolactin synthesis and release, as well as chronic activation of ERK1/2-sensitive human prolactin and GH promoters.
  • [MeSH-major] GTP-Binding Protein alpha Subunits, Gs / genetics. Gene Expression Regulation, Enzymologic. Growth Hormone / secretion. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. Prolactin / secretion. Somatotrophs / metabolism
  • [MeSH-minor] Adenylyl Cyclases / metabolism. Animals. Cell Line. Cyclic AMP / metabolism. Doxycycline / pharmacology. Enzyme Activation. Oncogene Proteins / genetics. Rats. Time Factors. Transfection. Transgenes / drug effects

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  • (PMID = 17363453.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins; 9002-62-4 / Prolactin; 9002-72-6 / Growth Hormone; E0399OZS9N / Cyclic AMP; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 3.6.1.- / Gnas protein, rat; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs; EC 4.6.1.1 / Adenylyl Cyclases; N12000U13O / Doxycycline
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77. Wasko R, Jaskuła M, Plewa R, Komarowska H, Poreba E, Goździcka-Józefiak A, Liebert W, Bednarek J, Sowiński J: The evaluation of ghrelin mRNA expression in human somatotroph adenomas. Neuro Endocrinol Lett; 2006 Feb-Apr;27(1-2):169-73
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The evaluation of ghrelin mRNA expression in human somatotroph adenomas.
  • Ghrelin is one of the peptides involved into GH-release, binding to specific GHS receptors on hypothalamus and pituitary.
  • The ghrelin peptide and ghrelin mRNA have been detected in several regions of hypothalamus, in normal pituitary, as well as in various types of pituitary adenoma, with different levels of expression in different tumour types.
  • We decided to determine the expression of ghrelin in somatotroph adenomas.
  • Human pituitary somatotroph adenoma tissues were obtained at the time of transsphenoidal surgery from 3 acromegalic patients and studied for ghrelin mRNA expression.
  • We wished to determine the number of copies of ghrelin gene within the single cell.
  • [MeSH-major] Adenoma / metabolism. Human Growth Hormone / metabolism. Peptide Hormones / biosynthesis. Pituitary Neoplasms / metabolism

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  • (PMID = 16648773.001).
  • [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 / Actins; 0 / DNA, Complementary; 0 / Ghrelin; 0 / Peptide Hormones; 0 / RNA, Messenger; 12629-01-5 / Human Growth Hormone; EC 1.2.1.- / Glyceraldehyde-3-Phosphate Dehydrogenases
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78. Meij BP, Auriemma E, Grinwis G, Buijtels JJ, Kooistra HS: Successful treatment of acromegaly in a diabetic cat with transsphenoidal hypophysectomy. J Feline Med Surg; 2010 May;12(5):406-10
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  • [Title] Successful treatment of acromegaly in a diabetic cat with transsphenoidal hypophysectomy.
  • Plasma concentrations of growth hormone (GH) (51 microg/l, reference range 0.8-7.2 microg/l) and insulin-like growth factor 1 (IGF-1) (3871 microg/l, reference range 39-590 microg/l) were highly elevated, whereas those of alpha-melanocyte-stimulating hormone, adrenocorticotropic hormone and cortisol were normal.
  • Computed tomography revealed a thick palatum molle and an enlarged pituitary gland, indicating a pituitary neoplasm.
  • Microsurgical transsphenoidal hypophysectomy was performed and microscopic examination of the surgical specimen revealed an acidophilic, infiltrative pituitary adenoma that showed positive immunostaining for GH.
  • One year after hypophysectomy the plasma concentrations of GH and IGF-1 were 2.4 microg/l and 113 microg/l, respectively.
  • PRACTICAL RELEVANCE: This is the first report detailing transsphenoidal hypophysectomy as a feasible and effective treatment for feline acromegaly due to a pituitary somatotroph adenoma.
  • The surgery is discussed in the context of human and other feline therapies for acromegaly.
  • [MeSH-major] Acromegaly / veterinary. Adenocarcinoma / veterinary. Cat Diseases / surgery. Hypophysectomy / veterinary
  • [MeSH-minor] Adrenocortical Hyperfunction / blood. Adrenocortical Hyperfunction / complications. Adrenocortical Hyperfunction / surgery. Adrenocortical Hyperfunction / veterinary. Animals. Blood Glucose / metabolism. Cats. Diabetes Mellitus / blood. Diabetes Mellitus / surgery. Diabetes Mellitus / veterinary. Growth Hormone / blood. Insulin-Like Growth Factor I / metabolism. Male. Sphenoid Bone. Treatment Outcome

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  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20417901.001).
  • [ISSN] 1532-2750
  • [Journal-full-title] Journal of feline medicine and surgery
  • [ISO-abbreviation] J. Feline Med. Surg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Blood Glucose; 67763-96-6 / Insulin-Like Growth Factor I; 9002-72-6 / Growth Hormone
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79. Pawlikowski M, Pisarek H, Kunert-Radek J, Radek M: Somatostatin receptors in GH-secreting pituitary adenomas--their relationship to the response to octreotide. Endokrynol Pol; 2008 May-Jun;59(3):196-9
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  • [Title] Somatostatin receptors in GH-secreting pituitary adenomas--their relationship to the response to octreotide.
  • Twenty pituitary adenomas, surgically removed from patients suffering from acromegaly, were studied.
  • The tumours were immunostained with anti-GH and anti-PRL antibodies and with antibodies raised against particular subtypes of somatostatin receptors (rsst1-5).
  • In 15 patients in whom the GH response to the acute administration of 200 ug octreotide was tested the correlation between the expression of rsst and the percentage of GH drop was estimated.
  • All the tumours were GH-immunopositive and in the majority (14/20) co-expression of PRL was also found.
  • All the adenomas examined expressed rsst2A (20/20) and rsst5 (12/12) receptor proteins.
  • The mixed (GH/PRL) adenomas showed a tendency to a higher expression of rsst2A + + rsst2B and a greater response to octreotide administration.
  • A significant positive correlation was found between rsst2A + rsst2B expressions and a drop in GH after octreotide.
  • To conclude, the GH-inhibiting effect of octreotide depends on the intensity of expression of both rsst2A and rsst2B.
  • Both isoforms of rsst2 mediate the same biological response (inhibition of GH secretion) in GH-secreting and GH/PRL-secreting adenomas.
  • [MeSH-major] Adenoma / drug therapy. Adenoma / metabolism. Growth Hormone-Secreting Pituitary Adenoma / drug therapy. Growth Hormone-Secreting Pituitary Adenoma / metabolism. Octreotide / therapeutic use. Receptors, Somatostatin / metabolism
  • [MeSH-minor] Acromegaly / etiology. Antineoplastic Agents / therapeutic use. Growth Hormone / drug effects. Growth Hormone / secretion. Humans. Immunohistochemistry

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  • (PMID = 18615392.001).
  • [ISSN] 0423-104X
  • [Journal-full-title] Endokrynologia Polska
  • [ISO-abbreviation] Endokrynol Pol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Receptors, Somatostatin; 9002-72-6 / Growth Hormone; RWM8CCW8GP / Octreotide
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80. Kirschner LS: PRKAR1A and the evolution of pituitary tumors. Mol Cell Endocrinol; 2010 Sep 15;326(1-2):3-7
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  • [Title] PRKAR1A and the evolution of pituitary tumors.
  • Carney complex (CNC) is an inherited tumor predisposition associated with pituitary tumors, including GH-producing pituitary adenomas and rare reports of prolactinomas.
  • This disease is caused by mutations in PRKAR1A, which encodes the type 1A regulatory subunit of the cAMP-dependent protein kinase, PKA.
  • Loss of PRKAR1A causes enhanced PKA signaling, which leads to pituitary tumorigenesis.
  • Mutations in the gene have not been detected in sporadic pituitary tumors, but there is some data to suggest that non-genomic mechanisms may cause loss of protein expression.
  • Unlike CNC patients, mice heterozygous for Prkar1a mutations do not develop pituitary tumors, although complete knockout of the gene in the Pit1 lineage of the pituitary produces GH-secreting pituitary adenomas.
  • These data indicate that complete loss of Prkar1a/PRKAR1A is able to cause pituitary tumors in mice and men.
  • The pattern of tumors is likely related to the signaling pathways employed in specific pituitary cell types.

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  • [Copyright] 2010 Elsevier Ireland Ltd. All rights reserved.
  • [Cites] Cancer Res. 2004 Dec 15;64(24):9193-8 [15604292.001]
  • [Cites] Hum Mol Genet. 2010 Apr 15;19(8):1387-98 [20080939.001]
  • [Cites] Genes Chromosomes Cancer. 2005 May;43(1):72-82 [15704128.001]
  • [Cites] Cancer Res. 2005 Jun 1;65(11):4506-14 [15930266.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jun 28;102(26):9218-23 [15972329.001]
  • [Cites] Lancet Oncol. 2005 Jul;6(7):501-8 [15992699.001]
  • [Cites] Genomics. 1999 Nov 15;62(1):21-33 [10585764.001]
  • [Cites] J Neurosurg. 2000 Mar;92(3):413-8 [10701527.001]
  • [Cites] J Pediatr Endocrinol Metab. 2000 Apr;13(4):373-9 [10776991.001]
  • [Cites] Oncogene. 2000 Apr 6;19(15):1875-84 [10773877.001]
  • [Cites] Methods Mol Biol. 2000;136:477-85 [10840735.001]
  • [Cites] Nat Genet. 2000 Sep;26(1):89-92 [10973256.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Oct;85(10):3860-5 [11061550.001]
  • [Cites] Hum Mol Genet. 2000 Dec 12;9(20):3037-46 [11115848.001]
  • [Cites] Endocrinology. 2001 Sep;142(9):3764-73 [11517152.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Sep;86(9):4041-6 [11549623.001]
  • [Cites] Endocr Rev. 2001 Oct;22(5):675-705 [11588148.001]
  • [Cites] Endocr Rev. 2001 Dec;22(6):724-63 [11739329.001]
  • [Cites] J Biol Chem. 2002 Jul 26;277(30):27294-304 [12004056.001]
  • [Cites] Clin Endocrinol (Oxf). 2002 Oct;57(4):443-8 [12354125.001]
  • [Cites] J Med Genet. 2002 Dec;39(12):e78 [12471216.001]
  • [Cites] Clin Endocrinol (Oxf). 2003 Apr;58(4):464-70 [12641630.001]
  • [Cites] J Mol Endocrinol. 2003 Apr;30(2):87-97 [12683933.001]
  • [Cites] J Med Genet. 2004 Aug;41(8):596-600 [15286154.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Sep 28;101(39):14222-7 [15371594.001]
  • [Cites] Medicine (Baltimore). 1985 Jul;64(4):270-83 [4010501.001]
  • [Cites] Nature. 1991 Mar 7;350(6313):74-7 [1848356.001]
  • [Cites] Recent Prog Horm Res. 1995;50:35-73 [7740167.001]
  • [Cites] Semin Dermatol. 1995 Jun;14(2):90-8 [7640202.001]
  • [Cites] Endocrinology. 1995 Sep;136(9):4147-50 [7649123.001]
  • [Cites] J Clin Invest. 1996 Feb 1;97(3):699-705 [8609225.001]
  • [Cites] Br J Dermatol. 1997 Apr;136(4):578-82 [9155962.001]
  • [Cites] Cancer Res. 2004 Dec 15;64(24):8811-5 [15604237.001]
  • [Cites] Cancer Res. 2005 Nov 15;65(22):10307-15 [16288019.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Dec;90(12):6721-4 [16204369.001]
  • [Cites] Science. 2006 May 26;312(5777):1228-30 [16728643.001]
  • [Cites] Nat Genet. 2006 Jul;38(7):794-800 [16767104.001]
  • [Cites] Orphanet J Rare Dis. 2006;1:21 [16756677.001]
  • [Cites] Curr Opin Oncol. 2007 Jan;19(1):24-9 [17133108.001]
  • [Cites] J Biol Chem. 2007 Dec 7;282(49):35924-32 [17916558.001]
  • [Cites] Genesis. 2008 Jan;46(1):37-42 [18196598.001]
  • [Cites] Mol Endocrinol. 2008 Feb;22(2):430-40 [17932105.001]
  • [Cites] Mol Endocrinol. 2008 Feb;22(2):380-7 [17975024.001]
  • [Cites] Circulation. 2008 Mar 18;117(11):1414-22 [18316483.001]
  • [Cites] Eur J Hum Genet. 2008 Oct;16(10):1245-53 [18431404.001]
  • [Cites] Horm Res. 2009;71(3):132-41 [19188737.001]
  • [Cites] J Clin Endocrinol Metab. 2009 Jun;94(6):2085-91 [19293268.001]
  • [Cites] Endocrinology. 2009 Jul;150(7):3177-85 [19342460.001]
  • [Cites] Endocr Relat Cancer. 2009 Sep;16(3):773-93 [19470615.001]
  • [Cites] Pituitary. 2004;7(2):73-82 [15761655.001]
  • (PMID = 20451576.001).
  • [ISSN] 1872-8057
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA112268; None / None / / R01 CA112268-05; United States / NCI NIH HHS / CA / R01 CA112268-05
  • [Publication-type] Journal Article; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit; 0 / PRKAR1A protein, human; 0 / Prkar1a protein, mouse; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases
  • [Other-IDs] NLM/ NIHMS211600; NLM/ PMC2922961
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81. Thodou E, Argyrakos T, Kontogeorgos G: Galectin-3 as a marker distinguishing functioning from silent corticotroph adenomas. Hormones (Athens); 2007 Jul-Sep;6(3):227-32
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  • [Title] Galectin-3 as a marker distinguishing functioning from silent corticotroph adenomas.
  • OBJECTIVE: Galectin-3 (Gal-3) belongs to the family of carbohydrate-binding proteins with high affinity for galactoside and is involved in many biological processes including cell growth and differentiation, cell adhesion, tumor progression, apoptosis and metastasis.
  • The aim of this study was to disclose differences in the expression of Gal-3 in silent and functioning corticotroph pituitary adenomas.
  • DESIGN: We examined 30 pituitary adenomas (19 functioning corticotroph, 11 silent corticotroph adenomas).
  • Two prolactinomas and 2 functioning somatotroph adenomas served as positive controls.
  • The independent variables t-test was used for comparison of the mean expression of Gal-3 in the two different corticotroph adenoma subgroups.
  • RESULTS: Eighteen of the functioning corticotroph adenomas (94.73%) were positive for Gal-3 with a cytoplasmic and focally membranous distribution; two cases also exhibited nuclear expression, whereas 9 of the silent corticotroph adenomas (81.81%) had zero or<1% expression of Gal-3 (p=0.001).
  • CONCLUSIONS: Gal-3 is highly expressed in functioning corticotroph adenomas of the pituitary gland, while silent adenomas exhibit very focal to null expression of Gal-3.
  • This observation can be used in the pathological diagnosis to separate functioning from silent corticotroph adenomas of the pituitary.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / diagnosis. Adenoma / diagnosis. Biomarkers, Tumor / metabolism. Galectin 3 / metabolism
  • [MeSH-minor] Humans. Immunohistochemistry. Pituitary Gland / metabolism

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  • (PMID = 17724007.001).
  • [ISSN] 1109-3099
  • [Journal-full-title] Hormones (Athens, Greece)
  • [ISO-abbreviation] Hormones (Athens)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Galectin 3
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82. Chang HP, Tseng YC, Chou TM: An enlarged sella turcica on cephalometric radiograph. Dentomaxillofac Radiol; 2005 Sep;34(5):308-12
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  • A 28-year-old male presented to the Orthodontic clinic for correction of his anterior crossbite due to mandibular prognathism as a result of pituitary adenoma with acromegaly.
  • We discuss the radiographic diagnosis of an enlarged sella turcica in intrasellar tumours and also emphasise the dentist's important role in the initial diagnosis of pituitary adenoma cases.
  • [MeSH-major] Acromegaly / radiography. Cephalometry. Sella Turcica / radiography
  • [MeSH-minor] Adenoma / complications. Adult. Humans. Male. Malocclusion, Angle Class III / etiology. Malocclusion, Angle Class III / radiography. Patient Care Planning. Pituitary Neoplasms / complications. Prognathism / etiology. Prognathism / radiography. Radiographic Magnification. Radiography, Panoramic

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  • (PMID = 16120882.001).
  • [ISSN] 0250-832X
  • [Journal-full-title] Dento maxillo facial radiology
  • [ISO-abbreviation] Dentomaxillofac Radiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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83. Roberts BK, Ouyang DL, Lad SP, Chang SD, Harsh GR 4th, Adler JR Jr, Soltys SG, Gibbs IC, Remedios L, Katznelson L: Efficacy and safety of CyberKnife radiosurgery for acromegaly. Pituitary; 2007;10(1):19-25
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  • [Title] Efficacy and safety of CyberKnife radiosurgery for acromegaly.
  • OBJECTIVE: Acromegaly is a disease characterized by GH hypersecretion, and is typically caused by a pituitary somatotroph adenoma.
  • The primary mode of therapy is surgery, and radiotherapy is utilized as an adjuvant strategy to treat persistent disease.
  • The aim of this study was to determine the efficacy and tolerability of CyberKnife stereotactic radiosurgery in acromegaly.
  • DESIGN: A retrospective review of biochemical and imaging data for subjects with acromegaly treated with CyberKnife stereotactic radiosurgery between 1998 and 2005 at Stanford University Hospital.
  • PATIENTS: Nine patients with active acromegaly were treated with radiosurgery using the CyberKnife (CK).
  • MEASUREMENTS: Biochemical response based on serum insulin-like growth factor-1 (IGF-1), anterior pituitary hormone function, and tumor size with MRI scans were analyzed.
  • Smaller tumor size was predictive of treatment success: baseline tumor volume was 1.28 cc (+/- 0.81, SD) vs. 3.93 cc (+/- 1.54) in subjects with a normal IGF-1 vs. those with persistent, active disease, respectively (P = 0.02).
  • The mean biologically effective dose (BED) was higher in subjects who achieved a normal IGF-1 vs. those with persistent, active disease, 172 Gy(3) (+/-28) vs. 94 Gy(3) (+/-17), respectively (P < 0.01).
  • At least one new anterior pituitary hormone deficiency was observed after CK in 3 (33%) patients: two developed hypogonadism, and one developed panhypopituitarism.
  • CONCLUSIONS: CK radiosurgery may be a valuable adjuvant therapy for the management of acromegaly.
  • [MeSH-major] Acromegaly / surgery. Growth Hormone-Secreting Pituitary Adenoma / surgery. Radiosurgery
  • [MeSH-minor] Adult. Female. Humans. Insulin-Like Growth Factor I / analysis. Magnetic Resonance Imaging. Male. Middle Aged. Retrospective Studies

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  • [ErratumIn] Pituitary. 2007;10(1):17. Remedios, Lynn [added]
  • [ErratumIn] Pituitary. 2007 Mar;10(1):17 [27519534.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Oct;83(10):3419-26 [9768641.001]
  • [Cites] Clin Endocrinol (Oxf). 1994 Jul;41(1):95-102 [8050136.001]
  • [Cites] Endocr Pract. 2004 May-Jun;10(3):213-25 [15382339.001]
  • [Cites] J Clin Endocrinol Metab. 2000 May;85(5):2068-71 [10843197.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Oct;85(10):3779-85 [11061538.001]
  • [Cites] Clin Endocrinol (Oxf). 2003 Feb;58(2):132-5 [12580925.001]
  • [Cites] Minim Invasive Neurosurg. 2005 Apr;48(2):91-6 [15906203.001]
  • [Cites] BMJ. 1992 May 23;304(6838):1343-6 [1611331.001]
  • [Cites] J Neurosurg. 2000 Dec;93 Suppl 3:6-9 [11143264.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1991 Aug;21(3):607-14 [1907958.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Jul;88(7):3105-12 [12843150.001]
  • [Cites] Metabolism. 1996 Aug;45(8 Suppl 1):111-4 [8769401.001]
  • [Cites] Q J Med. 1989 Feb;70(262):145-60 [2594955.001]
  • [Cites] Neurosurgery. 1999 Jun;44(6):1299-306; discussion 1306-7 [10371630.001]
  • [Cites] Neurosurgery. 1998 Jan;42(1):172-8 [9442520.001]
  • [Cites] Neurosurgery. 2001 Jun;48(6):1239-43; discussion 1244-5 [11383725.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1994 Oct 15;30(3):557-65 [7928486.001]
  • [Cites] Neurosurg Clin N Am. 2004 Oct;15(4):467-79, x [15450882.001]
  • [Cites] Eur J Endocrinol. 2001 Dec;145(6):717-26 [11720896.001]
  • [Cites] J Neurosurg. 1998 Jun;88(6):1002-8 [9609294.001]
  • [Cites] J Neurosurg. 2005 Apr;102(4):678-91 [15871511.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Jul;85(7):2476-82 [10902796.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Oct;82(10):3187-91 [9329336.001]
  • [Cites] J Clin Endocrinol Metab. 1995 Dec;80(12):3395-402 [8530571.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Oct;83(10):3411-8 [9768640.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Mar;85(3):1287-9 [10720077.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1995 Sep 30;33(2):307-14 [7673017.001]
  • [Cites] Clin Endocrinol (Oxf). 1999 May;50(5):561-7 [10468920.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1997 Sep 1;39(2):437-44 [9308948.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1993 Jan 15;25(2):381-5 [8420891.001]
  • [Cites] Clin Endocrinol (Oxf). 1993 Jun;38(6):571-8 [8334743.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Aug;90(8):4483-8 [15899958.001]
  • [Cites] Neurosurgery. 2003 Jan;52(1):140-6; discussion 146-7 [12493111.001]
  • [Cites] Clin Endocrinol (Oxf). 1979 May;10(5):469-79 [113142.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Nov;88(11):5334-40 [14602770.001]
  • [Cites] Growth Horm IGF Res. 2005 Jul;15 Suppl A:S31-5 [16023876.001]
  • [Cites] Acta Neurochir Suppl. 1994;62:33-8 [7717132.001]
  • [Cites] Clin Endocrinol (Oxf). 1998 Mar;48(3):331-7 [9578824.001]
  • [Cites] Exp Clin Endocrinol Diabetes. 2005 Apr;113(4):219-24 [15891958.001]
  • (PMID = 17273921.001).
  • [ISSN] 1386-341X
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 67763-96-6 / Insulin-Like Growth Factor I
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84. Gola M, Doga M, Bonadonna S, Mazziotti G, Vescovi PP, Giustina A: Neuroendocrine tumors secreting growth hormone-releasing hormone: Pathophysiological and clinical aspects. Pituitary; 2006;9(3):221-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neuroendocrine tumors secreting growth hormone-releasing hormone: Pathophysiological and clinical aspects.
  • Hypothalamic GHRH is secreted into the portal system, binds to specific surface receptors of the somatotroph cell and elicits intracellular signals that modulate pituitary GH synthesis and/or secretion.
  • Excessive peripheral production of GHRH by a tumor source would therefore be expected to cause somatotroph cell hyperstimulation, increased GH secretion and eventually pituitary acromegaly.
  • Immunoreactive GHRH is present in several tumors, including carcinoid tumors, pancreatic cell tumors, small cell lung cancers, endometrial tumors, adrenal adenomas, and pheochromocytomas which have been reported to secrete GHRH.
  • Acromegaly in these patients, however, is uncommon.
  • The distinction of pituitary vs. extrapituitary acromegaly is extremely important in planning effective management.
  • Regardless of the cause, GH and IGF-1 are invariably elevated and GH levels fail to suppress (<1 microg/l) after an oral glucose load in all forms of acromegaly.
  • Dynamic pituitary tests are not helpful in distinguishing acromegalic patients with pituitary tumors from those harbouring extrapituitary tumors.
  • Plasma GHRH levels are usually elevated in patients with peripheral GHRH-secreting tumors, and are normal or low in patients with pituitary acromegaly.
  • Unique and unexpected clinical features in an acromegalic patient, including respiratory wheezing or dyspnea, facial flushing, peptic ulcers, or renal stones sometimes are helpful in alerting the physician to diagnosing non pituitary endocrine tumors.
  • If no facility to measure plasma GHRH is available, and in the absence of MRI evidence of pituitary adenoma, a CT scan of the thorax and abdominal ultrasound could be performed to exclude with good approximation the possibility of an ectopic GHRH syndrome.
  • Surgical resection of the tumor secreting ectopic GHRH should be the logical approach to a patient with ectopic GHRH syndrome.
  • Standard chemotherapy directed at GHRH-producing carcinoid tumors is generally unsuccessful in controlling the activated GH axis.
  • Somatostatin analogs provide an effective option for medical management of carcinoid patients, especially those with recurrent disease.
  • In fact, long-acting somatostatin analogs may be able to control not only the ectopic hormonal secretion syndrome, but also, in some instances, tumor growth.
  • Therefore, although cytotoxic chemotherapy, pituitary surgery, or irradiation still remain available therapeutic options, long-acting somatostatin analogs are now preferred as a second-line therapy in patients with carcinoid tumors and ectopic GHRH-syndrome.
  • [MeSH-major] Acromegaly / etiology. Adenoma / secretion. Carcinoid Tumor / secretion. Growth Hormone-Releasing Hormone / secretion. Growth Hormone-Secreting Pituitary Adenoma / secretion. Neuroendocrine Tumors / secretion. Paraneoplastic Endocrine Syndromes / etiology
  • [MeSH-minor] Animals. Biomarkers, Tumor / blood. Diagnosis, Differential. Human Growth Hormone / blood. Humans. Insulin-Like Growth Factor I / metabolism. Treatment Outcome. Up-Regulation

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  • [Cites] Endocrinol Metab Clin North Am. 1992 Sep;21(3):539-51 [1521511.001]
  • [Cites] Endocrinology. 1997 Nov;138(11):4543-51 [9348176.001]
  • [Cites] Eur J Endocrinol. 2005 Dec;153(6):737-40 [16322377.001]
  • [Cites] Semin Oncol. 1987 Sep;14(3):343-53 [2820064.001]
  • [Cites] Biochem Biophys Res Commun. 1982 Nov 16;109(1):152-8 [7159418.001]
  • [Cites] Endocrinology. 1985 Aug;117(2):457-67 [2862007.001]
  • [Cites] Endocr J. 1993 Feb;40(1):133-9 [7951487.001]
  • [Cites] J Endocrinol Invest. 1993 Sep;16(8):585-90 [8258646.001]
  • [Cites] Nature. 1983 Feb 17-23;301(5901):607-8 [6402707.001]
  • [Cites] Endocr Rev. 1998 Dec;19(6):717-97 [9861545.001]
  • [Cites] Endocr Rev. 1988 Aug;9(3):357-73 [3145190.001]
  • [Cites] Metabolism. 1991 May;40(5):519-23 [2023538.001]
  • [Cites] Domest Anim Endocrinol. 1997 Sep;14(5):358-66 [9347256.001]
  • [Cites] J Neurosci. 1996 Dec 15;16(24):8140-8 [8987839.001]
  • [Cites] J Endocrinol Invest. 2003 Feb;26(2):163-9 [12739745.001]
  • [Cites] Nature. 1983 Jun 9-15;303(5917):532-5 [6406907.001]
  • [Cites] J Clin Endocrinol Metab. 1984 May;58(5):796-803 [6423659.001]
  • [Cites] J Clin Endocrinol Metab. 1989 May;68(5):917-24 [2565913.001]
  • [Cites] Proc Soc Exp Biol Med. 1990 Mar;193(3):232-5 [2106141.001]
  • [Cites] Neurosurgery. 2002 Jun;50(6):1356-9; discussion 1360 [12015856.001]
  • [Cites] J Neuroendocrinol. 1989 Apr 1;1(2):109-15 [19210467.001]
  • [Cites] Endocrinology. 1976 Mar;98(3):580-9 [177264.001]
  • [Cites] Clin Endocrinol (Oxf). 2001 Mar;54(3):301-7 [11298081.001]
  • [Cites] Neuroendocrinology. 1990 May;51(5):572-5 [1693757.001]
  • [Cites] J Clin Endocrinol Metab. 1995 Nov;80(11):3321-6 [7593445.001]
  • [Cites] Metabolism. 1990 Sep;39(9 Suppl 2):40-2 [1976218.001]
  • [Cites] N Engl J Med. 1990 Aug 2;323(5):322-7 [2164153.001]
  • [Cites] Endocrinology. 1984 Nov;115(5):2032-4 [6436012.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Jun;88(6):2797-802 [12788890.001]
  • [Cites] J Clin Endocrinol Metab. 1984 Aug;59(2):197-201 [6330151.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Apr;90(4):2104-9 [15671091.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Apr;82(4):1210-9 [9100598.001]
  • [Cites] Endocrinology. 1993 Sep;133(3):1029-34 [8103446.001]
  • [Cites] Pharmacol Res. 1996 Nov-Dec;34(5-6):247-68 [9076850.001]
  • [Cites] J Clin Endocrinol Metab. 1984 Nov;59(5):846-9 [6434585.001]
  • [Cites] Cancer. 1988 Jan 15;61(2):221-6 [2891432.001]
  • [Cites] Metabolism. 1992 Dec;41(12):1291-4 [1281259.001]
  • [Cites] Ann Oncol. 2001;12 Suppl 2:S89-94 [11762359.001]
  • [Cites] Endocrinol Jpn. 1989 Apr;36(2):229-36 [2550207.001]
  • [Cites] J Clin Endocrinol Metab. 1989 Jan;68(1):180-5 [2491860.001]
  • [Cites] J Clin Invest. 1980 Jan;65(1):43-54 [6243140.001]
  • [Cites] Physiol Rev. 1999 Apr;79(2):511-607 [10221989.001]
  • [Cites] J Clin Endocrinol Metab. 1989 Jan;68(1):22-8 [2491864.001]
  • [Cites] Clin Endocrinol (Oxf). 1987 Sep;27(3):297-306 [2892599.001]
  • [Cites] FEBS Lett. 1996 Sep 23;394(1):1-4 [8925914.001]
  • [Cites] J Clin Endocrinol Metab. 1987 Mar;64(3):585-91 [3102543.001]
  • [Cites] Endocrinology. 1985 Jul;117(1):424-6 [2988927.001]
  • [Cites] J Endocrinol Invest. 2003;26(8 Suppl):4-7 [15233203.001]
  • [Cites] Nature. 1982 Nov 18;300(5889):276-8 [6292724.001]
  • [Cites] J Clin Invest. 1990 Jul;86(1):17-24 [1973173.001]
  • [Cites] Endocrinology. 1972 Oct;91(4):1071-8 [5051331.001]
  • [Cites] J Endocrinol Invest. 2003 Dec;26(12):1242-7 [15055479.001]
  • [Cites] J Endocrinol Invest. 2005;28(11 Suppl International):43-7 [16625844.001]
  • [Cites] J Clin Invest. 1982 Nov;70(5):965-77 [6290540.001]
  • [Cites] Endocr Rev. 1991 Nov;12(4):450-82 [1684746.001]
  • [Cites] Endocrinology. 1984 Apr;114(4):1082-5 [6423368.001]
  • [Cites] Endocrinology. 1992 Mar;130(3):1097-102 [1537276.001]
  • [Cites] Clin Endocrinol (Oxf). 1986 Feb;24(2):135-40 [2871948.001]
  • [Cites] Nature. 1983 Nov 3-9;306(5938):84-5 [6415487.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Feb;85(2):526-9 [10690849.001]
  • [Cites] Nature. 1985 Mar 21-27;314(6008):279-81 [2858817.001]
  • [Cites] Endocrinology. 1985 Oct;117(4):1598-601 [3928335.001]
  • [Cites] Lancet. 1984 Aug 18;2(8399):401-2 [6147476.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Sep;83(9):3104-9 [9745411.001]
  • [Cites] Endocrinology. 1983 Nov;113(5):1726-31 [6194979.001]
  • [Cites] Nature. 1993 Jul 15;364(6434):208-13 [8391647.001]
  • [Cites] Eur J Endocrinol. 1995 Jan;132(1):12-24 [7850005.001]
  • [Cites] Am J Clin Pathol. 1986 Jan;85(1):13-20 [3000164.001]
  • [Cites] Eur J Endocrinol. 1998 Jul;139(1):59-71 [9703380.001]
  • [Cites] Clin Endocrinol (Oxf). 1976 Sep;5(5):503-13 [991433.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Sep;87(9):4054-8 [12213843.001]
  • [Cites] Science. 1982 Nov 5;218(4572):585-7 [6812220.001]
  • [Cites] Clin Endocrinol (Oxf). 1989 Apr;30(4):367-77 [2574645.001]
  • [Cites] Endocrinology. 1996 Apr;137(4):1326-31 [8625907.001]
  • [Cites] Endocr Rev. 1986 Aug;7(3):223-53 [2874984.001]
  • [Cites] Am J Med. 1984 Apr;76(4):605-16 [6424465.001]
  • [Cites] Science. 1975 Feb 7;187(4175):447-9 [1111113.001]
  • [Cites] J Clin Endocrinol Metab. 1985 Feb;60(2):370-5 [3917460.001]
  • [Cites] Cancer. 1991 May 15;67(10):2538-42 [2015554.001]
  • [Cites] J Thorac Cardiovasc Surg. 2004 Oct;128(4):631-2 [15457172.001]
  • [Cites] Endocrinol Metab Clin North Am. 1992 Sep;21(3):575-95 [1521513.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Aug;86(8):3989-95 [11502843.001]
  • [Cites] J Clin Endocrinol Metab. 1989 Feb;68(2):499-504 [2493033.001]
  • [Cites] Adv Tech Stand Neurosurg. 1995;22:3-53 [7495421.001]
  • [Cites] J Clin Endocrinol Metab. 1984 Oct;59(4):747-51 [6434578.001]
  • [Cites] Annu Rev Med. 1990;41:447-55 [2184742.001]
  • [Cites] J Endocrinol Invest. 1993 Jan;16(1):69-81 [8445159.001]
  • [Cites] Br Med J (Clin Res Ed). 1986 Apr 12;292(6526):981-2 [2870758.001]
  • [Cites] J Clin Endocrinol Metab. 1984 Jan;58(1):212-4 [6417155.001]
  • [Cites] Science. 1985 Oct 25;230(4724):461-3 [2864742.001]
  • [Cites] Mol Endocrinol. 1992 Oct;6(10):1734-44 [1333056.001]
  • [Cites] Eur J Endocrinol. 1997 Jun;136(6):553-65 [9225715.001]
  • [Cites] Ir J Med Sci. 2004 Oct-Dec;173(4):215-6 [16323617.001]
  • [Cites] Acta Endocrinol (Copenh). 1985 May;109(1):13-8 [3923754.001]
  • [Cites] Endocrinology. 1991 Feb;128(2):1151-8 [1671214.001]
  • [Cites] J Endocrinol Invest. 1994 Oct;17(9):717-22 [7868816.001]
  • [Cites] Brain Res. 1989 Feb 27;481(1):8-15 [2565134.001]
  • [Cites] Eur J Endocrinol. 1995 Sep;133(3):320-4 [7581949.001]
  • [Cites] Endocrinology. 1985 Apr;116(4):1334-40 [3918850.001]
  • (PMID = 17036195.001).
  • [ISSN] 1573-7403
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I; 9034-39-3 / Growth Hormone-Releasing Hormone
  • [Number-of-references] 101
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85. Barbieri F, Bajetto A, Stumm R, Pattarozzi A, Porcile C, Zona G, Dorcaratto A, Ravetti JL, Minuto F, Spaziante R, Schettini G, Ferone D, Florio T: Overexpression of stromal cell-derived factor 1 and its receptor CXCR4 induces autocrine/paracrine cell proliferation in human pituitary adenomas. Clin Cancer Res; 2008 Aug 15;14(16):5022-32
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  • [Title] Overexpression of stromal cell-derived factor 1 and its receptor CXCR4 induces autocrine/paracrine cell proliferation in human pituitary adenomas.
  • PURPOSE: Hypothalamic or locally produced growth factors and cytokines control pituitary development, functioning, and cell division.
  • We evaluated the expression of the chemokine stromal cell-derived factor 1 (SDF1) and its receptor CXCR4 in human pituitary adenomas and normal pituitary tissues and their role in cell proliferation.
  • EXPERIMENTAL DESIGN: The expression of SDF1 and CXCR4 in 65 human pituitary adenomas and 4 human normal pituitaries was determined by reverse transcription-PCR, immunohistochemistry, and confocal immunofluorescence.
  • The proliferative effect of SDF1 was evaluated in eight fibroblast-free human pituitary adenoma cell cultures.
  • RESULTS: CXCR4 mRNA was expressed in 92% of growth hormone (GH)-secreting pituitary adenomas (GHoma) and 81% of nonfunctioning pituitary adenomas (NFPA), whereas SDF1 was identified in 63% and 78% of GHomas and NFPAs, respectively.
  • In normal tissues, CXCR4 and SDF1 were expressed only in a subset of anterior pituitary cells, with a lower expression of SDF1 compared with its cognate receptor.
  • CXCR4 and SDF1 were not confined to a specific cell population in the anterior pituitary but colocalized with discrete subpopulations of GH-, prolactin-, and adrenocorticorticotropic hormone-secreting cells.
  • In six of eight pituitary adenoma primary cultures, SDF1 induced a statistically significant increase in DNA synthesis that was prevented by the treatment with the CXCR4 antagonist AMD3100 or somatostatin.
  • CONCLUSIONS: CXCR4 and SDF1 are overexpressed in human pituitary adenomas and CXCR4 activation may contribute to pituitary cell proliferation and, possibly, to adenoma development in humans.
  • [MeSH-major] Chemokine CXCL12 / biosynthesis. Pituitary Neoplasms / metabolism. Receptors, CXCR4 / biosynthesis
  • [MeSH-minor] Cell Proliferation. Fluorescent Antibody Technique. Humans. Immunohistochemistry. In Situ Hybridization. Microscopy, Confocal. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction. Up-Regulation

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  • (PMID = 18698020.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CXCR4 protein, human; 0 / Chemokine CXCL12; 0 / RNA, Messenger; 0 / Receptors, CXCR4
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86. Taguchi T, Takao T, Iwasaki Y, Oyama K, Yamada S, Inoue M, Terada Y: Diagnostic value of 18F-dihydroxyphenylalanine positron emission tomography for growth hormone-producing pituitary adenoma. Pituitary; 2010;13(1):78-9
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  • [Title] Diagnostic value of 18F-dihydroxyphenylalanine positron emission tomography for growth hormone-producing pituitary adenoma.
  • A 55-year-old woman with signs of acromegaly was referred to our hospital.
  • Endocrinological examinations showed that she had high levels of growth hormone (GH; 5.54 ng ml(-1); normal range: 0.66-3.68 ng ml(-1)) and insulin-like growth factor-I (IGF-I; 508 ng ml(-1); normal range: 37-266 ng ml(-1)) levels, incomplete suppression of serum GH following a 75-gram oral glucose tolerance test (oGTT; trough GH 3.66 ng ml(-1)), and paradoxical GH responses to a TRH provocation test (peak GH 38.9 ng ml(-1)).
  • Dynamic magnetic resonance imaging (MRI) suggested the presence of an intrasellar mass lesion (5.9 x 2.8 mm) in the left part of her pituitary gland (Fig.
  • Subsequent histological analysis confirmed the diagnosis of a GH-producing pituitary adenoma.
  • After removal, serum IGF-I levels decreased to a normal range (178 ng ml(-1)), and serum GH was appropriately suppressed during oGTT (trough GH 0.30 ng ml(-1)), suggesting that complete resection was obtained [1].
  • PET scans are reported to be a valuable tool for the detection of pituitary adenomas [2-4].
  • This case clearly showed that FDG-PET is also useful for re-evaluation of the disease after surgery.
  • PET scans are recommended for patients with equivocal pituitary mass lesions on conventional MRI, and for follow-up examinations after surgery.
  • [MeSH-major] Dihydroxyphenylalanine. Fluorine Radioisotopes. Growth Hormone-Secreting Pituitary Adenoma / diagnosis. Positron-Emission Tomography / methods

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  • [Cites] Eur J Nucl Med Mol Imaging. 2006 Feb;33(2):169-78 [16228237.001]
  • [Cites] Neuroendocrinology. 2006;83(3-4):205-10 [17047384.001]
  • [Cites] J Clin Endocrinol Metab. 2009 Feb;94(2):523-7 [19033371.001]
  • [Cites] Radiology. 1990 Oct;177(1):39-44 [2399336.001]
  • (PMID = 19915981.001).
  • [ISSN] 1573-7403
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Case Reports; Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Fluorine Radioisotopes; 63-84-3 / Dihydroxyphenylalanine
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87. Trouillas J, Labat-Moleur F, Sturm N, Kujas M, Heymann MF, Figarella-Branger D, Patey M, Mazucca M, Decullier E, Vergès B, Chabre O, Calender A, Groupe d'études des Tumeurs Endocrines: Pituitary tumors and hyperplasia in multiple endocrine neoplasia type 1 syndrome (MEN1): a case-control study in a series of 77 patients versus 2509 non-MEN1 patients. Am J Surg Pathol; 2008 Apr;32(4):534-43
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  • [Title] Pituitary tumors and hyperplasia in multiple endocrine neoplasia type 1 syndrome (MEN1): a case-control study in a series of 77 patients versus 2509 non-MEN1 patients.
  • Patients affected by the multiple endocrine neoplasia type I syndrome (MEN1) display a high incidence of pituitary adenomas, though it is still unknown whether these pituitary tumors have specific pathologic features that would distinguish them from sporadic pituitary adenomas.
  • Pituitary tissue specimens of 77 MEN1 patients from the GTE (Groupe d'étude des Tumeurs Endocrines) register were compared with unselected 2509 non-MEN1 sporadic pituitary tumors and also to a control subgroup of 296 cases, where 1 MEN1 tumor was matched with 4 sporadic tumors of the same hormonal immunoprofile.
  • Histologic analysis took into account 33 items, including immunocytochemical data, the proliferative marker Ki-67, and an examination of the juxtatumoral pituitary.
  • MEN1 patients with large pituitary tumors (grade IV) were younger than non-MEN1 patients.
  • MEN1 tumors had no other characteristic histologic features and no predominance of any one hormone producing subtype.
  • However, plurihormonal adenomas versus monohormonal and nonimmunoreactive adenomas were more frequent in MEN1 tumors (39%) than in the control non-MEN1 group (P = 0.001).
  • Especially, the growth hormone and prolactin plurihormonality with unusual association with follicle-stimulating hormone, luteinizing hormone, or adrenocorticotropic hormone was more frequent in MEN1 tumors.
  • In addition, multiple adenomas were significantly more frequent (4% vs. 0.1%; P < 0.0001), especially prolactin-adrenocorticotropic hormone.
  • Somatotroph hyperplasia, with or without a microadenoma was found in only 3 MEN1 patients, with growth hormone-releasing hormone hypersecretion by a pancreatic tumor in 2 of them.
  • [MeSH-major] Adenoma / pathology. Multiple Endocrine Neoplasia Type 1 / pathology. Pituitary Gland / pathology. Pituitary Neoplasms / pathology
  • [MeSH-minor] Adolescent. Adrenocorticotropic Hormone / analysis. Adult. Aged. Aged, 80 and over. Case-Control Studies. Cell Proliferation. Female. Follicle Stimulating Hormone / analysis. Gene Expression Regulation, Neoplastic. Human Growth Hormone / analysis. Humans. Hyperplasia. Immunohistochemistry. Ki-67 Antigen / analysis. Luteinizing Hormone / analysis. Male. Middle Aged. Mutation. Neoplasm Invasiveness. Neoplasm Staging. Prolactin / analysis. Proto-Oncogene Proteins / genetics. Thyrotropin / analysis


88. Minniti G, Jaffrain-Rea ML, Osti M, Esposito V, Santoro A, Solda F, Gargiulo P, Tamburrano G, Enrici RM: The long-term efficacy of conventional radiotherapy in patients with GH-secreting pituitary adenomas. Clin Endocrinol (Oxf); 2005 Feb;62(2):210-6
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  • [Title] The long-term efficacy of conventional radiotherapy in patients with GH-secreting pituitary adenomas.
  • OBJECTIVE: To assess the long-term efficacy and safety of conventional radiotherapy (RT) in the control of acromegaly according to recent stringent criteria of cure.
  • PATIENTS AND METHODS: Forty-seven patients with active acromegaly were treated with conventional RT between 1982 and 1994.
  • All patients were first operated on and successively irradiated at a dose of 45-50 Gy in 25-28 fractions for persistent (n = 40) or recurrent (n = 7) disease.
  • MEASUREMENTS: Long-term GH/IGF-I secretion and local tumour control were evaluated regularly, and possible side-effects were searched for systematically, especially in terms of secondary endocrine dysfunction.
  • Biochemical cure of acromegaly was defined by glucose-suppressed plasma GH levels below 1 microg/l during an oral glucose tolerance test (OGTT) and normal age-corrected IGF-I values.
  • Suppression of GH during OGTT was seen in 9% of patients at 2 years, 29% at 5 years, 52% at 10 years, and 77% at 15 years.
  • Normalization of GH/IGF-I mainly depended on pre-RT levels.
  • CONCLUSION: Conventional RT is effective in the long-term control of GH-secreting pituitary adenomas, although with a high prevalence of progressive hypopituitarism.
  • [MeSH-major] Acromegaly / radiotherapy. Adenoma / radiotherapy. Adenoma / secretion. Growth Hormone / secretion. Pituitary Neoplasms / radiotherapy. Pituitary Neoplasms / secretion
  • [MeSH-minor] Adult. Female. Follow-Up Studies. Glucose Tolerance Test. Humans. Insulin-Like Growth Factor I / analysis. Male. Middle Aged. Retrospective Studies. Survival Rate. Treatment Outcome

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  • (PMID = 15670198.001).
  • [ISSN] 0300-0664
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 67763-96-6 / Insulin-Like Growth Factor I; 9002-72-6 / Growth Hormone
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89. Castinetti F, Reynaud R, Saveanu A, Quentien MH, Albarel F, Barlier A, Enjalbert A, Brue T: [Clinical and genetic aspects of combined pituitary hormone deficiencies]. Ann Endocrinol (Paris); 2008 Feb;69(1):7-17
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  • [Title] [Clinical and genetic aspects of combined pituitary hormone deficiencies].
  • [Transliterated title] Déficit hypophysaire combiné multiple : aspects cliniques et génétiques.
  • DEFINITION: Congenital hypopituitarism is characterized by multiple pituitary hormone deficiency, including somatotroph, thyrotroph, lactotroph, corticotroph or gonadotroph deficiencies, due to mutations of pituitary transcription factors involved in pituitary ontogenesis.
  • INCIDENCE: Congenital hypopituitarism is rare compared with the high incidence of hypopituitarism induced by pituitary adenomas, transsphenoidal surgery or radiotherapy.
  • CLINICAL SIGNS: Clinical presentation is variable, depending on the type and severity of deficiencies and on the age at diagnosis.
  • DIAGNOSIS: A diagnosis of combined pituitary hormone deficiency (CPHD) must be suspected when evident causes of hypopituitarism (sellar tumor, postsurgical or radioinduced hypopituitarism...) have been ruled out.
  • AETIOLOGY: Congenital hypopituitarism is due to mutations of several genes encoding pituitary transcription factors.
  • Phenotype varies with the factor involved: PROP1 (somatolactotroph, thyrotroph, gonadotroph and sometimes corticotroph deficiencies; pituitary hyper and hypoplasia), POU1F1 (somatolactotroph and thyrotroph deficiencies, pituitary hypoplasia), HESX1 (variable pituitary deficiencies, septo-optic dysplasia), and less frequently LHX3 (somatolactotroph, thyrotroph and gonadotroph deficiencies, limited head and neck rotation) and LHX4 (variable pituitary deficiencies, ectopic neurohypophysis, cerebral abnormalities).
  • MANAGEMENT: An appropriate replacement of hormone deficiencies is required.
  • PROGNOSIS: It is equivalent to patients without pituitary deficiencies if treatment is started immediately when diagnosis is confirmed, and if a specialized follow-up is performed.
  • [MeSH-major] Hypopituitarism / genetics. Pituitary Hormones / deficiency
  • [MeSH-minor] Diagnosis, Differential. Homeodomain Proteins / genetics. Hormone Replacement Therapy. Humans. Transcription Factor Pit-1 / genetics

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  • (PMID = 18291347.001).
  • [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 / HESX1 protein, human; 0 / Homeodomain Proteins; 0 / POU1F1 protein, human; 0 / Pituitary Hormones; 0 / Transcription Factor Pit-1
  • [Number-of-references] 40
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90. Tahir A, Chahal HS, Korbonits M: Molecular genetics of the aip gene in familial pituitary tumorigenesis. Prog Brain Res; 2010;182:229-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular genetics of the aip gene in familial pituitary tumorigenesis.
  • Pituitary adenomas usually occur as sporadic tumors, but familial cases are now increasingly identified.
  • As opposed to multiple endocrine neoplasia type 1 and Carney complex, in familial isolated pituitary adenoma (FIPA) syndrome no other disease is associated with the familial occurrence of pituitary adenomas.
  • It is an autosomal dominant disease with incomplete variable penetrance.
  • Patients with AIP mutations have an overwhelming predominance of somatotroph and lactotroph adenomas, which often present in childhood or young adulthood.
  • AIP, originally identified as a molecular co-chaperone of several nuclear receptors, is thought to act as a tumor suppressor gene; overexpression of wild-type, but not mutant AIP, reduces cell proliferation while knockdown of AIP stimulates it.
  • AIP is shown to bind various proteins, including the aryl hydrocarbon receptor, Hsp90, phosphodiesterases, survivin, RET and the glucocorticoid receptor, but currently it is not clear which interaction has the leading role in pituitary tumorigenesis.
  • This chapter summarizes the available clinical and molecular data regarding the role of AIP in the pituitary gland.
  • [MeSH-major] Family Health. Intracellular Signaling Peptides and Proteins / genetics. Molecular Imaging. Pituitary Neoplasms / etiology. Pituitary Neoplasms / genetics
  • [MeSH-minor] Cell Proliferation. Chromosomes, Human, Pair 11. Humans. Male. Mutation / genetics. Pituitary Gland / metabolism

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  • [Copyright] Copyright 2010 Elsevier B.V. All rights reserved.
  • (PMID = 20541668.001).
  • [ISSN] 1875-7855
  • [Journal-full-title] Progress in brain research
  • [ISO-abbreviation] Prog. Brain Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / aryl hydrocarbon receptor-interacting protein
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91. Daems T, Verhelst J, Michotte A, Abrams P, De Ridder D, Abs R: Modification of hormonal secretion in clinically silent pituitary adenomas. Pituitary; 2009;12(1):80-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Modification of hormonal secretion in clinically silent pituitary adenomas.
  • BACKGROUND: Silent pituitary adenomas are a subtype of adenomas characterized by positive immunoreactivity for one or more hormones classically secreted by normal pituitary cells but without clinical expression, although in some occasions enhanced or changed secretory activity can develop over time.
  • Silent corticotroph adenomas are the classical example of this phenomenon.
  • PATIENTS AND METHODS: A series of about 500 pituitary adenomas seen over a period of 20 years were screened for modification in hormonal secretion.
  • RESULTS: Two cases were retrieved, one silent somatotroph adenoma and one thyrotroph adenoma, both without specific clinical features or biochemical abnormalities, which presented 20 years after initial surgery with evidence of acromegaly and hyperthyroidism, respectively.
  • While the acromegaly was controlled by a combination of somatostatin analogs and growth hormone (GH) receptor antagonist therapy, neurosurgery was necessary to manage the thyrotroph adenoma.
  • Immunohistochemical examination demonstrated an increase in the number of thyroid stimulating hormone (TSH)-immunoreactive cells compared to the first tissue.
  • Apparently, the mechanisms responsible for the secretory modifications are different, being a change in secretory capacity in the silent somatotroph adenoma and a quantitative change in the silent thyrotroph adenoma.
  • CONCLUSIONS: These two cases, one somatotroph and one thyrotroph adenoma, are an illustration that clinically silent pituitary adenomas may in rare circumstances evolve over time and become active, as previously demonstrated in silent corticotroph adenomas.
  • [MeSH-major] Pituitary Neoplasms / metabolism
  • [MeSH-minor] Acromegaly / drug therapy. Acromegaly / metabolism. Acromegaly / surgery. Adult. Human Growth Hormone / secretion. Humans. Immunohistochemistry. Insulin-Like Growth Factor I / secretion. Male. Thyrotropin / secretion

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  • [Cites] Neurosurgery. 2000 Sep;47(3):723-9; discussion 729-30 [10981760.001]
  • [Cites] Pituitary. 2000 Oct;3(2):117-22 [11141695.001]
  • [Cites] Neuropathology. 2001 Dec;21(4):288-93 [11837535.001]
  • [Cites] Am J Pathol. 1989 Feb;134(2):345-53 [2464941.001]
  • [Cites] Mod Pathol. 1988 May;1(3):212-5 [3237702.001]
  • [Cites] Endocr Pathol. 2005 Summer;16(2):107-14 [16199895.001]
  • [Cites] Pituitary. 2007;10 (1):35-45 [17410413.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Apr;90(4):2117-21 [15671111.001]
  • [Cites] Aust N Z J Med. 1987 Apr;17(2):249-51 [3039955.001]
  • [Cites] Neurosurgery. 1994 Jul;35(1):39-44 [7936150.001]
  • [Cites] Clin Endocrinol (Oxf). 1985 Feb;22(2):147-53 [2985300.001]
  • [Cites] Pathol Res Pract. 1991 Dec;187(8):943-9 [1792190.001]
  • [Cites] Acta Neuropathol. 2006 Jan;111(1):1-7 [16328527.001]
  • [Cites] Hum Pathol. 1992 Dec;23(12):1332-9 [1468769.001]
  • [Cites] Pituitary. 1999 May;1(3-4):233-41 [11081203.001]
  • [Cites] J Clin Endocrinol Metab. 1993 Feb;76(2):352-6 [8432778.001]
  • [Cites] Endocr Pathol. 2006 Summer;17(2):191-9 [17159252.001]
  • [Cites] Hum Pathol. 2004 Sep;35(9):1137-47 [15343517.001]
  • [Cites] Clin Endocrinol (Oxf). 2003 Jan;58(1):59-64 [12519413.001]
  • [Cites] Neurol India. 2000 Dec;48(4):374-7 [11146605.001]
  • [Cites] Br J Neurosurg. 2005 Feb;19(1):38-42 [16147581.001]
  • [Cites] Neurosurgery. 2003 Nov;53(5):1076-84; discussion 1084-5 [14580274.001]
  • [Cites] J Neurosurg. 1987 Jun;66(6):806-11 [3572509.001]
  • [Cites] Neurosurgery. 2005 May;56(5):E1154; discussion E1154 [15854264.001]
  • [Cites] Acta Neuropathol. 2001 Nov;102(5):435-40 [11699555.001]
  • [Cites] Acta Endocrinol (Copenh). 1988 Aug;118(4):533-7 [2840793.001]
  • [Cites] J Neurosurg. 1987 Feb;66(2):244-50 [3543255.001]
  • [Cites] Eur J Endocrinol. 2003 Jul;149(1):17-22 [12824861.001]
  • [Cites] J Clin Neurosci. 2005 Apr;12(3):318-20 [15851094.001]
  • (PMID = 18350381.001).
  • [ISSN] 1573-7403
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I; 9002-71-5 / Thyrotropin
  • [Number-of-references] 30
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92. Fougner SL, Lekva T, Borota OC, Hald JK, Bollerslev J, Berg JP: The expression of E-cadherin in somatotroph pituitary adenomas is related to tumor size, invasiveness, and somatostatin analog response. J Clin Endocrinol Metab; 2010 May;95(5):2334-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The expression of E-cadherin in somatotroph pituitary adenomas is related to tumor size, invasiveness, and somatostatin analog response.
  • CONTEXT: Appropriate cell-to-cell adhesion is fundamental for the epithelial phenotype of pituitary cells.
  • In somatotroph adenomas, a variable and reduced expression of E-cadherin has been demonstrated.
  • In addition, nuclear translocation of E-cadherin was found to correlate with pituitary tumor invasion.
  • OBJECTIVE: The objective was to examine the protein expression of E-cadherin in somatotroph pituitary adenomas in relation to adenoma size, invasiveness, and somatostatin analog (SMS) efficacy.
  • Adenoma E-cadherin protein expression was analyzed by Western blot (61 patients) and immunohistochemistry (IHC) (80 patients) with antibodies directed against both extracellular and intracellular domains (IHC).
  • RESULTS: Membranous E-cadherin was lost in several adenomas.
  • The E-cadherin level correlated positively to tumor reduction after SMS treatment, and adenomas with nuclear E-cadherin staining had lower IGF-I reduction and tumor shrinkage.
  • Preoperatively treated adenomas had reduced E-cadherin protein levels, but the IHC expression was unaltered.
  • CONCLUSION: Reduced E-cadherin expression may correlate to a dedifferentiated phenotype in the somatotroph pituitary adenomas.
  • [MeSH-major] Cadherins / genetics. Peptide Fragments / therapeutic use. Pituitary Neoplasms / genetics. Somatostatin / therapeutic use
  • [MeSH-minor] Acromegaly / complications. Acromegaly / surgery. Adult. Female. Growth Hormone / blood. Humans. Immunohistochemistry. Insulin-Like Growth Factor I / metabolism. Magnetic Resonance Imaging. Male. Middle Aged. Neoplasm Invasiveness