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1. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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2. Hubina E, Nanzer AM, Hanson MR, Ciccarelli E, Losa M, Gaia D, Papotti M, Terreni MR, Khalaf S, Jordan S, Czirják S, Hanzély Z, Nagy GM, Góth MI, Grossman AB, Korbonits M: Somatostatin analogues stimulate p27 expression and inhibit the MAP kinase pathway in pituitary tumours. Eur J Endocrinol; 2006 Aug;155(2):371-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Somatostatin analogues stimulate p27 expression and inhibit the MAP kinase pathway in pituitary tumours.
  • OBJECTIVES: Somatostatin (SST) analogues play an important role in the medical management of somatotroph pituitary adenomas and new agonists have the potential to be effective in a wider group of pituitary and other tumours.
  • The anti-proliferative effect of SST occurs through multiple mechanisms, one of which is cell-cycle arrest, where p27, a cyclin-dependent kinase inhibitor, is an important regulator.
  • METHODS: Human pituitary adenoma cells and rat pituitary cell line (GH3) were cultured and treated in vitro with octreotide and the broad-spectrum SST agonist SOM230 (pasireotide).
  • RESULTS: We detected upregulation of p27 protein levels with SST analogue treatment in vitro in human pituitary adenoma samples. pERK1/2 was inhibited by SST analogues in both the human samples and GH3 cells.
  • CONCLUSIONS: This study demonstrates that SST-mediated growth inhibition is associated with the downregulation of pERK and upregulation of p27.

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  • (PMID = 16868153.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 10028-17-8 / Tritium; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 51110-01-1 / Somatostatin; 98H1T17066 / pasireotide; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; RWM8CCW8GP / Octreotide; VC2W18DGKR / Thymidine
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3. 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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4. 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


5. 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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6. 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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7. Moran C, Behan LA, Draman MS, King T, Smith D, Sreenan S, Thompson C, Agha A: Spontaneous recovery from severe cardiac failure after acute hypotensive infarction of a somatotroph adenoma. Clin Endocrinol (Oxf); 2008 Feb;68(2):321-2
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Spontaneous recovery from severe cardiac failure after acute hypotensive infarction of a somatotroph adenoma.
  • [MeSH-major] Growth Hormone-Secreting Pituitary Adenoma / pathology. Heart Failure / pathology. Infarction / pathology

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  • (PMID = 17760886.001).
  • [ISSN] 1365-2265
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
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8. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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9. 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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10. Plöckinger U, Albrecht S, Mawrin C, Saeger W, Buchfelder M, Petersenn S, Schulz S: Selective loss of somatostatin receptor 2 in octreotide-resistant growth hormone-secreting adenomas. J Clin Endocrinol Metab; 2008 Apr;93(4):1203-10
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Selective loss of somatostatin receptor 2 in octreotide-resistant growth hormone-secreting adenomas.
  • Although sst2A and sst5 mRNAs are consistently expressed in GH-secreting adenomas, octreotide controls GH secretion only in 65% of acromegalic patients.
  • Hence, we investigated the immunocytochemical expression of sst in a large group of somatotroph tumors.
  • In group B octreotide reduced GH secretion by more than 50% in 14 patients (70%) (GH responders).
  • Six patients with less than 50% GH suppression were considered GH nonresponders.
  • We used a panel of extensively characterized antibodies to determine the immunocytochemical sst status in somatotroph adenomas and compared their expression between the groups.
  • A similar pattern was found in the GH responders of group B.
  • In contrast, none of the GH nonresponders exhibited detectable sst2A (sst2A: GH responders vs. GH nonresponders, P < 0.0001), whereas sst5 was found in 70%.
  • CONCLUSIONS: Our findings suggest that octreotide resistance in GH-secreting adenomas occurs due to a selective loss of sst2A.
  • [MeSH-major] Adenoma / chemistry. Antineoplastic Agents, Hormonal / therapeutic use. Growth Hormone-Secreting Pituitary Adenoma / chemistry. Octreotide / therapeutic use. Receptors, Somatostatin / analysis
  • [MeSH-minor] Adult. Aged. Amino Acid Sequence. Female. Human Growth Hormone / blood. Humans. Immunohistochemistry. Male. Middle Aged. Molecular Sequence Data

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  • (PMID = 18198230.001).
  • [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 / Antineoplastic Agents, Hormonal; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 12629-01-5 / Human Growth Hormone; RWM8CCW8GP / Octreotide
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11. 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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  • (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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12. 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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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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  • [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. Tunici P, Yu JS: Pituitary adenoma stem cells. Methods Mol Biol; 2009;568:195-201
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  • [Title] Pituitary adenoma stem cells.
  • The identification of a subpopulation of brain tumor cells with potent tumorigenic capacity strengthens the cancer stem cell hypothesis of the origin of the tumors that has recently attracted the attention of many researchers.
  • These cells express stem cell markers, and when differentiated they express glial and neuronal markers.
  • More recently we have isolated tumor stem-like cells also from benign tumors like pituitary adenomas.
  • Cells derived from pituitary adenomas are able to grow as floating aggregates resembling the neurospheres (typical of normal stem cells) in a medium supplemented by growth factors (EGF and bFGF).
  • The immunocytochemical analysis revealed that pituitary tumor stem-like cells are positives for nestin and, when grown for ten days in differentiation medium they express GFAP, BIII tubulin, and S-100.
  • In vitro tumor stem-like cells derived from a patient with a somatotroph adenoma showed high production of growth hormone and prolactin, while cells derived from the same patient but grown in presence of fetal bovine serum showed no production of hormones.
  • [MeSH-major] Cell Culture Techniques / methods. Neoplastic Stem Cells / pathology. Pituitary Neoplasms / pathology
  • [MeSH-minor] Human Growth Hormone / metabolism. Humans. Immunohistochemistry. Prolactin / metabolism

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  • (PMID = 19582428.001).
  • [ISSN] 1064-3745
  • [Journal-full-title] Methods in molecular biology (Clifton, N.J.)
  • [ISO-abbreviation] Methods Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 12629-01-5 / Human Growth Hormone; 9002-62-4 / Prolactin
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15. 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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16. Beuschlein F, Hancke K, Petrick M, Göbel H, Honegger J, Reincke M: Growth hormone receptor mRNA expression in non-functioning and somatotroph pituitary adenomas: implications for growth hormone substitution therapy? Exp Clin Endocrinol Diabetes; 2005 Apr;113(4):214-8
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  • [Title] Growth hormone receptor mRNA expression in non-functioning and somatotroph pituitary adenomas: implications for growth hormone substitution therapy?
  • The use of growth hormone (GH) in patients with GH deficiency induced by pituitary adenoma is widely accepted, but the safety of this mitogenic hormone, particularly in patients with residual tumor after neurosurgery, continues to be a concern.
  • Since the mitogenic potency of GH is dependent upon the presence of the GH receptor (GH-R) and the subsequent IGF-1/IGF receptor (IGF-1-R) system we investigated the expression of the members of the growth hormone cascade in endocrine inactive and GH-producing pituitary adenomas.
  • Tissue specimens of 18 clinically non-functioning pituitary adenomas and 6 GH-producing adenomas were collected following transsphenoidal surgery while normal cadaver pituitary glands served as controls.
  • After RNA extraction, semi-quantitative RT-PCR amplification with specific primers for GH, GH-R, IGF-1 and IGF-1-R was performed.
  • Applying this sensitive RT-PCR based approach, GH-R expression was demonstrated in all normal pituitaries, most inactive adenomas (94%), and the majority of GH-producing adenomas (66%).
  • Both IGF-1 and IGF-1-R mRNA was detectable in the majority of inactive (72% and 77%, respectively) and somatotrophic adenomas (83% and 83%).
  • While IGF-1-R mRNA was expressed in all normal pituitary specimen studied, IGF-1 was detectable in only 55% of them.
  • In summary, expression of members of the GH-IGF-1 cascade could be demonstrated in a substantial subset of patients with non-functioning and GH-producing pituitary adenomas.
  • These factors might serve as a substrate for the transduction of mitogenic effects of GH on remnant pituitary tumors during GH replacement therapy.
  • Therefore, GH therapy should be carefully considered and patients on GH therapy kept under close observation.
  • [MeSH-major] Adenoma / genetics. Growth Hormone / analogs & derivatives. Growth Hormone / therapeutic use. Pituitary Neoplasms / genetics. RNA, Messenger / genetics. Receptors, Somatotropin / genetics
  • [MeSH-minor] Acromegaly / genetics. DNA Primers. Gene Expression Regulation, Neoplastic. Humans. Insulin-Like Growth Factor I / genetics. Receptor, IGF Type 1 / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 15891957.001).
  • [ISSN] 0947-7349
  • [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 / DNA Primers; 0 / RNA, Messenger; 0 / Receptors, Somatotropin; 67763-96-6 / Insulin-Like Growth Factor I; 9002-72-6 / Growth Hormone; EC 2.7.10.1 / Receptor, IGF Type 1
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17. 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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18. Rotondo F, Scheithauer BW, Kovacs K, Bell DC: Rab3B immunoexpression in human pituitary adenomas. Appl Immunohistochem Mol Morphol; 2009 May;17(3):185-8
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  • [Title] Rab3B immunoexpression in human pituitary adenomas.
  • To shed light on its presence in the normal human pituitary and in adenomas, a detailed immunohistochemical study of 130 surgically removed human pituitary adenomas was undertaken, including 23 somatotroph, 32 lactotroph, 19 functional corticotroph, 10 silent subtype 1 and 8 silent subtype 2 corticotroph adenomas, 12 gonadotroph hormone producing, 10 thyrotroph, 7 silent subtype 3 adenomas, and 9 null cell adenomas, 5 of the latter being of oncocytic type.
  • Among the 32 prolactin lactotroph adenomas, 10 had been treated preoperatively with bromocriptine, a dopamine agonist.
  • Among the 23 somatotroph adenomas, 10 were pretreated with octreotide, a long acting somatostatin analog.
  • The results showed Rab3B immunopositivity to be strongest in corticotroph adenomas followed by thyrotroph, lactotroph, gonadotroph, null cell, and somatotroph adenomas.
  • No difference was noted between endocrinologically active and silent corticotroph adenomas.
  • Our results add new information to the view that Rab3B is involved in the regulation of pituitary hormone secretion.

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  • (PMID = 19384079.001).
  • [ISSN] 1533-4058
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 3A64E3G5ZO / Bromocriptine; EC 3.6.1.- / RAB3B protein, human; EC 3.6.5.2 / rab3 GTP-Binding Proteins; RWM8CCW8GP / Octreotide
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19. 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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  • [ISSN] 0172-8113
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
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20. 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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  • (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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21. 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.


22. 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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  • [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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23. 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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  • (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
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24. 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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25. 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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26. 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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27. 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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28. 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]
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  • (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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29. 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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  • [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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30. 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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31. 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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  • (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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32. 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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33. 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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  • (PMID = 15765245.001).
  • [ISSN] 0344-5607
  • [Journal-full-title] Neurosurgical review
  • [ISO-abbreviation] Neurosurg Rev
  • [Language] eng
  • [Publication-type] Journal Article
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34. 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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  • [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


35. Schaaf C, Shan B, Buchfelder M, Losa M, Kreutzer J, Rachinger W, Stalla GK, Schilling T, Arzt E, Perone MJ, Renner U: Curcumin acts as anti-tumorigenic and hormone-suppressive agent in murine and human pituitary tumour cells in vitro and in vivo. Endocr Relat Cancer; 2009 Dec;16(4):1339-50
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  • [Title] Curcumin acts as anti-tumorigenic and hormone-suppressive agent in murine and human pituitary tumour cells in vitro and in vivo.
  • Therefore, we have studied its effect in pituitary tumour cell lines and adenomas.
  • Proliferation of lactosomatotroph GH3 and somatotroph MtT/S rat pituitary cells as well as of corticotroph AtT20 mouse pituitary cells was inhibited by curcumin in monolayer cell culture and in colony formation assay in soft agar.
  • Fluorescence-activated cell sorting (FACS) analysis demonstrated curcumin-induced cell cycle arrest at G2/M.
  • Analysis of cell cycle proteins by immunoblotting showed reduction in cyclin D(1), cyclin-dependent kinase 4 and no change in p27(kip).
  • Growth of GH3 tumours in athymic nude mice was suppressed by curcumin in vivo.
  • In endocrine pituitary tumour cell lines, GH, ACTH and prolactin production were inhibited by curcumin.
  • Studies in 25 human pituitary adenoma cell cultures have confirmed the anti-tumorigenic and hormone-suppressive effects of curcumin.
  • Altogether, the results described in this report suggest this natural compound as a good candidate for therapeutic use on pituitary tumours.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Curcumin / pharmacology. Pituitary Hormones / metabolism. Pituitary Neoplasms / drug therapy. Pituitary Neoplasms / pathology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Blotting, Western. Caspase 3 / metabolism. Cell Cycle / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Cyclin D1 / metabolism. Cyclin-Dependent Kinase 4 / metabolism. Flow Cytometry. Humans. Male. Mice. Mice, Nude. Rats

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  • (PMID = 19726538.001).
  • [ISSN] 1479-6821
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Pituitary Hormones; 136601-57-5 / Cyclin D1; EC 2.7.11.22 / Cyclin-Dependent Kinase 4; EC 3.4.22.- / Caspase 3; IT942ZTH98 / Curcumin
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36. Fracassi F, Gandini G, Diana A, Preziosi R, Ingh TS, Famigli-Bergamini P, Kooistra HS: Acromegaly due to a somatroph adenoma in a dog. Domest Anim Endocrinol; 2007 Jan;32(1):43-54
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acromegaly due to a somatroph adenoma in a dog.
  • The basal serum growth hormone (GH) concentration was markedly elevated (23microg/l) and did not decrease during a glucose tolerance test or after somatostatin administration.
  • The serum insulin-like growth factor-1 concentration was also markedly elevated (1254microg/l).
  • CT scanning of the skull showed an enlarged pituitary gland with normal enhancement pattern.
  • The pituitary gland contained an acidophilic adenoma that immunostained positively for GH (and negatively for ACTH and alpha-MSH).
  • In conclusion, this Dalmatian dog with acromegaly and insulin resistance represents the first case of GH hypersecretion proven to be due to a somatotroph adenoma.
  • [MeSH-major] Acromegaly / veterinary. Adenoma / veterinary. Dog Diseases / pathology. Pituitary Neoplasms / veterinary
  • [MeSH-minor] Animals. Dogs. Fatal Outcome. Growth Hormone / blood. Insulin Resistance. Male. Spinal Osteophytosis / complications. Spinal Osteophytosis / pathology. Spinal Osteophytosis / veterinary

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  • (PMID = 16472961.001).
  • [ISSN] 0739-7240
  • [Journal-full-title] Domestic animal endocrinology
  • [ISO-abbreviation] Domest. Anim. Endocrinol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 9002-72-6 / Growth Hormone
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37. Lania AG, Ferrero S, Pivonello R, Mantovani G, Peverelli E, Di Sarno A, Beck-Peccoz P, Spada A, Colao A: Evolution of an aggressive prolactinoma into a growth hormone secreting pituitary tumor coincident with GNAS gene mutation. J Clin Endocrinol Metab; 2010 Jan;95(1):13-7
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  • [Title] Evolution of an aggressive prolactinoma into a growth hormone secreting pituitary tumor coincident with GNAS gene mutation.
  • CONTEXT: Mixed PRL- and GH-secreting pituitary adenomas are relatively common because somatotrophs and lactotrophs share the common somato-mammotroph progenitor lineage.
  • Conversely, the occurrence of a prolactinoma evolving into clinically and biochemically active acromegaly is a rare phenomenon.
  • OBJECTIVE AND RESULTS: We report a patient with a prolactinoma who after 15 yr of disease control by bromocriptine became resistant to dopaminergic drugs and due to the rapid tumor growth was submitted to four neurosurgeries and two stereotactic radiotherapies in the subsequent 5 yr.
  • Unexpectedly, in the last 1.5 yr, after the fourth neurosurgery and second gamma-knife, she complained of signs and symptoms of acromegaly that was biochemically confirmed.
  • Although samples from the initial surgery were positive for prolactin and negative for GH, about 10% of GH-positive cells were detected in tissue from the last surgery, consistent with the observed clinical shift to acromegaly.
  • CONCLUSIONS: These observations suggest that 1)treatment of prolactinomas resistant to dopaminergic drugs is still a challenge, and 2) the appearance of gsp oncogene in a prolactinoma evolving into acromegaly might be the underlying mechanism of this rare transition, further confirming that this mutational change is associated with somatotroph growth and transformation.
  • [MeSH-major] GTP-Binding Protein alpha Subunits, Gs / genetics. Growth Hormone-Secreting Pituitary Adenoma / genetics. Growth Hormone-Secreting Pituitary Adenoma / pathology. Pituitary Neoplasms / pathology. Prolactinoma / pathology
  • [MeSH-minor] DNA Mutational Analysis. Disease Progression. Female. Follow-Up Studies. Humans. Middle Aged. Mutation / physiology. Neoplasm Invasiveness

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  • (PMID = 19890024.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.6.1.- / GNAS protein, human; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs
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38. 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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39. Remick AK, Wood CE, Cann JA, Gee MK, Feiste EA, Kock ND, Cline JM: Histologic and immunohistochemical characterization of spontaneous pituitary adenomas in fourteen cynomolgus macaques (Macaca fascicularis). Vet Pathol; 2006 Jul;43(4):484-93
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  • [Title] Histologic and immunohistochemical characterization of spontaneous pituitary adenomas in fourteen cynomolgus macaques (Macaca fascicularis).
  • Pituitary adenomas were identified in 14 of 491 (2.9%) cynomolgus macaques evaluated from 1994 to 2004.
  • Seven of the pituitary adenomas caused gross enlargement of the pituitary gland that was visible on postmortem examination, whereas the remaining 7 were multifocal microadenomas identified on histologic examination.
  • A total of 35 adenomas were identified in the 14 macaques, 6 of which were being treated for diabetes mellitus.
  • Mean (+/- SD) pituitary weight was 0.31 +/- 0.42 g, compared with 0.07 +/- 0.02 g for 430 historical control animals (P < 0.0001).
  • Immunohistochemical staining for follicle-stimulating hormone, luteinizing hormone, prolactin, human growth hormone, thyroid-stimulating hormone, and adrenocorticotropic hormone was applied to pituitary tissue from all cases.
  • Immunostaining revealed 22 of 35 (62.9%) lactotroph adenomas, 5 of 35 (14.3%) plurihormonal cell adenomas, 3 of 35 (8.6%) corticotroph adenomas, 2 of 35 (5.7%) null cell adenomas, 1 of 35 (2.9%) somatotroph adenomas, 1 of 35 (2.9%) mixed corticotroph-somatotroph adenomas, 1 of 35 (2.9%) mixed lactotroph-corticotroph adenomas, 0 of 35 gonadotroph adenomas, and 0 of 35 thyrotroph adenomas.
  • This study represents the first extensive retrospective case series performed to evaluate the histologic and immunohistochemical characteristics of pituitary adenomas in cynomolgus macaques.
  • Our findings indicated that macaque pituitary adenomas frequently had mixed histologic appearance and hormone expression, and that, similar to human pituitary adenomas, prolactin-secreting neoplasms were the most prevalent type.
  • [MeSH-major] Macaca fascicularis. Monkey Diseases / pathology. Pituitary Neoplasms / veterinary. Prolactinoma / veterinary
  • [MeSH-minor] Adrenocorticotropic Hormone / biosynthesis. Animals. Female. Follicle Stimulating Hormone / biosynthesis. Human Growth Hormone / biosynthesis. Immunohistochemistry / veterinary. Luteinizing Hormone / biosynthesis. Male. Prevalence. Prolactin / biosynthesis. Retrospective Studies. Thyrotropin / biosynthesis

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  • (PMID = 16846990.001).
  • [ISSN] 0300-9858
  • [Journal-full-title] Veterinary pathology
  • [ISO-abbreviation] Vet. Pathol.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / T32 RR07009
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 12629-01-5 / Human Growth Hormone; 9002-60-2 / Adrenocorticotropic Hormone; 9002-62-4 / Prolactin; 9002-67-9 / Luteinizing Hormone; 9002-68-0 / Follicle Stimulating Hormone; 9002-71-5 / Thyrotropin
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40. 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


41. Zatelli MC, Ambrosio MR, Bondanelli M, degli Uberti EC: In vitro testing of new somatostatin analogs on pituitary tumor cells. Mol Cell Endocrinol; 2008 May 14;286(1-2):187-91
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  • [Title] In vitro testing of new somatostatin analogs on pituitary tumor cells.
  • Somatostatin has been discovered as a somatotroph release inhibitory factor (SRIF), and, indeed, it has been demonstrated that SRIF and its analogs can inhibit pituitary tumor hormone secretion and control neoplastic bulk.
  • Several in vitro studies have contributed to the current knowledge of the mechanisms by which SRIF and its analogs may influence pituitary adenomas, opening the way to new possible therapeutic strategies.
  • This review focuses on the results obtained by testing several SRIF analogs in vitro on pituitary adenomas, concerning both secretory activity and cell viability.
  • These studies provide the basis for further investigations, both at basic and clinical level, of the application of SRIF analogs in the pituitary field.
  • [MeSH-major] Adenoma / drug therapy. Antineoplastic Agents, Hormonal / therapeutic use. Pituitary Neoplasms / drug therapy. Somatostatin / analogs & derivatives. Somatostatin / therapeutic use
  • [MeSH-minor] Cell Survival / drug effects. Drug Resistance, Neoplasm. Humans. Tumor Cells, Cultured

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  • (PMID = 18243520.001).
  • [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; 51110-01-1 / Somatostatin
  • [Number-of-references] 42
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42. 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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43. 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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  • [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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44. 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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  • (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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45. 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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  • [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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46. 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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47. 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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  • [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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48. Wasko R, Jaskula M, Kotwicka M, Andrusiewicz M, Jankowska A, Liebert W, Sowinski J: The expression of ghrelin in somatotroph and other types of pituitary adenomas. Neuro Endocrinol Lett; 2008 Dec;29(6):929-38
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  • [Title] The expression of ghrelin in somatotroph and other types of pituitary adenomas.
  • OBJECTIVES: It has been suggested that ghrelin synthesized locally in pituitary regulates the function and growth of pituitary cells in autocrine/paracrine way and might be an important factor of pituitary tumorogenesis.
  • The expression of ghrelin receptor in neoplastic cells of pituitary adenomas has also been demonstrated.
  • In vitro studies confirmed that ghrelin stimulates the proliferation of somatotroph cells in GH3 cell line.
  • This study showed the presence of ghrelin mRNA and its protein in different types of pituitary adenomas.
  • DESIGN: The samples of 37 pituitary adenomas were obtained during standard neurosurgical tumor removal.
  • The study tissues included 20 somatotroph tumors (15 patients treated and 5 patients untreated with octreotide LAR before the surgery), 12 nonfunctioning adenomas, 4 prolactinomas and 1 ACTH-secreting tumor.
  • Expression of ghrelin mRNA was studied in 28 pituitary adenomas by RT-PCR.
  • RESULTS: The presence of ghrelin gene transcripts was demonstrated in 10 out of 15 examined somatotroph tumors (obtained from patients treated with octreotide LAR before the surgery) and also in 2 out of 4 samples of prolactinomas, 7 out of 8 of nonfunctioning tumors and in 2 samples of normal pituitary.
  • Immunohistochemical analyses revealed the presence of the protein in all 5 examined somatotroph tumors obtained from patients not treated prior to the surgery and in 10 out of 15 tumors obtained from patients treated with octreotide LAR.
  • The peptide was detected also in 10 out of 12 examined nonfunctioning tumors and in 2 examined PRL-secreting tumors.
  • CONCLUSIONS: The study demonstrated that ghrelin gene is expressed in somatotroph adenomas, both treated and untreated with octreotide LAR before the surgery, and also in other types of pituitary adenomas (prolactinomas and nonfunctioning adenomas).
  • [MeSH-major] Adenoma / metabolism. Ghrelin / metabolism. Pituitary Neoplasms / metabolism. Somatotrophs / metabolism

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  • (PMID = 19112387.001).
  • [ISSN] 0172-780X
  • [Journal-full-title] Neuro endocrinology letters
  • [ISO-abbreviation] Neuro Endocrinol. Lett.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Sweden
  • [Chemical-registry-number] 0 / Ghrelin; 0 / RNA, Messenger
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49. 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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50. 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


51. Kontogeorgos G, Mourouti G, Kyrodimou E, Liapi-Avgeri G, Parasi E: Ganglion cell containing pituitary adenomas: signs of neuronal differentiation in adenoma cells. Acta Neuropathol; 2006 Jul;112(1):21-8
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  • [Title] Ganglion cell containing pituitary adenomas: signs of neuronal differentiation in adenoma cells.
  • Ganglion cell containing pituitary adenomas are rare.
  • Recently accumulated information suggests a common origin for their neuronal and pituitary constituents.
  • The objective of this study was to report the clinical and morphologic findings of pituitary gangliocytomas and study their immunoprofile using neuronal markers.
  • Seven cases of pituitary gangliocytomas retrieved from 1,322 sellar lesions were studied.
  • All tumors were removed from patients with mild acromegaly.
  • Histologically they were biphasic composed of pituitary adenoma and clusters of ganglion cells embedded in a variably dense neuropil substrate.
  • All adenomas belonged to the category of sparsely granulated somatotroph adenoma and were positive for growth hormone, whereas in five tumors, a few adenoma cells were also positive for prolactin.
  • Interestingly, all tumors contained varying numbers of adenoma cells with NFP-positive, dot-like areas of cytoplasmic reactivity, mostly tiny paranuclear, a finding not previously reported in human pituitary gangliocytomas.
  • The presence of NFP in pituitary adenomas indicates neuronal differentiation in adenoma cells, suggesting a common origin for neuronal and pituitary adenoma cell elements in gangliocytomas.
  • [MeSH-major] Adenoma / classification. Adenoma / pathology. Ganglioneuroma / classification. Ganglioneuroma / pathology. Pituitary Neoplasms / classification. Pituitary Neoplasms / pathology
  • [MeSH-minor] Acromegaly / etiology. Female. Humans. Immunohistochemistry. Male. Middle Aged. Neurofilament Proteins / metabolism. Sella Turcica / pathology

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  • (PMID = 16699777.001).
  • [ISSN] 0001-6322
  • [Journal-full-title] Acta neuropathologica
  • [ISO-abbreviation] Acta Neuropathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Neurofilament Proteins
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52. Picard C, Silvy M, Gerard C, Buffat C, Lavaque E, Figarella-Branger D, Dufour H, Gabert J, Beckers A, Brue T, Enjalbert A, Barlier A: Gs alpha overexpression and loss of Gs alpha imprinting in human somatotroph adenomas: association with tumor size and response to pharmacologic treatment. Int J Cancer; 2007 Sep 15;121(6):1245-52
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  • [Title] Gs alpha overexpression and loss of Gs alpha imprinting in human somatotroph adenomas: association with tumor size and response to pharmacologic treatment.
  • Gs alpha is paternally silenced in normal pituitary, but Gs alpha imprinting relaxation is found in some tumoral tissue.
  • In addition, Gs alpha mRNA levels are high in some somatotroph adenomas not bearing the active Gs alpha mutant, the gsp oncogene.
  • We compared the expression and imprinting of 4 transcripts of GNAS locus (NESP55, XL alpha s, exon 1A, Gs alpha) of 60 somatotroph adenomas with those of 23 lactotroph adenomas.
  • [MeSH-major] Adenoma / genetics. Drug Resistance, Neoplasm / genetics. GTP-Binding Protein alpha Subunits, Gs / genetics. Genomic Imprinting. Growth Hormone-Secreting Pituitary Adenoma / genetics

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17514647.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / RNA, Messenger; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs; RWM8CCW8GP / Octreotide
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53. 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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54. 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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  • (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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55. 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.
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  • (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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56. 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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57. 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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58. 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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  • (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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59. 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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60. 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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61. 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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62. 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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63. 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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64. 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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65. 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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  • [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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  • (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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66. 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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67. Damjanovic SS, Neskovic AN, Petakov MS, Popovic V, Macut D, Vukojevic P, Joksimovic MM: Clinical indicators of biochemical remission in acromegaly: does incomplete disease control always mean therapeutic failure? Clin Endocrinol (Oxf); 2005 Apr;62(4):410-7
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  • [Title] Clinical indicators of biochemical remission in acromegaly: does incomplete disease control always mean therapeutic failure?
  • OBJECTIVE: Correction of GH and IGF-I levels are associated with improvements in insulin secretion, cardiac performance and body composition in patients with acromegaly, but whether these parallel post-treatment levels of GH-IGF-I axis activity is undefined.
  • We investigate whether various biochemical outcomes after transsphenoidal pituitary surgery (TSS) in these patients are associated with clinically relevant differences in cardiac performance, insulin resistance and body composition.
  • DESIGN: Cross-sectional study of consecutive patients with acromegaly admitted to the hospital between 2001 and 2002.
  • PATIENTS AND METHODS: Forty-one patients after TSS for somatotroph pituitary adenoma and 23 patients with naive acromegaly serving as positive controls were enrolled in the study.
  • Mean daily GH levels (mGH), IGF-I, leptin and lipid levels, glucose, insulin and GH concentrations during oral glucose tolerance test (oGTT) were measured in all study participants.
  • RESULTS: We found no difference in cardiac indices, insulin resistance, body composition and leptin levels between patients with complete biochemical remission and those with inadequately controlled disease (P > 0.05 for all) after TSS.
  • A similar decrease in LVM(i) was observed in controlled (108.4 +/- 30.0 g/m(2); P = 0.015) and inadequately controlled disease (108.8 +/- 30.7 g/m(2); P = 0.03) in comparison with naive disease (160.3 +/- 80.6 g/m(2)).
  • In controlled and inadequately controlled disease, R(HOMA) index was lower (2.2 +/- 1.4; P = 0.001 and 3.1 +/- 2.0; P = 0.05 vs. 5.1 +/- 3.1) while leptin concentration was higher (14.9 +/- 8.7 microg/l, P = 0.004 and 12.8 +/- 7.8 microg/l, P = 0.05 vs. 7.4 +/- 3.8 microg/l) than in naive disease.
  • Similar results were obtained if the definition of cure included both normal IGF-I levels and the ability to achieve GH nadir < 1 microg/l during oGTT.
  • CONCLUSION: This study shows that cardiac indices, insulin resistance and body composition were not different between patients with complete biochemical remission and those with discordant GH and IGF-I levels.
  • It appears that even incomplete disease control after TSS can result in improvement of these clinical markers.
  • [MeSH-major] Acromegaly / surgery
  • [MeSH-minor] Absorptiometry, Photon. Adenoma / blood. Adenoma / complications. Adenoma / surgery. Adult. Aged. Area Under Curve. Biomarkers / blood. Blood Glucose / analysis. Body Composition. Echocardiography. Female. Growth Hormone / blood. Humans. Insulin / blood. Insulin-Like Growth Factor I / analysis. Leptin / blood. Lipids / blood. Logistic Models. Male. Middle Aged. Pituitary Neoplasms / blood. Pituitary Neoplasms / complications. Pituitary Neoplasms / surgery. Remission Induction. Treatment Failure

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  • (PMID = 15807870.001).
  • [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] 0 / Biomarkers; 0 / Blood Glucose; 0 / Insulin; 0 / Leptin; 0 / Lipids; 67763-96-6 / Insulin-Like Growth Factor I; 9002-72-6 / Growth Hormone
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68. 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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  • 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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69. 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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  • [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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70. 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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  • [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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71. 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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72. Iván G, Szigeti-Csúcs N, Oláh M, Nagy GM, Góth MI: Treatment of pituitary tumors: dopamine agonists. Endocrine; 2005 Oct;28(1):101-10
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  • [Title] Treatment of pituitary tumors: dopamine agonists.
  • In the hypothalamopituitary system its function is a dominant and tonic inhibitory regulation of pituitary hormone secretion including prolactin- and proopiomelanocortin-derived hormones.
  • It is well known that dopamine agonists, such as bromocriptine, pergolide, quinagolide, cabergoline, and lisuride, can inhibit PRL secretion by binding to the D(2) dopamine receptors located on normal as well as tumorous pituitary cells.
  • Furthermore, dopamine agonists can also be used in other pituitary tumors.
  • Therefore, in addition to prolactinomas, targets of dopamine agonist therapy are somatotroph tumors, nonfunctioning pituitary tumors, corticotroph pituitary tumors, Nelson's syndrome, gonadotropinomas, and thyrotropin-secreting pituitary tumors.
  • It is also an option for the treatment of pituitary disease during pregnancy.
  • Differences between the effectiveness and the resistance of different dopaminergic agents as well as the future perspectives of them in the therapy of pituitary tumors are discussed.
  • [MeSH-major] Adenoma / drug therapy. Dopamine Agonists / pharmacology. Pituitary Neoplasms / drug therapy

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  • (PMID = 16311416.001).
  • [ISSN] 1355-008X
  • [Journal-full-title] Endocrine
  • [ISO-abbreviation] Endocrine
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dopamine Agonists; 0 / Ergolines; 0 / Receptors, Dopamine; 3A64E3G5ZO / Bromocriptine; LL60K9J05T / cabergoline; VTD58H1Z2X / Dopamine
  • [Number-of-references] 71
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73. 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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  • [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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  • (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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74. Bhayana S, Booth GL, Asa SL, Kovacs K, Ezzat S: The implication of somatotroph adenoma phenotype to somatostatin analog responsiveness in acromegaly. J Clin Endocrinol Metab; 2005 Nov;90(11):6290-5
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  • [Title] The implication of somatotroph adenoma phenotype to somatostatin analog responsiveness in acromegaly.
  • CONTEXT: Persistently elevated GH and IGF-I levels are associated with increased mortality.
  • OBJECTIVE: The objective of this study was to examine the significance of somatotroph adenoma type on response to SSA.
  • PATIENTS: Forty patients with acromegaly were studied.
  • MAIN OUTCOME MEASURES: Normalization of IGF-I levels and GH responses were the main outcome measures.
  • RESULTS: Univariate analysis revealed that responders were more likely to have densely granulated somatotroph adenomas (80% vs. 43.8%; P = 0.024), to be older (51.3 vs. 38.2 yr; P < 0.003), to have smaller tumors (stage < or =3; 78.6% vs. 35.7%; P = 0.022), to have lower baseline IGF-I (453 vs. 716 microg/liter; P < 0.001) and GH levels (2.7 vs. 7.8 microg/liter; P < 0.05), and to require a lower maximum dose of SSA (24 vs. 31 mg every 4 wk; P = 0.013).
  • Multivariate analysis confirmed that a densely granulated adenoma was the strongest predictor of complete response [adjusted odds ratio (OR), 58.41; 95% confidence interval (CI), 1.24-1000.00; P = 0.04] compared with other covariates, including older age at time of diagnosis (OR, 1.15/yr; 95% CI, 1.01-1.31; P = 0.03), and tumor stage of 3 or less (OR, 29.77; 95% CI, 1.01-885.45; P < 0.05).
  • CONCLUSIONS: Somatotroph tumor type represents a strong clinical predictor of response to SSA treatment and will help to identify patients who warrant more vigilant management of their disease.
  • [MeSH-major] Acromegaly / drug therapy. Adenoma / drug therapy. Octreotide / therapeutic use. Pituitary Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Female. Human Growth Hormone / blood. Humans. Insulin-Like Growth Factor I / analysis. Male. Middle Aged. Multivariate Analysis. Phenotype. Retrospective Studies

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  • (PMID = 16118335.001).
  • [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] 12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I; RWM8CCW8GP / Octreotide
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75. 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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76. 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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  • [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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77. 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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78. Kirschner LS: PRKAR1A and the evolution of pituitary tumors. Mol Cell Endocrinol; 2010 Sep 15;326(1-2):3-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
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  • (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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79. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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80. Metzler M, Luedecke DK, Saeger W, Grueters A, Haberl H, Kiess W, Repp R, Rascher W, Doetsch J: Low prevalence of Gs alpha mutations in śomatotroph adenomas of children and adolescents. Cancer Genet Cytogenet; 2006 Apr 15;166(2):146-51
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  • [Title] Low prevalence of Gs alpha mutations in śomatotroph adenomas of children and adolescents.
  • Mutations in the gene coding for the alpha-subunit of the heterotrimeric stimulatory G protein Gs are the most frequently identified molecular events in the development of somatotroph adenomas in adults.
  • In children and adolescents, somatotroph adenomas are rare, and only two cases with the Gs alpha mutation have been reported so far.
  • In this study, we therefore investigated the prevalence of activating Gs alpha mutations in 17 patients younger than 20 years with pituitary growth hormone-secreting adenomas and examined the characteristics of mutation-positive cases.
  • Interestingly, in contrast to the remaining cases, the adenomas positive for the Gs alpha mutation proved to be nonsporadic, but part of a syndrome associated with endocrine tumors in both individuals.
  • In contrast to the findings in adult cases, somatotroph adenomas in young patients seem to carry somatic Gs alpha mutations at a lower frequency, and germ-line or early postzygotic mutational events may be responsible for the shortened latency of tumorigenesis.
  • [MeSH-major] GTP-Binding Protein alpha Subunits, Gs / genetics. Growth Hormone-Secreting Pituitary Adenoma / genetics. Mutation / genetics

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  • (PMID = 16631471.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs
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81. 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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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. 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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84. 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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85. 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]
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  • (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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86. 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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87. 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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88. Korbonits M, Carlsen E: Recent clinical and pathophysiological advances in non-functioning pituitary adenomas. Horm Res; 2009 Apr;71 Suppl 2:123-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Recent clinical and pathophysiological advances in non-functioning pituitary adenomas.
  • Pituitary adenomas are being recognized and diagnosed with increasing frequency.
  • One of the most common forms of pituitary lesion is the clinically non-functioning pituitary adenoma (NFPA), which is often diagnosed incidentally.
  • The vast majority of pituitary adenomas are sporadic, but familial adenomas can occur in the multiple pituitary adenoma type 1 syndrome, in Carney complex or in familial isolated pituitary adenoma.
  • NFPA often show hormone synthesis on tissue immunostaining without causing clinical symptoms.
  • Most often these are silent gonadotroph adenomas, with silent corticotroph or somatotroph adenomas occurring less frequently.
  • It is unclear why these silent adenomas do not release hormones at a clinically recognizable level, although it is probable that there is a continuum between fully functional and completely silent adenomas.
  • Temozolomide has been successfully used for the treatment of a few aggressive pituitary adenomas, and the response to this drug could be influenced by the expression of the DNA repair enzyme O-6-methylguanine DNA methyltransferase.
  • The early diagnosis, prediction of long-term outcome and treatment of NFPAs remain a challenge for endocrinologists.
  • [MeSH-major] Growth Hormone-Secreting Pituitary Adenoma. Prolactinoma
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / diagnosis. ACTH-Secreting Pituitary Adenoma / metabolism. ACTH-Secreting Pituitary Adenoma / pathology. ACTH-Secreting Pituitary Adenoma / therapy. Female. Humans. Male

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  • [Copyright] Copyright 2009 S. Karger AG, Basel.
  • (PMID = 19407508.001).
  • [ISSN] 1423-0046
  • [Journal-full-title] Hormone research
  • [ISO-abbreviation] Horm. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Number-of-references] 58
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89. Abbassioun K, Amirjamshidi M, Mehrazin A, Khalatbary I, Keynama M, Bokai H, Abdollahi M: A prospective analysis of 151 cases of patients with acromegaly operated by one neurosurgeon: a follow-up of more than 23 years. Surg Neurol; 2006 Jul;66(1):26-31; discussion 31
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  • [Title] A prospective analysis of 151 cases of patients with acromegaly operated by one neurosurgeon: a follow-up of more than 23 years.
  • BACKGROUND: Transsphenoidal adenomectomy has been the accepted surgical management for treatment of growth hormone (GH)-secreting pituitary adenomas.
  • Although the goal of treatment might be to keep the GH level in the reference range, the actual definition of success in control of acromegaly is not yet clear.
  • The preoperative hormonal studies documenting the high GH and/or insulin-like growth factor were available in all the cases.
  • RESULTS: There were 90 patients with pure GH-secreting adenoma (59.6%) with the highest GH level of 235 mU/L.
  • A second group of 12 patients had normal GH level but elevated serum level of insulin-like growth factor 1 (8%).
  • The group with mixed secretion of GH and prolactin included 49 cases (32.4%).
  • Normal postoperative serum GH level could be achieved in 98 patients (94.2%) of 104 cases with full follow-up.
  • CONCLUSION: In the developing countries, early diagnosis and proper surgical extirpation of the GH-secreting adenoma by an experienced and dedicated pituitary surgeon is mandatory to reduce the mortality and increase the chance of cure of this rather mortal endocrionopathy.
  • [MeSH-major] Acromegaly / surgery. Adenoma / surgery. Growth Hormone-Secreting Pituitary Adenoma / surgery. Hypophysectomy / methods
  • [MeSH-minor] Adolescent. Adult. Aged. Cerebrospinal Fluid Rhinorrhea / etiology. Cerebrospinal Fluid Rhinorrhea / physiopathology. Diabetes Insipidus / etiology. Diabetes Insipidus / physiopathology. Early Diagnosis. Female. Follow-Up Studies. Growth Hormone / blood. Growth Hormone / secretion. Humans. Hypopituitarism / etiology. Hypopituitarism / physiopathology. Insulin-Like Growth Factor I / metabolism. Insulin-Like Growth Factor I / secretion. Male. Middle Aged. Pituitary Gland / physiopathology. Pituitary Gland / secretion. Pituitary Gland / surgery. Postoperative Complications / etiology. Postoperative Complications / physiopathology. Prolactin / blood. Prolactin / secretion. Prospective Studies. Sella Turcica / anatomy & histology. Sella Turcica / pathology. Sella Turcica / surgery. Sphenoid Bone / anatomy & histology. Sphenoid Bone / pathology. Sphenoid Bone / surgery. Treatment Outcome

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  • (PMID = 16793431.001).
  • [ISSN] 0090-3019
  • [Journal-full-title] Surgical neurology
  • [ISO-abbreviation] Surg Neurol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 67763-96-6 / Insulin-Like Growth Factor I; 9002-62-4 / Prolactin; 9002-72-6 / Growth Hormone
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90. Jaffe CA: Clinically non-functioning pituitary adenoma. Pituitary; 2006;9(4):317-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinically non-functioning pituitary adenoma.
  • Non-functioning pituitary tumors are relatively common.
  • A large number of these tumors are incidentally found pituitary microadenomas (<1 cm) and are usually of no clinical importance.
  • Visual field defects are present in roughly 70% of patients with non-functioning macroadenoma at the time of diagnosis and the majority of these patients have at least growth deficiency and hypogonadism.
  • By immunocytochemistry, the large majority of these tumors are glycoprotein producing and less commonly they are non-functioning somatotroph, lactotroph or corticotoph adenomas.
  • Surgery improves visual defects in the majority of patients and a lesser number will recover pituitary function.
  • In the past, pituitary radiation was commonly administered following pituitary surgery; however the need for routine radiation has recently been reevaluated.
  • Close follow-up with surveillance pituitary scans should be performed after surgery and radiation therapy reserved for patients having significant tumor recurrence.
  • [MeSH-major] Adenoma / diagnosis. Adenoma / therapy. Pituitary Neoplasms / diagnosis. Pituitary Neoplasms / therapy
  • [MeSH-minor] Algorithms. Antineoplastic Agents, Hormonal. Biomarkers / blood. Growth Disorders / etiology. Growth Disorders / therapy. Humans. Hypogonadism / etiology. Hypogonadism / therapy. Hypophysectomy. Hypopituitarism / etiology. Hypopituitarism / therapy. Practice Guidelines as Topic. Radiotherapy, Adjuvant. Recurrence. Treatment Outcome. Vision Disorders / etiology. Vision Disorders / therapy

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  • (PMID = 17082898.001).
  • [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 / Antineoplastic Agents, Hormonal; 0 / Biomarkers
  • [Number-of-references] 17
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91. 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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92. Flitsch J, Lüdecke DK, Saeger W, Veit JA, Metternich FU: [Acromegaly-associated lesions of the nasal mucosa. Case report]. HNO; 2009 Aug;57(8):845-50
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  • [Title] [Acromegaly-associated lesions of the nasal mucosa. Case report].
  • Acromegaly is a rare disease caused by a growth-hormone-secreting pituitary adenoma.
  • Besides these "cosmetic" symptoms, the disease is associated with hypertension and diabetes mellitus, as well as with an increased risk for adenomas and carcinomas of the colon.
  • The average time span from first symptom to diagnosis is well over 6 years; a single determination of insulin-like growth factor 1 in serum can confirm the disease.
  • The treatment of choice remains surgical resection of the adenoma in suitable patients, whereas in extensive disease with invasion of surrounding tissue, drug therapy and/or radiotherapy may be necessary.
  • [MeSH-major] Acromegaly / complications. Acromegaly / surgery. Adenoma / etiology. Adenoma / surgery. Nasal Mucosa / surgery. Nose Neoplasms / etiology. Nose Neoplasms / surgery

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  • [Cites] Clin Endocrinol (Oxf). 1994 Jul;41(1):95-102 [8050136.001]
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  • (PMID = 19557321.001).
  • [ISSN] 1433-0458
  • [Journal-full-title] HNO
  • [ISO-abbreviation] HNO
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
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93. Nishioka H, Haraoka J: Biochemical cure of acromegaly after transsphenoidal surgery despite residual tumor on magnetic resonance imaging: case report. Neurol Med Chir (Tokyo); 2008 Jul;48(7):311-3
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  • [Title] Biochemical cure of acromegaly after transsphenoidal surgery despite residual tumor on magnetic resonance imaging: case report.
  • A 52-year-old acromegalic woman underwent transsphenoidal removal of a pituitary macroadenoma.
  • Postoperative magnetic resonance (MR) imaging demonstrated small residual tumor, but her acromegaly was "cured" using current strict criteria.
  • The histological diagnosis was somatotroph cell adenoma with fibrous bodies.
  • Biochemical cure may not reflect total removal of the tumor, particularly if the growth hormone secretory activity of the residual tumor is low.
  • Careful evaluation of postoperative MR imaging is always necessary to interpret surgical outcome, even if biochemical cure in acromegaly has been achieved.
  • [MeSH-major] Growth Hormone / blood. Growth Hormone-Secreting Pituitary Adenoma / surgery. Insulin-Like Growth Factor I / metabolism. Magnetic Resonance Imaging. Neoplasm, Residual / diagnosis. Pituitary Neoplasms / surgery. Postoperative Complications / diagnosis. Sphenoid Sinus / surgery
  • [MeSH-minor] Female. Follow-Up Studies. Humans. Middle Aged. Pituitary Function Tests. Pituitary Gland / pathology. Pituitary Gland / surgery

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  • (PMID = 18654051.001).
  • [ISSN] 1349-8029
  • [Journal-full-title] Neurologia medico-chirurgica
  • [ISO-abbreviation] Neurol. Med. Chir. (Tokyo)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 67763-96-6 / Insulin-Like Growth Factor I; 9002-72-6 / Growth Hormone
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94. Noh SJ, Ahn JY, Lee KS, Kim SH: Pituitary adenoma and concomitant Rathke's cleft cyst. Acta Neurochir (Wien); 2007 Dec;149(12):1223-8
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  • [Title] Pituitary adenoma and concomitant Rathke's cleft cyst.
  • Although pituitary adenomas and Rathke's cleft cysts have a shared ancestry, they rarely occur simultaneously.
  • Only 32 reports involving a pituitary adenoma and a concomitant Rathke's cleft cyst were identified upon review of the literature.
  • Next to growth hormone, Prolactin was the most commonly hypersecreted pituitary hormone.
  • Here, we report a patient with a growth hormone- secreting pituitary adenoma associated with a Rathke's cleft cyst.
  • When a non-enhancing cyst-like structure is demonstrated on imaging in a patient with a pituitary adenoma, the possibility of a coexisting Rathke's cleft cyst should be considered.
  • [MeSH-major] Adenoma / surgery. Central Nervous System Cysts / surgery. Growth Hormone-Secreting Pituitary Adenoma / surgery. Neoplasms, Multiple Primary / surgery. Pituitary Neoplasms / surgery
  • [MeSH-minor] Diagnosis, Differential. Female. Humans. Image Processing, Computer-Assisted. Magnetic Resonance Imaging. Middle Aged. Neuronavigation. Pituitary Gland / pathology

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  • (PMID = 17914599.001).
  • [ISSN] 0942-0940
  • [Journal-full-title] Acta neurochirurgica
  • [ISO-abbreviation] Acta Neurochir (Wien)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Austria
  • [Number-of-references] 28
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95. Andrioli M, Pecori Giraldi F, Losa M, Terreni M, Invitti C, Cavagnini F: Cushing's disease due to double pituitary ACTH-secreting adenomas: the first case report. Endocr J; 2010;57(9):833-7
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  • [Title] Cushing's disease due to double pituitary ACTH-secreting adenomas: the first case report.
  • Double pituitary adenomas are rare occurrences in autoptical, surgical and neuroradiological series and are mostly due to non-functioning pituitary adenomas, GH-secreting and prolactin-secreting adenomas.
  • ACTH secreting tumours are more rare and, to our knowledge, two distinct ACTH-producing adenomas within the same pituitary have never been reported.
  • We herewith describe a 56 year old woman with Cushing' s disease due to two clearly distinct ACTH-secreting pituitary adenomas.
  • She presented with signs and symptoms of hypercortisolism and hormonal testing was indicative for pituitary-dependent Cushing' s syndrome.
  • Sellar MRI visualized an asymmetric pituitary gland with suspect lesions in both the right and the left pituitary lobes.
  • Pathology confirmed the existence of two distinct adenomas located in different sites in the gland.
  • Our case indicates that double ACTH-secreting pituitary adenomas may occur in patients with Cushing' s disease.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / pathology. Adenoma / pathology. Neoplasms, Multiple Primary / pathology. Pituitary ACTH Hypersecretion / etiology
  • [MeSH-minor] Cushing Syndrome / etiology. Female. Humans. Middle Aged. Pituitary Neoplasms / pathology

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  • (PMID = 20595779.001).
  • [ISSN] 1348-4540
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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96. Fusco A, Zatelli MC, Bianchi A, Cimino V, Tilaro L, Veltri F, Angelini F, Lauriola L, Vellone V, Doglietto F, Ambrosio MR, Maira G, Giustina A, degli Uberti EC, Pontecorvi A, De Marinis L: Prognostic significance of the Ki-67 labeling index in growth hormone-secreting pituitary adenomas. J Clin Endocrinol Metab; 2008 Jul;93(7):2746-50
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  • [Title] Prognostic significance of the Ki-67 labeling index in growth hormone-secreting pituitary adenomas.
  • OBJECTIVE: The aim of the study was to evaluate the Ki-67 index prognostic relevance in a group of acromegalic patients who underwent transsphenoidal surgery for a GH-secreting pituitary adenoma.
  • The Ki-67 index was determined by immunohistochemistry on tissue samples obtained from each adenoma after surgery.
  • Periodical pituitary magnetic resonance imaging and hormonal evaluation were performed during the follow-up.
  • Pituitary magnetic resonance imaging showed residual/recurrent disease in 25 of 68 patients after 6 months.
  • No correlation was found between Ki-67 index and age, tumor size, GH, or IGF-I plasma levels.
  • We suggest routine Ki-67 evaluation in GH-secreting pituitary adenomas.
  • [MeSH-major] Adenoma / pathology. Growth Hormone-Secreting Pituitary Adenoma / pathology. Ki-67 Antigen / analysis

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  • (PMID = 18460561.001).
  • [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 / Ki-67 Antigen; 51110-01-1 / Somatostatin
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97. Drutel A, Caron P, Archambeaud F: [New medical treatments in pituitary adenomas]. Ann Endocrinol (Paris); 2008 Sep;69 Suppl 1:S16-28
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  • [Title] [New medical treatments in pituitary adenomas].
  • Currently, the role of dopaminergic and somatostatinergic agonists in the treatment of pituitary adenomas is quite well established.
  • Nevertheless, a clearer understanding of the expression of dopaminergic and somatostatinergic receptors at the cellular level of pituitary adenomas as well as the development of newer analogues compounds may drastically change current therapeutic modalities.
  • In the midst of GH-secreting pituitary adenomas, a positive correlation exists between the expression of Sst2 mRNA and the inhibition of GH release by somatostatin analogues.
  • The involvement of Sst5 subtype in adenomas resistant to preferential Sst2 agonists has recently been proved.
  • SOM-230 could therefore allow for much more effective methods in treating patients suffering from acromegaly.
  • Besides, the use of a chimeric molecule presenting a binding affinity to both Sst2 and D2 subtypes (BIM-23A287) inhibits the secretion of GH in ways similar to the Sst2 or D2 agonists used alone or concurrently but however in a concentration 50 times lower than that of the latter.
  • The discovery of Sst5 and D2 subtypes at the level of corticotropic adenomas reveals newer therapeutic perspectives with promising preliminary results with the use of SOM-230 ; these finding lead to a rise in interest in cabergoline.
  • In the midst of non-functioning pituitary adenomas, the expression of Sst2, Sst3 and D2 receptors will perhaps allow the use of combined therapies associating the new somatostatin analogues to the dopaminergic agonists or even use dopastatin (BIM-23A760, chimeric molecule Sst2-Sst5-D2).
  • Nevertheless, it seems that adenomas resistant to dopaminergic agonist due to a lack of expression of D2 receptor fail to express Sst5 receptors as well.
  • On the other hand, dopastatin appears to be more efficient than cabergoline in the management of this type of adenomas.
  • Therefore, the growing awareness concerning the mechanisms involved in the control of pituitary secretions as well as cellular proliferation will perhaps allow physicians to treat the pathology of pituitary adenomas, macroadenomas in particular, using solely pharmacological means instead of invasive surgical procedures and/or radiotherapy.
  • [MeSH-major] Adenoma / drug therapy. Pituitary Neoplasms / drug therapy

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  • (PMID = 18954854.001).
  • [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 / Dopamine Agonists; 0 / Peptides, Cyclic; 0 / Receptors, Dopamine; 0 / Receptors, Somatostatin; 118992-92-0 / lanreotide; 51110-01-1 / Somatostatin; RWM8CCW8GP / Octreotide
  • [Number-of-references] 49
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98. 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


99. 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