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1. Zhan X, Desiderio DM: The use of variations in proteomes to predict, prevent, and personalize treatment for clinically nonfunctional pituitary adenomas. EPMA J; 2010 Sep;1(3):439-59

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  • [Title] The use of variations in proteomes to predict, prevent, and personalize treatment for clinically nonfunctional pituitary adenomas.
  • Pituitary adenomas account for ∼10% of intracranial tumors, and they cause the compression of nearby structures and the inappropriate expression of pituitary hormones.
  • Unlike functional pituitary adenomas, nonfunctional (NF) pituitary adenomas account for ∼30% of pituitary tumors, and are large enough to cause blindness; because they do not cause any clinical hormone hypersecretion, they are difficult to detect at an early stage; and hypopituitarism results.
  • No effective molecular biomarkers or chemical therapy have been approved for the clinical setting.
  • Because an NF pituitary adenoma is highly heterogeneous, differences in the proteins (the proteome) can distinguish among those heterogeneity structures.
  • Changes in protein expression and protein modifications, individually or in combination, might be biomarkers to predict the disease, monitor the tumor progression, and develop an accurate molecular classification for personalized patient treatment.
  • The modalities of proteomic variation might also be useful in the interventional prevention and personalized treatment of patients to halt the occurrence and progression of NF pituitary adenomas.

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  • [Cites] Horm Res. 1992;38(3-4):164-70 [1306849.001]
  • [Cites] J Clin Invest. 1990 Jul;86(1):336-40 [1973174.001]
  • [Cites] J Clin Endocrinol Metab. 1990 Dec;71(6):1427-33 [1977759.001]
  • [Cites] Neuroendocrinology. 1997 Dec;66(6):426-31 [9430448.001]
  • [Cites] Horm Res. 1999;51(5):242-7 [10559669.001]
  • [Cites] Front Neuroendocrinol. 2000 Jul;21(3):174-98 [10882539.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Jun;86(6):2631-7 [11397864.001]
  • [Cites] Science. 2001 Sep 14;293(5537):2101-5 [11474067.001]
  • [Cites] Anal Biochem. 2001 Oct 1;297(1):25-31 [11567524.001]
  • [Cites] Proteomics. 2001 Mar;1(3):377-96 [11680884.001]
  • [Cites] Anal Chem. 2001 Dec 1;73(23):5683-90 [11774908.001]
  • [Cites] Lancet. 2002 Feb 16;359(9306):572-7 [11867112.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jun 11;99(12):7900-5 [12060738.001]
  • [Cites] Science. 2002 Dec 6;298(5600):1911-2 [12471242.001]
  • [Cites] Nature. 2003 Mar 13;422(6928):198-207 [12634793.001]
  • [Cites] Proteomics. 2003 May;3(5):699-713 [12748949.001]
  • [Cites] Clin Chem. 2003 Aug;49(8):1272-5 [12881441.001]
  • [Cites] J Clin Invest. 2003 Dec;112(11):1603-18 [14660734.001]
  • [Cites] Expert Rev Mol Med. 2002 Apr;4(9):1-19 [14987393.001]
  • [Cites] Mol Cell Proteomics. 2004 Apr;3(4):367-78 [14990683.001]
  • [Cites] J Natl Cancer Inst. 2004 Mar 3;96(5):353-6 [14996856.001]
  • [Cites] Anal Chem. 2004 Mar 15;76(6):1560-70 [15018552.001]
  • [Cites] Oncogene. 2004 Apr 12;23(16):2838-49 [15077147.001]
  • [Cites] J Proteome Res. 2004 Mar-Apr;3(2):179-96 [15113093.001]
  • [Cites] Clin Cancer Res. 2005 Feb 1;11(3):963-5 [15709159.001]
  • [Cites] Mol Cell Proteomics. 2005 Sep;4(9):1341-9 [15970584.001]
  • [Cites] Mitochondrion. 2004 Sep;4(5-6):755-62 [16120430.001]
  • [Cites] Science. 2005 Sep 9;309(5741):1682-3 [16150998.001]
  • [Cites] Cancer Res. 2005 Nov 15;65(22):10214-22 [16288009.001]
  • [Cites] Chem Biol Interact. 2006 Mar 10;160(1):1-40 [16430879.001]
  • [Cites] Oncogene. 2006 Aug 7;25(34):4812-30 [16892093.001]
  • [Cites] Mol Cell Proteomics. 2006 Oct;5(10):1840-52 [16896061.001]
  • [Cites] Curr Mol Med. 2007 Feb;7(1):121-31 [17311537.001]
  • [Cites] Drug News Perspect. 2007 Mar;20(2):109-17 [17440634.001]
  • [Cites] Oncogene. 2007 May 14;26(22):3279-90 [17496922.001]
  • [Cites] Mol Cell Proteomics. 2008 May;7(5):853-63 [17951628.001]
  • [Cites] Antioxid Redox Signal. 2008 Mar;10(3):635-40 [17999628.001]
  • [Cites] Cell. 2008 Jul 11;134(1):112-23 [18614015.001]
  • [Cites] J Immunol. 2008 Sep 1;181(5):3540-8 [18714027.001]
  • [Cites] J Intern Med. 2009 Feb;265(2):193-209 [19192036.001]
  • [Cites] Methods Mol Biol. 2009;509:123-34 [19212718.001]
  • [Cites] BMC Med Genomics. 2010;3:13 [20426862.001]
  • [Cites] Biochim Biophys Acta. 1991 May 2;1089(1):95-102 [2025653.001]
  • [Cites] Cancer. 1980 Aug 1;46(3):537-42 [6249483.001]
  • [Cites] Acta Neurochir (Wien). 1980;51(3-4):195-201 [7368994.001]
  • [Cites] Biochem Biophys Res Commun. 1994 Dec 30;205(3):1785-9 [7811265.001]
  • [Cites] J Endocrinol Invest. 1993 Nov;16(10):807-16 [8144855.001]
  • [Cites] J Clin Endocrinol Metab. 1997 May;82(5):1516-21 [9141543.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Sep;82(9):2944-9 [9284724.001]
  • [Cites] Electrophoresis. 1997 Oct;18(11):2071-7 [9420172.001]
  • [Cites] Clin Endocrinol (Oxf). 2000 Sep;53(3):337-44 [10971451.001]
  • [Cites] Pituitary. 1999 Nov;2(3):225-31 [11081158.001]
  • [Cites] Minerva Endocrinol. 2000 Sep-Dec;25(3-4):55-9 [11338396.001]
  • [Cites] Trends Pharmacol Sci. 2002 Jan;23(1):40-5 [11804650.001]
  • [Cites] J Mass Spectrom. 2002 Feb;37(2):133-45 [11857757.001]
  • [Cites] Mol Cell Proteomics. 2002 Feb;1(2):117-24 [12096129.001]
  • [Cites] J Endocrinol. 2002 Sep;174(3):379-86 [12208657.001]
  • [Cites] Rapid Commun Mass Spectrom. 2002;16(22):2115-23 [12415544.001]
  • [Cites] J Am Soc Mass Spectrom. 2003 Jan;14(1):1-7 [12504328.001]
  • [Cites] Biochim Biophys Acta. 2002 Dec 30;1585(2-3):193-201 [12531554.001]
  • [Cites] Electrophoresis. 2003 Jun;24(11):1818-33 [12783459.001]
  • [Cites] Electrophoresis. 2003 Jun;24(11):1834-46 [12783460.001]
  • [Cites] Proteomics. 2004 Mar;4(3):587-98 [14997482.001]
  • [Cites] Trends Mol Med. 2004 Mar;10(3):125-9 [15102355.001]
  • [Cites] Front Horm Res. 2004;32:34-62 [15281339.001]
  • [Cites] Front Horm Res. 2004;32:110-26 [15281342.001]
  • [Cites] Mass Spectrom Rev. 2005 Nov-Dec;24(6):783-813 [15495141.001]
  • [Cites] Biochem Biophys Res Commun. 2004 Dec 24;325(4):1180-6 [15555551.001]
  • [Cites] Am J Gastroenterol. 2005 Feb;100(2):414-23 [15667502.001]
  • [Cites] Proteomics. 2005 Apr;5(5):1228-41 [15717326.001]
  • [Cites] Rapid Commun Mass Spectrom. 2005;19(7):865-70 [15724237.001]
  • [Cites] Free Radic Biol Med. 2005 May 15;38(10):1278-95 [15855047.001]
  • [Cites] Science. 2005 Sep 9;309(5741):1735-9 [16151014.001]
  • [Cites] J Natl Cancer Inst. 2005 Dec 21;97(24):1800-1 [16368937.001]
  • [Cites] Br Med Bull. 2005;75-76:81-97 [16684928.001]
  • [Cites] Expert Rev Proteomics. 2006 Jun;3(3):297-309 [16771702.001]
  • [Cites] Anal Biochem. 2006 Jul 15;354(2):279-89 [16777052.001]
  • [Cites] Eur Respir J. 2007 Apr;29(4):643-50 [17182653.001]
  • [Cites] Eur J Endocrinol. 2007 Feb;156(2):203-16 [17287410.001]
  • [Cites] Clin Endocrinol (Oxf). 2007 Mar;66(3):348-52 [17302867.001]
  • [Cites] Med Hypotheses. 2007;69(4):826-8 [17368752.001]
  • [Cites] J Proteome Res. 2007 Nov;6(11):4200-9 [17902639.001]
  • [Cites] Pituitary. 2008;11(3):231-45 [18183490.001]
  • [Cites] J Cancer Res Clin Oncol. 2008 Jul;134(7):769-76 [18202856.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Apr;93(4):1211-6 [18230656.001]
  • [Cites] Pharmacol Res. 2008 May;57(5):325-31 [18455424.001]
  • [Cites] IUBMB Life. 2008 Jul;60(7):441-7 [18465793.001]
  • [Cites] Neurochem Res. 2008 Dec;33(12):2502-9 [18998208.001]
  • [Cites] Front Biosci (Landmark Ed). 2009;14:4376-85 [19273356.001]
  • [Cites] J Proteome Res. 2009 Dec;8(12):5511-22 [19845411.001]
  • [Cites] Proteomics. 2010 Feb;10(4):731-48 [19953541.001]
  • [Cites] Proteomics. 2010 Jan;10(2):343-7 [20029838.001]
  • [Cites] Proteome Sci. 2010;8:2 [20205839.001]
  • (PMID = 23199087.001).
  • [ISSN] 1878-5077
  • [Journal-full-title] The EPMA journal
  • [ISO-abbreviation] EPMA J
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / S10 RR016679
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Other-IDs] NLM/ PMC3405333
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2. Arimura A, Li M, Batuman V: Potential protective action of pituitary adenylate cyclase-activating polypeptide (PACAP38) on in vitro and in vivo models of myeloma kidney injury. Blood; 2006 Jan 15;107(2):661-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Potential protective action of pituitary adenylate cyclase-activating polypeptide (PACAP38) on in vitro and in vivo models of myeloma kidney injury.
  • The most common type of renal injury in multiple myeloma is chronic tubulointerstitial nephropathy associated with casts in tubule lumens, an entity referred to as "myeloma kidney" that often progresses to end-stage kidney diseases.
  • Here, we report that pituitary adenylate cyclase-activating polypeptide with 38 residues (PACAP38) dramatically prevents injury of cultured renal proximal tubule cells caused by myeloma light chains through suppression of proinflammatory cytokines production, by inhibiting p38 MAPK and translocation of NFkappaB via both PAC(1) and VPAC(1) receptors.
  • [MeSH-major] Kidney / drug effects. Kidney / injuries. Models, Animal. Multiple Myeloma / drug therapy. Peptide Fragments / therapeutic use. Pituitary Adenylate Cyclase-Activating Polypeptide / therapeutic use. Protective Agents / therapeutic use
  • [MeSH-minor] Animals. Anti-Inflammatory Agents / pharmacology. Bone Marrow / metabolism. Cell Adhesion. Chemokine CCL2 / metabolism. Dexamethasone / pharmacology. Immunoglobulin Light Chains / adverse effects. In Vitro Techniques. Interleukin-6 / metabolism. Male. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. NF-kappa B / metabolism. Protein Transport. Rats. Rats, Sprague-Dawley. Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide, Type I / genetics. Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide, Type I / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Stromal Cells / cytology. Stromal Cells / metabolism. Tumor Necrosis Factor-alpha / metabolism. p38 Mitogen-Activated Protein Kinases / metabolism

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  • (PMID = 16204306.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [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 / Anti-Inflammatory Agents; 0 / Ccl2 protein, rat; 0 / Chemokine CCL2; 0 / Immunoglobulin Light Chains; 0 / Interleukin-6; 0 / NF-kappa B; 0 / Peptide Fragments; 0 / Pituitary Adenylate Cyclase-Activating Polypeptide; 0 / Protective Agents; 0 / Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide, Type I; 0 / Tumor Necrosis Factor-alpha; 0 / pituitary adenylate cyclase-activating-peptide (1-38), pig; 7S5I7G3JQL / Dexamethasone; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases
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3. McIntyre DJ, Robinson SP, Howe FA, Griffiths JR, Ryan AJ, Blakey DC, Peers IS, Waterton JC: Single dose of the antivascular agent, ZD6126 (N-acetylcolchinol-O-phosphate), reduces perfusion for at least 96 hours in the GH3 prolactinoma rat tumor model. Neoplasia; 2004 Mar-Apr;6(2):150-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Single dose of the antivascular agent, ZD6126 (N-acetylcolchinol-O-phosphate), reduces perfusion for at least 96 hours in the GH3 prolactinoma rat tumor model.
  • Tumor vasculature is an attractive therapeutic target as it differs structurally from normal vasculature, and the destruction of a single vessel can lead to the death of many tumor cells.
  • The effects of antivascular drugs are frequently short term, with regrowth beginning less than 24 hours posttreatment.
  • The tumors were examined with dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) 24 hours pretreatment and posttreatment, and at a single time between 48 and 96 hours posttreatment.
  • No evidence of recovery of perfusion was observed even at the longest (96-hour) time point.
  • Involvement of a statistician at the project planning stage and the use of DCE-MRI, which permits noninvasive quantitation of parameters related to blood flow in intact animals, allowed this highly significant result to be obtained using only eight rats.
  • [MeSH-major] Neovascularization, Pathologic / drug therapy. Organophosphorus Compounds / administration & dosage. Pituitary Neoplasms / blood supply. Prolactinoma / blood supply
  • [MeSH-minor] Animals. Disease Models, Animal. Magnetic Resonance Imaging. Necrosis. Rats. Rats, Inbred WF. Regional Blood Flow / drug effects

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  • [Cites] Clin Cancer Res. 2000 Apr;6(4):1498-507 [10778982.001]
  • [Cites] J Magn Reson Imaging. 1999 Sep;10(3):254-9 [10508284.001]
  • [Cites] Cancer. 2001 Jun 15;91(12):2230-7 [11413510.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2002 May 1;53(1):164-71 [12007956.001]
  • [Cites] Clin Cancer Res. 2002 Jun;8(6):1974-83 [12060643.001]
  • [Cites] Cancer Res. 2002 Jul 1;62(13):3711-5 [12097279.001]
  • [Cites] Int J Oncol. 2002 Oct;21(4):717-26 [12239609.001]
  • [Cites] Cancer Res. 2002 Nov 15;62(22):6371-5 [12438217.001]
  • [Cites] Cancer Res. 2002 Dec 15;62(24):7247-53 [12499266.001]
  • [Cites] Br J Cancer. 2003 May 19;88(10):1592-7 [12771928.001]
  • [Cites] Radiology. 2003 Jul;228(1):271-8 [12832588.001]
  • [Cites] J Clin Oncol. 2003 Aug 1;21(15):2831-42 [12807936.001]
  • [Cites] J Endocrinol. 1981 Mar;88(3):463-9 [7217831.001]
  • [Cites] Radiat Res. 1988 Apr;114(1):64-76 [2895486.001]
  • [Cites] Nat Med. 1995 Jan;1(1):27-31 [7584949.001]
  • [Cites] Eur J Cancer. 2000 Sep;36(14):1833-43 [10974632.001]
  • (PMID = 15140404.001).
  • [ISSN] 1522-8002
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / N-acetylcochinol-O-phosphate; 0 / Organophosphorus Compounds
  • [Other-IDs] NLM/ PMC1502085
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4. Talvinen K, Tuikkala J, Grönroos J, Huhtinen H, Kronqvist P, Aittokallio T, Nevalainen O, Hiekkanen H, Nevalainen T, Sundström J: Biochemical and clinical approaches in evaluating the prognosis of colon cancer. Anticancer Res; 2006 Nov-Dec;26(6C):4745-51
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • To achieve optimal treatment results, the risk estimation of recurrence should be as accurate as possible.
  • MATERIALS AND METHODS: Tissue material from tumour and normal mucosa was taken from six patients and was analysed to screen aberrantly expressed genes using cDNA microarray.
  • For this purpose a tissue array material of 114 colorectal cancer patients was obtained.
  • CONCLUSION: Tumour stage is superior in estimating the prognosis of patients with colonic cancer compared with the grading of cell cycle regulators or histological grade of the cancer.
  • The study of regional lymph nodes is essential to identify the patients who would benefit from adjuvant chemotherapy.

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  • (PMID = 17214335.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Neoplasm Proteins; 0 / Securin; 0 / pituitary tumor-transforming protein 1, human; EC 3.1.3.16 / CDC25B protein, human; EC 3.1.3.48 / cdc25 Phosphatases
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5. Prieto-Tenreiro A, Díaz-Guardiola P: Long term treatment of a thyrotropin-secreting microadenoma with somatostatin analogues. Arq Bras Endocrinol Metabol; 2010;54(5):502-6
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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 treatment of a thyrotropin-secreting microadenoma with somatostatin analogues.
  • Thyrotropin (TSH) secreting pituitary adenomas (TSH-omas) account for < 1% of all pituitary adenomas and are a rare cause of hyperthyroidism.
  • The diagnosis is often made at the stage of macroadenoma because of the aggressive nature of the tumor and due to the fact that patients are mistakenly treated for more common primary hyperthyroidism for a long time.
  • First line therapy is transsphenoidal resection of the tumor, which can cure one-third of the patients completely.
  • However, if surgery is not possible or curative, pituitary radiotherapy and/or somatostatin analogs (SSA) can be useful.
  • As transsphenoidal surgery was not considered effective, medical therapy with a somatostatin analogue was initiated.
  • Currently, at four years of follow-up, the patient continues on this treatment and remains euthyroid and asymptomatic.
  • We report a case of successful long-term treatment with SSA, after unsuccessful surgery.
  • [MeSH-major] Adenoma / drug therapy. Antineoplastic Agents, Hormonal / therapeutic use. Peptides, Cyclic / therapeutic use. Pituitary Neoplasms / drug therapy. Somatostatin / analogs & derivatives. Thyrotropin / secretion

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  • (PMID = 20694413.001).
  • [ISSN] 1677-9487
  • [Journal-full-title] Arquivos brasileiros de endocrinologia e metabologia
  • [ISO-abbreviation] Arq Bras Endocrinol Metabol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Peptides, Cyclic; 118992-92-0 / lanreotide; 51110-01-1 / Somatostatin; 9002-71-5 / Thyrotropin
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6. Pelosi G, Volante M, Papotti M, Sonzogni A, Masullo M, Viale G: Peptide receptors in neuroendocrine tumors of the lung as potential tools for radionuclide diagnosis and therapy. Q J Nucl Med Mol Imaging; 2006 Dec;50(4):272-87
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  • [Title] Peptide receptors in neuroendocrine tumors of the lung as potential tools for radionuclide diagnosis and therapy.
  • The standard treatment of typical or atypical carcinoids is the complete surgical resection, whereas the role of radio-chemotherapy in a multimodality treatment or for palliation remains controversial.
  • Conversely, high-grade neuroendocrine carcinomas are in primis treated by aggressive combination chemotherapy, deserving surgical resection for uncommon low-stage tumors.
  • Since evidence has been accumulated that neuroendocrine tumors of the lung are supplied with a wide array of peptide receptors detectable on cell membranes by immunohistochemical methods, innovative strategies for diagnosis and radiometabolic therapy have been devised to target these molecules for the correct clinical management of the patients.
  • In this paper, the structural and functional aspects and the clinical applications of the detection of several peptide receptors in pulmonary neuroendocrine tumors will be reviewed, including somatostatin receptors, vasoactive intestinal peptide/pituitary adenylate cyclase activating peptide family receptors, cholecystokinin /gastrin receptors, bombesin/gastrin releasing peptide receptors, neurotensin receptors, substance P receptors, neuroepeptide Y receptors, calcitonin/calcitonin gene-related peptide receptors, atrial natriuretic peptide receptors, glucagon-like-peptide-1 receptors, oxytocin receptors and endothelin receptors.
  • Only a detailed knowledge of the peptide receptor distribution in these tumor types, especially in uncommon neoplasms such as atypical carcinoids and large cell neuroendocrine carcinomas, is pivotal for planning the most adequate interventions for the patients' diagnosis and therapy.
  • [MeSH-minor] Drug Delivery Systems / methods. Humans. Radiopharmaceuticals / pharmacokinetics. Radiopharmaceuticals / therapeutic use

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  • (PMID = 17043625.001).
  • [ISSN] 1824-4785
  • [Journal-full-title] The quarterly journal of nuclear medicine and molecular imaging : official publication of the Italian Association of Nuclear Medicine (AIMN) [and] the International Association of Radiopharmacology (IAR), [and] Section of the Society of Radiopharmaceutical Chemistry and Biology
  • [ISO-abbreviation] Q J Nucl Med Mol Imaging
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Radioisotopes; 0 / Radiopharmaceuticals; 0 / Receptors, Peptide
  • [Number-of-references] 166
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7. Vomachka AJ, Pratt SL, Lockefeer JA, Horseman ND: Prolactin gene-disruption arrests mammary gland development and retards T-antigen-induced tumor growth. Oncogene; 2000 Feb 21;19(8):1077-84
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  • [Title] Prolactin gene-disruption arrests mammary gland development and retards T-antigen-induced tumor growth.
  • Prolactin (PRL), interacting with other hormones from the pituitary, gonad, and placenta, activates specific signals that drive the appropriately timed morphological and functional development of the mammary gland.
  • Replacement therapy with PRL injections stimulated a modest degree of lobular budding and ductal arborization (3.75+/-0.9).
  • Pituitary transplants to the kidney capsule of PRL-/- mice restored lobular budding and ductal arborization, to the full extent of that seen in control animals (20. 3+/-5.5).
  • Pregnancy, established by mating progesterone-treated PRL-/- females with PRL-/- males, led to complete morphological development of the mammary gland, appropriate to the gestational stage.
  • PRL treatment stimulated tyrosine phosphorylation and DNA binding activity of Stat5a, but not Stat1 in PRL-/- or PRL+/- females, and Stat5a, but not Stat1, was elevated by estradiol within 24 h.
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Animals. DNA-Binding Proteins / drug effects. DNA-Binding Proteins / metabolism. Female. Mice. Mice, Mutant Strains. Mice, Transgenic. Phosphorylation / drug effects. Pituitary Gland / transplantation. Pregnancy. STAT1 Transcription Factor. STAT5 Transcription Factor. Trans-Activators / drug effects. Trans-Activators / metabolism. Tyrosine / metabolism

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  • (PMID = 10713693.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0 / Antigens, Polyomavirus Transforming; 0 / DNA-Binding Proteins; 0 / Milk Proteins; 0 / STAT1 Transcription Factor; 0 / STAT5 Transcription Factor; 0 / Stat1 protein, mouse; 0 / Stat5a protein, mouse; 0 / Trans-Activators; 42HK56048U / Tyrosine; 9002-62-4 / Prolactin
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8. Perrin G, Stevenaert A, Jouanneau E: [Technical aspects and surgical strategy for removal of corticotroph pituitary adenoma]. Neurochirurgie; 2002 May;48(2-3 Pt 2):186-214
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  • [Title] [Technical aspects and surgical strategy for removal of corticotroph pituitary adenoma].
  • The development of transsphenoidal microsurgery and the refinement of endocrinological and radiological diagnostic procedures have afforded therapeutic options appropriate for each individual case in patients with pituitary-dependent hypercortisolism.
  • Compared with other secreting pituitary tumors, the corticotroph adenoma seems to be the most biologically active tumor.
  • Clinical evidence of hypercortisolism mainly occurs at an early stage of tumor growth when the tumor is very small, below the detection threshold of modern imaging techniques.
  • While the treatment of large tumors remains difficult due to the non-discrete boundary lines of the tumor and extension or invasion, surgical removal of very tiny tumors requires reliable preoperative or peroperative identification in order to achieve total tumor resection for clinical remission and pituitary preservation to prevent hypopituitarism.
  • We report here the state-of-the-art of surgical management of corticotroph pituitary adenoma focusing on preoperative radiological and biological data required for performing guided intrasellar surgical exploration and reliable tumor identification.
  • Different technical aspects of the nasosphenoidal approaches are reported as well as the modified transdiaphragmatic or transtubercular transcisternal approaches to tumors in a suprasellar localization or lying along the pituitary stalk.
  • Guidelines are given for peroperative tumor identification with macroscopic assessment or histological control with frozen section biopsies.
  • Different techniques for tumor removal are discussed from selective microadenomectomy to enlarged pituitary resection and total hypophysectomy.
  • Methods for preoperative guidance of total tumor removal are proposed including histological or biological assessment of normal adjacent pituitary tissue. the strategy of surgical intrasellar exploration and tumor resection is outlined using a set of algorithms.
  • The first is devoted to positive preoperative documentation of the tumor.
  • The second is proposed for the surgical scenario where there is no preoperative MRI evidence of the tumor.
  • Revision surgical management after surgical failure or tumor recurrence is described.
  • Special guidelines for surgical treatment of large clinically silent corticotroph macroadenomas are given with emphasis on the high risk of recurrence in comparison with other silent pituitary tumors such as gonadotroph or immunonegative adenomas.
  • [MeSH-major] Adenoma / surgery. Cushing Syndrome / surgery. Hypophysectomy / methods. Pituitary Neoplasms / surgery
  • [MeSH-minor] ACTH Syndrome, Ectopic / complications. ACTH Syndrome, Ectopic / surgery. Adrenocorticotropic Hormone / secretion. Anti-Bacterial Agents / therapeutic use. Cortisone / therapeutic use. Deamino Arginine Vasopressin / therapeutic use. Diabetes Insipidus / drug therapy. Diabetes Insipidus / etiology. Diagnostic Imaging. Endoscopy. Humans. Magnetic Resonance Imaging. Petrosal Sinus Sampling. Postoperative Complications / prevention & control. Premedication. Reoperation

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  • (PMID = 12058125.001).
  • [ISSN] 0028-3770
  • [Journal-full-title] Neuro-Chirurgie
  • [ISO-abbreviation] Neurochirurgie
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 9002-60-2 / Adrenocorticotropic Hormone; ENR1LLB0FP / Deamino Arginine Vasopressin; V27W9254FZ / Cortisone
  • [Number-of-references] 191
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9. Zieliński G, Podgórski JK, Koziarski A, Warczyńska A, Zgliczyński W, Makowska A: [Surgical treatment of invasive pituitary adenomas (somatotropinoma or corticotropinoma)]. Neurol Neurochir Pol; 2003 Nov-Dec;37(6):1239-55
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  • [Title] [Surgical treatment of invasive pituitary adenomas (somatotropinoma or corticotropinoma)].
  • [Transliterated title] Leczenie operacyjne czynnych hormonalnie (wydzielajacych GH lub ACTH) inwazyjnych gruczolaków przysadki mózgowej.
  • AIM OF THE STUDY: To evaluate efficiency of the transcranial epidural approach in the treatment of invasive GH- or ACTH-secreting pituitary adenomas with extension to the cavernous sinus.
  • MATERIAL AND METHODS: During the past two years (from January 2000 to December 2001) 14 patients with invasive GH- or ACTH-secreting pituitary adenomas extending to the cavernous sinus were operated on using the transcranial epidural approach.
  • Parasellar extension of the tumor was measured using the Knosp scale--in all the cases there was an extension to the cavernous sinus, in stage III (4 patients) or stage IV (10 patients).
  • There was no deterioration of pituitary function and no cases of diabetes insipidus in our group.
  • CONCLUSION: Transcranial epidural approach is an alternative to radiotherapy and/or prolonged medication in the treatment of invasive GH- or ACTH-secreting pituitary adenomas.
  • [MeSH-major] Adenoma / surgery. Adrenocorticotropic Hormone / secretion. Growth Hormone / secretion. Neurosurgical Procedures / methods. Pituitary Neoplasms / surgery
  • [MeSH-minor] Adult. Aged. Cavernous Sinus / pathology. Female. Humans. Hypophysectomy / methods. Male. Middle Aged. Neoplasm Invasiveness. Retrospective Studies. Treatment Outcome

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  • (PMID = 15174237.001).
  • [ISSN] 0028-3843
  • [Journal-full-title] Neurologia i neurochirurgia polska
  • [ISO-abbreviation] Neurol. Neurochir. Pol.
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone; 9002-72-6 / Growth Hormone
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10. Kadashev BA, Kutin MA, Kalinin PL, Trunin IuK, Alekseev SN, Shkarubo AN: [Comparative assessment of the results of different surgical treatments in patients with pituitary adenomas infiltrating the cavernous sinus]. Zh Vopr Neirokhir Im N N Burdenko; 2004 Jul-Sep;(3):14-7; discussion 17
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  • [Title] [Comparative assessment of the results of different surgical treatments in patients with pituitary adenomas infiltrating the cavernous sinus].
  • Benign pituitary tumors or adenomas are highly common, occasionally inclined to infiltrate the adjacent structures, the cavernous sinus in particular.
  • Despite the fact that drug and radiation therapy are at present widely used treatments, surgical procedures remain highly topical.
  • Different modifications of two basic surgical methods (transcranial intradural and transsphenoidal) that fail to completely remove a tumor from the cavernous sinus in most cases are mostly frequently used as before.
  • Attempts to improve surgical procedures and introduction of current technologies have led to the emergence of an extradural method for tumor removal from the cavernous sinus and to the introduction of endoscopic monitoring during transsphenoidal operations.
  • A strategy of two-stage removal of pituitary tumors has simultaneously been developed.
  • The paper presents the results of surgical treatment of 297 patients with pituitary adenomas growing into the cavernous sinus, by using currently available procedures: transsphenoidal, transcranial intradural, and intra-extradural, and two-stage ones.
  • The findings have confirmed that transsphenoidal removal of pituitary adenomas is the safest method.
  • However, this method has a number of limitations in cases with tumor being grown into the cavernous sinus especially when there is a medial displacement of the intracavernous segment of the internal carotid artery.
  • Moreover, secondary tumor nodes that may be removed by transcranial intradural access are a contraindication to its use.
  • With this, attempts to remove a tumor from the cavernous sinus fail to ensure the desired completeness of removal from the cavernous sinus.
  • The application of an intra-extradural access is the most adequate procedure for tumor removal from the cavernous sinus.
  • The two-stage removal is the most adequate procedure in cases of simultaneously significant spread of a tumor intracranially and into the structures of the base of the skull.
  • [MeSH-major] Adenoma / surgery. Cavernous Sinus / pathology. Neurosurgical Procedures / methods. Pituitary Neoplasms / surgery. Vascular Neoplasms / surgery

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  • (PMID = 15490633.001).
  • [ISSN] 0042-8817
  • [Journal-full-title] Zhurnal voprosy neĭrokhirurgii imeni N. N. Burdenko
  • [ISO-abbreviation] Zh Vopr Neirokhir Im N N Burdenko
  • [Language] rus
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Russia
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11. Bevan JS, Atkin SL, Atkinson AB, Bouloux PM, Hanna F, Harris PE, James RA, McConnell M, Roberts GA, Scanlon MF, Stewart PM, Teasdale E, Turner HE, Wass JA, Wardlaw JM: Primary medical therapy for acromegaly: an open, prospective, multicenter study of the effects of subcutaneous and intramuscular slow-release octreotide on growth hormone, insulin-like growth factor-I, and tumor size. J Clin Endocrinol Metab; 2002 Oct;87(10):4554-63
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  • [Title] Primary medical therapy for acromegaly: an open, prospective, multicenter study of the effects of subcutaneous and intramuscular slow-release octreotide on growth hormone, insulin-like growth factor-I, and tumor size.
  • There are few data on the use of the somatostatin analog octreotide (Oct) as primary medical therapy.
  • For the first 24 wk (phase 1), patients received sc Oct in an initial dose of 100 microg, 3 times daily, increased to 200 micro g three times daily after 4 wk in the 13 patients whose mean serum GH remained greater than 5 mU/liter (2 microg/liter).
  • Five-point GH profiles were performed at 0, 4, 12, and 24 wk, and high resolution pituitary imaging using a standard protocol was performed at 0, 12, and 24 wk (magnetic resonance imaging in 25 patients and computed tomography in 2).
  • Tumor dimensions and volumes were calculated by a central, reporting neuroradiologist, and the results were audited by a second, independent neuroradiologist.
  • Further GH profiles were performed at 36 and 48 wk, and pituitary imaging was performed at 48 wk.
  • All 27 tumors shrank during sc Oct; for microadenomas the median tumor volume reduction was 49% (range, 12-73), and for macroadenomas it was 43% (range, 6-92).
  • In the 15 patients given Oct-LAR (10 macroadenomas), wk 48 scans showed a further overall median tumor volume reduction of 24%.
  • At the end of the study 79% of patients had mean serum GH levels below 5 mU/liter, 53% had normal IGF-I levels, and 73% showed greater than 30% tumor shrinkage.
  • Twenty-nine percent of patients achieved all 3 targets, but no patient with pretreatment GH levels above 50 mU/liter did so at any stage of the study.
  • Primary medical therapy with Oct offers the prospect of normalization of GH/IGF-I levels together with substantial tumor shrinkage in a significant subset of acromegalic patients.
  • [MeSH-major] Acromegaly / drug therapy. Antineoplastic Agents, Hormonal / administration & dosage. Human Growth Hormone / blood. Insulin-Like Growth Factor I / analysis. Octreotide / administration & dosage. Pituitary Neoplasms / pathology
  • [MeSH-minor] Adenoma / drug therapy. Adenoma / pathology. Adenoma / physiopathology. Adult. Aged. Delayed-Action Preparations. Female. Humans. Injections, Intramuscular. Injections, Subcutaneous. Magnetic Resonance Imaging. Male. Middle Aged. Pituitary Gland, Anterior / pathology. Pituitary Gland, Anterior / physiopathology. Prospective Studies. Tomography, X-Ray Computed

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  • (PMID = 12364434.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Delayed-Action Preparations; 12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I; RWM8CCW8GP / Octreotide
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12. Seiz M, Radek M, Buslei R, Kreutzer J, Hofmann B, Kottler U, Doerfler A, Nimsky C, Fahlbusch R: Alveolar rhabdomyosarcoma of the clivus with intrasellar expansion: Case report. Zentralbl Neurochir; 2006 Nov;67(4):219-22
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  • However, a primarily intracranial localization of this tumor entity is rare.
  • We report on a 3-year-old boy presenting with double vision due to left VI (th) nerve palsy.
  • MRI scans visualized an enhancing mass lesion in the upper clivus compressing the cavernous sinus and the pituitary gland.
  • Staging identified a metastatic lesion in the fourth thoracic vertebra resulting in the diagnosis of stage IV disease.
  • Treatment modality included stereotactic radio- and chemotherapy.
  • [MeSH-major] Pituitary Neoplasms / surgery. Rhabdomyosarcoma / surgery
  • [MeSH-minor] Abducens Nerve Diseases / etiology. Abducens Nerve Diseases / pathology. Adrenocorticotropic Hormone / deficiency. Angiography. Antineoplastic Agents / administration & dosage. Antineoplastic Agents, Phytogenic / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain / pathology. Carboplatin / administration & dosage. Child, Preschool. Etoposide / administration & dosage. Human Growth Hormone / deficiency. Humans. Magnetic Resonance Imaging. Male. Radiosurgery. Sella Turcica / pathology. Sella Turcica / surgery. Spine / pathology

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  • (PMID = 17139605.001).
  • [ISSN] 0044-4251
  • [Journal-full-title] Zentralblatt für Neurochirurgie
  • [ISO-abbreviation] Zentralbl. Neurochir.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Phytogenic; 12629-01-5 / Human Growth Hormone; 6PLQ3CP4P3 / Etoposide; 9002-60-2 / Adrenocorticotropic Hormone; BG3F62OND5 / Carboplatin
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13. Fleseriu M, Delashaw JB Jr, Cook DM: Acromegaly: a review of current medical therapy and new drugs on the horizon. Neurosurg Focus; 2010 Oct;29(4):E15
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acromegaly: a review of current medical therapy and new drugs on the horizon.
  • Acromegaly is a disease that results from a growth hormone (GH)–secreting pituitary tumor.
  • Clinically, the disease is characterized by excessive skeletal growth, soft tissue enlargement with disfigurement, and increased risk of cardiovascular death.
  • The goals of treatment are the removal or reduction of the tumor mass via surgery and normalization of GH secretion.
  • Another treatment goal is the preservation of normal pituitary function if possible.
  • Transsphenoidal surgery by an experienced neurosurgeon is usually the first line of therapy, especially for small tumors.
  • Surgeon expertise is crucial for outcome, with dedicated pituitary surgeons having better results.
  • However, overall cure rates remain low because patients with these tumors usually present at an incurable stage.
  • Therefore, medical therapy to control excess GH secretion plays a significant role in a large proportion of patients with acromegaly who are not cured by surgery or other forms of therapy, such as radiotherapy, and/or are awaiting the effects of radiotherapy.
  • In the past decade major progress has occurred in the development of highly specific and selective pharmacological agents that have greatly facilitated more aggressive management of active acromegaly.
  • Treatment approach should be individualized and take into consideration a patient's tumor size and location, symptoms, comorbid conditions, and preferences.
  • Because a surgical cure can be difficult to achieve, all patients, even those with what seems to be a clinically and biochemically inactive disease, should undergo long-term biochemical testing and pituitary MR imaging.
  • [MeSH-major] Acromegaly / drug therapy. Acromegaly / surgery. Adenoma / drug therapy. Adenoma / surgery. Human Growth Hormone / secretion. Pituitary Neoplasms / drug therapy. Pituitary Neoplasms / surgery
  • [MeSH-minor] Humans. Insulin-Like Growth Factor I / analysis. Insulin-Like Growth Factor I / secretion. Octreotide / therapeutic use. Radiotherapy, Adjuvant / methods

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  • (PMID = 20887125.001).
  • [ISSN] 1092-0684
  • [Journal-full-title] Neurosurgical focus
  • [ISO-abbreviation] Neurosurg Focus
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I; RWM8CCW8GP / Octreotide
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14. Kumar SS, Ayuk J, Murray RD: Current therapy and drug pipeline for the treatment of patients with acromegaly. Adv Ther; 2009 Apr;26(4):383-403
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  • [Title] Current therapy and drug pipeline for the treatment of patients with acromegaly.
  • The etiology is almost exclusively an underlying pituitary adenoma.
  • Current therapeutic interventions include surgery, radiotherapy, and medical therapy.
  • Radiotherapy is efficacious in controlling tumor growth and GH secretion; still, achievement of biochemical targets may take up to a decade and a number of safety issues have been raised with this treatment modality.
  • Medical therapy, therefore, has an important role as adjuvant therapy in patients who fail to achieve control with surgery, or while awaiting the effects of radiotherapy to be realized.
  • Furthermore, medical therapy is increasingly being used as primary therapy.
  • Current medical therapies include dopaminergic agonists, somatostatin analogs, and GH receptor (GHR) antagonists.
  • The currently available GHR antagonist pegvisomant effectively controls insulin-like growth factor-I levels in over 90% of patients; however, it has no effect on the tumor itself and has considerable financial implications.
  • Other innovations to improve convenience of currently available drugs are also being investigated.
  • CONCLUSION: Significant advances in under standing of the somatostatin and dopaminergic system have aided drug development.
  • This may lead to new clinically available therapies enabling control of acromegaly in a larger proportion of patients, and at an earlier stage in their disease management.
  • [MeSH-major] Acromegaly / drug therapy
  • [MeSH-minor] Adenoma / complications. Combined Modality Therapy. Dopamine / analogs & derivatives. Dopamine / therapeutic use. Dopamine Agonists / therapeutic use. Drug Discovery. Drug Evaluation. Human Growth Hormone / analogs & derivatives. Human Growth Hormone / therapeutic use. Humans. Insulin-Like Growth Factor Binding Protein 1 / blood. Insulin-Like Growth Factor Binding Protein 1 / drug effects. Pituitary Neoplasms / complications. Radiotherapy / methods. Radiotherapy / trends. Receptors, Dopamine D2 / drug effects. Receptors, Somatotropin / antagonists & inhibitors. Somatostatin / analogs & derivatives. Somatostatin / therapeutic use. Treatment Outcome

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  • (PMID = 19444656.001).
  • [ISSN] 1865-8652
  • [Journal-full-title] Advances in therapy
  • [ISO-abbreviation] Adv Ther
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BIM 23A760; 0 / Dopamine Agonists; 0 / Insulin-Like Growth Factor Binding Protein 1; 0 / Receptors, Dopamine D2; 0 / Receptors, Somatotropin; 0 / pegvisomant; 12629-01-5 / Human Growth Hormone; 51110-01-1 / Somatostatin; 98H1T17066 / pasireotide; VTD58H1Z2X / Dopamine
  • [Number-of-references] 93
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15. Iwai Y, Yamanaka K, Ishiguro T, Morikawa T, Matsuzaka Y, Komiyama M, Yasui T: [Results of treatment for male prolactinomas]. No Shinkei Geka; 2002 Dec;30(12):1285-92
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  • [Title] [Results of treatment for male prolactinomas].
  • We evaluated the results of medical treatment for male prolactinomas.
  • The age was 25 to 54 years old (mean 43 years) and the chief clinical symptoms were visual acuity/field defect in three patients, pituitary apoplexy in one patient, disturbance of ejection in one patient, generalized convulsion in one patient, headache in one patient and general fatigue in one patient.
  • In only one patient, the operation was performed due to pituitary apoplexy.
  • All the patients were treated by medication, with bromocriptine being used in seven patients and terguride in one.
  • The follow-up period was 0.8 to 13 years (mean 5.9 years) and, in all patients, the medical treatment was continued.
  • The tumor decreased in size in all patients and the serum prolactin level at the last follow-up observation was 0.5 to 70.5 ng/ml (mean 26.9 ng/ml).
  • All the neurological symptoms disappeared in the early stage of treatment.
  • As for the complications of medical treatment; in one patient, orthostatic hypotension occurred during the initial administration of bromocriptine and one patient suffered CSF leakage two months after the administration of bromocriptine, so the repair of the sella floor by transsphenoidal surgery was necessary.
  • The medical treatment for male prolactinomas is effective for a long term and should be the primary treatment for the male prolactinomas.
  • In conclusion, patients can maintain a good quality of life for a long time by using dopamine agonists.
  • [MeSH-major] Bromocriptine / therapeutic use. Dopamine Agonists / therapeutic use. Lisuride / analogs & derivatives. Lisuride / therapeutic use. Pituitary Neoplasms / drug therapy. Prolactinoma / drug therapy
  • [MeSH-minor] Adult. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Pituitary Apoplexy / drug therapy. Prolactin / blood

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  • (PMID = 12491580.001).
  • [ISSN] 0301-2603
  • [Journal-full-title] No shinkei geka. Neurological surgery
  • [ISO-abbreviation] No Shinkei Geka
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Dopamine Agonists; 21OJT43Q88 / dironyl; 3A64E3G5ZO / Bromocriptine; 9002-62-4 / Prolactin; E0QN3D755O / Lisuride
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16. Nakagawa H, Yamamoto K: [A case of small cell lung cancer complicated by Cushing syndrome]. Nihon Kokyuki Gakkai Zasshi; 2008 Mar;46(3):210-5
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  • After a systemic examination, Stage IV small cell lung cancer with Cushing's syndrome was diagnosed.
  • Marked increases in ACTH levels were observed, but no abnormality was found in the pituitary MRI findings, and therefore ACTH-producing small cell lung cancer was suspected.
  • Chemotherapy was administered in addition to appropriate treatment for Cushing's syndrome.
  • The tumor temporarily began to decrease in size, but hypercortisolemia remained, and thus adrenal hormone synthesis-inhibiting therapy was concurrently administered.
  • Therefore, from an early stage, it is believed that adrenal cortical hormone synthesis-inhibiting therapy should be performed concurrently with chemotherapy, if hypercortisolemia cannot be controlled by radiation and chemotherapy alone.

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  • (PMID = 18409568.001).
  • [ISSN] 1343-3490
  • [Journal-full-title] Nihon Kokyūki Gakkai zasshi = the journal of the Japanese Respiratory Society
  • [ISO-abbreviation] Nihon Kokyuki Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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17. Kianmanesh R, O'toole D, Sauvanet A, Ruszniewski P, Belghiti J: [Surgical treatment of gastric, enteric, and pancreatic endocrine tumors Part 1. Treatment of primary endocrine tumors]. J Chir (Paris); 2005 May-Jun;142(3):132-49
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  • [Title] [Surgical treatment of gastric, enteric, and pancreatic endocrine tumors Part 1. Treatment of primary endocrine tumors].
  • [Transliterated title] Traitement chirurgical des tumeurs endocrines gastro-entéro-pancréatiques.
  • They are classified into two principal types: gastrointestinal ET's (formerly called carcinoid tumors) which are the most common, and pancreaticoduodenal ET's.
  • Poorly-differentiated ET's have a poor prognosis and are treated by chemotherapy.
  • Surgical excision is the only curative treatment of well-differentiated ET's.
  • The surgical goals are to: 1. prolong survival by resecting the primary tumor and any nodal or hepatic metastases, 2. control the symptoms related to hormonal secretion, 3. prevent or treat local complications.
  • The most common sites of gastrointestinal ET's ( carcinoids) are the appendix and the rectum; these are often small (<1 cm), benign, and discovered fortuitously at the time of appendectomy or colonoscopic removal.
  • They are usually malignant and of advanced stage at diagnosis presenting as a palpable or obstructing mass or as liver metastases.
  • Insulinoma and gastrinoma (cause of the Zollinger-Ellison syndrome) are the most common functional ET's. 80% are sporadic; in these cases, tumor size, location, and malignant potential determine the type of resection which may vary from a simple enucleation to a formal pancreatectomy.
  • In 10-20% of cases, pancreaticoduodenal ET presents in the setting of multiple endocrine neoplasia (NEM type I), an autosomal-dominant genetic disease with multifocal endocrine involvement of the pituitary, parathyroid, pancreas, and adrenal glands.
  • For insulinoma with NEM-I, enucleation of lesions in the pancreatic head plus a caudal pancreatectomy is the most appropriate procedure.
  • [MeSH-major] Carcinoid Tumor / surgery. Carcinoma, Islet Cell / surgery. Carcinoma, Neuroendocrine / surgery. Insulinoma / surgery. Intestinal Neoplasms / surgery. Multiple Endocrine Neoplasia Type 1 / surgery. Pancreatic Neoplasms / surgery. Stomach Neoplasms / surgery. Zollinger-Ellison Syndrome / surgery

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  • (PMID = 16142076.001).
  • [ISSN] 0021-7697
  • [Journal-full-title] Journal de chirurgie
  • [ISO-abbreviation] J Chir (Paris)
  • [Language] fre
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Number-of-references] 236
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18. Riffaud L, Saikali S, Leray E, Hamlat A, Haegelen C, Vauleon E, Lesimple T: Survival and prognostic factors in a series of adults with medulloblastomas. J Neurosurg; 2009 Sep;111(3):478-87
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  • Staging according to the Chang classification showed 4 patients with tumors invading the brainstem (2 with Stage T3b and 2 with Stage T4), 3 patients with metastases (2 with Stage M2 and 1 with Stage M3), and 1 patient in whom the stage was unknown (Stage MX) who died 10 days postoperatively.
  • All patients except the one whose status was classified as Stage MX underwent craniospinal radiotherapy at our institution.
  • Seven patients received chemotherapy before radiotherapy.
  • The median overall survival time was 17.7 years.
  • The median event-free survival time was 17.9 years.
  • Univariate analysis showed that survival was significantly correlated with sex (women had a better prognosis than men) and M stage (patients without metastases had a better outcome).
  • Patient age, duration of symptoms, Karnofsky Performance Scale score at presentation, hydrocephalus, tumor location, brainstem invasion, extent of resection, histological subtype, preradiotherapy chemotherapy, risk group, and period of presentation were not significant variables.
  • Multivariate analysis identified sex and M stage as well as the period of presentation as independent prognostic factors for overall and event-free survival times.
  • Eleven patients suffered tumor recurrence within a median time of 4.2 years.
  • All patients in whom the tumor recurred have died despite aggressive treatments.
  • The median survival time after diagnosis of recurrence was 2.5 years.
  • Questionnaires on quality of life and cognition showed high scores in favor of limited negative effects in the perception of mental and physical health after treatment.
  • The authors observed 1 supposed second malignancy (thyroid carcinoma) and no evidence of pituitary dysfunction.
  • Tumor recurrences should be treated with aggressive therapies as some patients may have sustained response.
  • Adjuvant chemotherapy should be given to high-risk patients, but its role in reducing recurrences, particularly distant ones, remains unclear in the standard-risk group.

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  • (PMID = 19231932.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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19. 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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  • OBJECTIVE: The objective of this study was to examine the significance of somatotroph adenoma type on response to SSA.
  • 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

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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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20. Kellner O, Voigt W, Schneyer U, Dempke W, Schmoll HJ: HCG induced hyperthyreosis in germ cell cancer. Anticancer Res; 2000 Nov-Dec;20(6D):5135-8
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  • AFP (the product of normal yolk sac) and HCG (produced by trophoblastic tissues) are frequently produced by germ cell tumors.
  • The a-subunit of the glycoprotein HCG is identical to that of several pituitary glycoprotein hormones (e.g.
  • A 24-year old patient was admitted to our clinic because of a widespread recurrence of a germ cell tumor (stage IIIC, Lugano classification).
  • The patient was then entered in our phase-II-study for relapsing germ cell carcinomas using a high-dose chemotherapy regime (paclitaxel 175 mg/m2, ifosfamide 9.000 mg/m2, carboplatin 900 mg/m2, etoposide 900 mg/m2) with subsequent retransfusion of collected stem cells.
  • After three courses of this protocol an excellent partial remission of the tumor lesions was achieved and the HCG value dramatically decreased.
  • In this case report we have demonstrated a clear positive correlation between HCG levels and thyroidal hormones in a patient with germ cell tumor suggesting a direct stimulation of hormone producing thyroidal cells by HCG, however, this was not associated with clinical symptoms of hyperthyreosis.
  • [MeSH-minor] Adult. Humans. Male. Thyroid Gland / drug effects

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  • (PMID = 11326684.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Chorionic Gonadotropin
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21. Sultanem K, Shu HK, Xia P, Akazawa C, Quivey JM, Verhey LJ, Fu KK: Three-dimensional intensity-modulated radiotherapy in the treatment of nasopharyngeal carcinoma: the University of California-San Francisco experience. Int J Radiat Oncol Biol Phys; 2000 Oct 1;48(3):711-22
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  • [Title] Three-dimensional intensity-modulated radiotherapy in the treatment of nasopharyngeal carcinoma: the University of California-San Francisco experience.
  • PURPOSE: To review our experience with three-dimensional intensity-modulated radiotherapy (IMRT) in the treatment of nasopharyngeal carcinoma.
  • According to the 1997 American Joint Committee on Cancer staging classification, 4 (12%) patients had Stage I disease, 6 (17%) had Stage II, 11 (32%) had Stage III, and 14 (40%) had Stage IV disease.
  • IMRT of the primary tumor was delivered using one of the following three techniques:.
  • A forward 3D treatment-planning system was used for the first two methods, and an inverse treatment planning system was used for the third method.
  • The prescribed dose was 65-70 Gy to the gross tumor volume (GTV) and positive neck nodes, 60 Gy to the clinical target volume (CTV), and 50-60 Gy to the clinically negative neck.
  • Eleven (32%) patients had fractionated high-dose-rate intracavitary brachytherapy boost to the primary tumor 1-2 weeks following external beam radiotherapy.
  • Acute and late normal tissue effects were graded according to the Radiation Therapy Oncology Group (RTOG) radiation morbidity scoring criteria.
  • Only 1 patient had a transient Grade 4 soft-tissue necrosis.
  • At 24 months after treatment, 50% of the evaluated patients had Grade 0, 50% had Grade 1, and none had Grade 2 xerostomia.
  • Analysis of the dose-volume histograms (DVHs) showed that the average maximum, mean, and minimum dose delivered were 79.5 Gy, 75.8 Gy, and 56.5 Gy to the GTV, and 78.9 Gy, 71.2 Gy, and 45.4 Gy to the CTV, respectively.
  • The average dose to 5% of the brain stem, optic chiasm, and right and left optic nerves was 48.3 Gy, 23.9 Gy, 15.0 Gy, and 14.9 Gy, respectively.
  • The average dose to 1 cc of the cervical spinal cord was 41.7 Gy.
  • The average dose to 50% of the right and left parotids, pituitary, right and left T-M joints, and ears was 43.
  • 2 Gy, 41.0 Gy, 46.3 Gy, 60.5 Gy, 58.3 Gy, 52.0 Gy, and 52.2 Gy, respectively.
  • CONCLUSION: 3D intensity-modulated radiotherapy provided improved target volume coverage and increased dose to the gross tumor with significant sparing of the salivary glands and other critical normal structures.
  • Local-regional control rate with combined IMRT and chemotherapy was excellent, although distant metastasis remained unabated.
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Analysis of Variance. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Disease Progression. Female. Follow-Up Studies. Humans. Male. Middle Aged. Neoplasm Staging. Radiation Injuries / pathology. Radiotherapy Dosage. Survival Analysis. Xerostomia / etiology

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  • (PMID = 11020568.001).
  • [ISSN] 0360-3016
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
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22. Nikou GC, Toubanakis C, Nikolaou P, Giannatou E, Marinou K, Safioleas M, Karamanolis D: Gastrinomas associated with MEN-1 syndrome: new insights for the diagnosis and management in a series of 11 patients. Hepatogastroenterology; 2005 Nov-Dec;52(66):1668-76
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  • Among 33 pts with ZES, we present in this study 11 pts with ZES and MEN-1 syndrome, describing our diagnostic and therapeutic approach.
  • A variety of other gastrointestinal peptides, as well as the general neuroendocrine tumor marker, Chromogranin-A (CgA) were also estimated.
  • The diagnosis of MEN-1 was based upon the presence of the other two MEN-1 related endocrinopathies (hyperparathyroidism, pituitary adenomas), revealed by estimation of several hormones (PTH, Prolactin, ACTH etc.) and performance of imaging studies of the pituitary and parathyroid glands.
  • RESULTS: At the time of presentation, 91% pts, had symptoms of peptic ulcer disease, refractory to treatment, while a history of colicky abdominal pain due to nephrolithiasis was also reported by 45% pts.
  • Serum gastrin levels at the time of diagnosis were greater than 1000pg/mL in 63.5% pts, while at the same time serum CgA levels were greater than 10 times the upper normal limit (<98ng/mL) in all pts.
  • OCTREOSCAN and EUS revealed the primary tumor (in duodenum or pancreas) in 64% pts, in whom conventional methods showed no abnormalities at the same time.
  • Parathyroid adenomas, pituitary adenomas and bronchial carcinoids were revealed in 11, 3 and 1 pts respectively, which were treated surgically.
  • Also, surgical treatment of pancreatic or duodenal gastrinomas was performed in 54.5% pts, while pts who already had metastases (45%), or developed them during the follow-up period (18%), were treated by somatostatin analogues (63.6%) and chemotherapy (27.3%).
  • A precise preoperative localization of all pancreaticoduodenal lesions, in combination with a surgical exploration and management by experienced surgeons, seems to be curative in pts without distal metastases.
  • Non-surgical treatment with somatostatin analogues and chemotherapy in pts with progressive disease seem to stabilize the disease, although further studies are needed.
  • A close clinical and biochemical follow-up of all pts, as well as their family members, is necessary in order to reveal and treat all MEN-1 related endocrinopathies and especially PETs, in an early stage.
  • [MeSH-major] Digestive System Neoplasms / diagnosis. Digestive System Neoplasms / therapy. Gastrinoma / diagnosis. Gastrinoma / therapy. Multiple Endocrine Neoplasia Type 1 / diagnosis. Multiple Endocrine Neoplasia Type 1 / therapy
  • [MeSH-minor] Adult. Aged. Combined Modality Therapy. Diagnostic Imaging / methods. Duodenal Neoplasms / complications. Duodenal Neoplasms / diagnosis. Duodenal Neoplasms / therapy. Endosonography / methods. Female. Follow-Up Studies. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Pancreatic Neoplasms / complications. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / therapy. Positron-Emission Tomography. Risk Assessment. Sampling Studies. Stomach Neoplasms / complications. Stomach Neoplasms / diagnosis. Stomach Neoplasms / therapy. Tomography, X-Ray Computed. Treatment Outcome

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  • (PMID = 16334754.001).
  • [ISSN] 0172-6390
  • [Journal-full-title] Hepato-gastroenterology
  • [ISO-abbreviation] Hepatogastroenterology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
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23. Toledano Y, Rot L, Greenman Y, Orlovsky S, Pauker Y, Olchovsky D, Eliash A, Bardicef O, Makhoul O, Tsvetov G, Gershinsky M, Cohen-Ouaqnine O, Ness-Abramof R, Adnan Z, Ilany J, Guttmann H, Sapir M, Benbassat C, Shimon I: Efficacy of long-term lanreotide treatment in patients with acromegaly. Pituitary; 2009;12(4):285-93
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  • [Title] Efficacy of long-term lanreotide treatment in patients with acromegaly.
  • We investigated the effectiveness of lanreotide for the treatment of active acromegaly in a retrospectively multicenter case series including 53 patients (24 male, 29 female; mean age at diagnosis, 49.5 +/- 13.9 years) with acromegaly treated with lanreotide in nine different centers.
  • Mean tumor diameter was 20 +/- 13 mm; mean basal levels of growth hormone (GH) and insulin-like growth factor I (IGF-I) were 21.3 +/- 26.3 and 579 +/- 177 mug/l, respectively.
  • The primary mode of treatment was surgery in 70% of patients.
  • Twenty-nine patients received only lanreotide (Prolonged Release, Autogel), whereas 24 subjects were also treated with octreotide at another treatment stage.
  • Primary therapy with lanreotide was administered in five patients.
  • During 36 months of lanreotide treatment, mean IGF-I levels decreased from 443 +/- 238 to 276 +/- 147 mug/l (P < 0.001), and mean GH levels, from 5.2 +/- 6.4 to 3.2 +/- 3.0 mug/l (P < 0.001).
  • Lanreotide is an effective treatment for active acromegaly.
  • [MeSH-major] Acromegaly / drug therapy. Antineoplastic Agents / therapeutic use. Peptides, Cyclic / therapeutic use. Somatostatin / analogs & derivatives
  • [MeSH-minor] Adult. Female. Human Growth Hormone / metabolism. Humans. Male. Middle Aged. Retrospective Studies. Somatomedins / metabolism. Treatment Outcome

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  • [Cites] J Clin Endocrinol Metab. 1998 Oct;83(10):3419-26 [9768641.001]
  • [Cites] Clin Endocrinol (Oxf). 1994 Jul;41(1):95-102 [8050136.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Nov;83(11):3808-16 [9814451.001]
  • [Cites] Eur J Endocrinol. 2004 Sep;151(3):317-24 [15362960.001]
  • [Cites] Clin Endocrinol (Oxf). 2000 Nov;53(5):577-86 [11106918.001]
  • [Cites] J Clin Endocrinol Metab. 1994 Sep;79(3):724-9 [7521350.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Nov;88(11):5258-65 [14602759.001]
  • [Cites] J Clin Endocrinol Metab. 1994 Feb;78(2):398-403 [8106629.001]
  • [Cites] Eur J Endocrinol. 2004 Apr;150(4):473-80 [15080776.001]
  • [Cites] Clin Endocrinol (Oxf). 2008 Aug;69(2):299-305 [18248639.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Aug;90(8):4465-73 [15886238.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Jul;89(7):3099-102 [15240576.001]
  • [Cites] Clin Endocrinol (Oxf). 2006 Feb;64(2):209-14 [16430722.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Jul;87(7):3013-8 [12107192.001]
  • [Cites] Clin Endocrinol (Oxf). 2002 Jan;56(1):65-71 [11849248.001]
  • [Cites] J Endocrinol. 1997 Oct;155 Suppl 1:S17-9; discussion S21 [9389991.001]
  • [Cites] Clin Endocrinol (Oxf). 2002 Jan;56(1):73-7 [11849249.001]
  • [Cites] J Endocrinol. 1997 Oct;155 Suppl 1:S3-6; discussion S7-8 [9389989.001]
  • [Cites] Exp Clin Endocrinol Diabetes. 2005 Mar;113(3):139-44 [15789272.001]
  • [Cites] J Clin Endocrinol Metab. 1993 Mar;76(3):721-7 [8095269.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Jul;90(7):4081-6 [15886256.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Feb;89(2):667-74 [14764779.001]
  • [Cites] Eur J Endocrinol. 1999 Sep;141(3):267-71 [10474124.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Aug;93(8):2957-68 [18477663.001]
  • [Cites] Eur J Endocrinol. 2008 Aug;159(2):89-95 [18524797.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Nov;86(11):5240-4 [11701684.001]
  • [Cites] J Clin Endocrinol Metab. 1995 Nov;80(11):3267-72 [7593436.001]
  • [Cites] Clin Endocrinol (Oxf). 2005 Sep;63(3):342-9 [16117824.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Jan;87(1):99-104 [11788630.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Apr;93(4):1324-30 [18230660.001]
  • [Cites] Clin Endocrinol (Oxf). 1995 Apr;42(4):417-23 [7750196.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Feb;85(2):526-9 [10690849.001]
  • [Cites] Ann Oncol. 1999;10 Suppl 2:S17-21 [10399028.001]
  • [Cites] J Clin Endocrinol Metab. 1991 Feb;72(2):374-81 [1991807.001]
  • [Cites] Clin Endocrinol (Oxf). 1993 Jun;38(6):589-93 [8334745.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Sep;87(9):4054-8 [12213843.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Jun;91(6):2112-8 [16537687.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Nov;85(11):4099-103 [11095439.001]
  • [Cites] Presse Med. 1993 Mar 27;22(11):526-31 [8099735.001]
  • [Cites] J Clin Endocrinol Metab. 1995 Apr;80(4):1386-92 [7714115.001]
  • [Cites] Clin Endocrinol (Oxf). 1999 Sep;51(3):275-80 [10469005.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Jun;89(6):2789-96 [15181059.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Mar;90(3):1377-82 [15585548.001]
  • [Cites] Life Sci. 1995;56(5):333-42 [7530798.001]
  • [Cites] Eur J Endocrinol. 2004 Apr;150(4):489-95 [15080778.001]
  • [Cites] Metabolism. 1996 Aug;45(8 Suppl 1):67-71 [8769387.001]
  • [Cites] N Engl J Med. 2006 Dec 14;355(24):2558-73 [17167139.001]
  • [Cites] Clin Endocrinol (Oxf). 2007 Oct;67(4):512-9 [17555511.001]
  • (PMID = 19266287.001).
  • [ISSN] 1573-7403
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Peptides, Cyclic; 0 / Somatomedins; 0G3DE8943Y / lanreotide; 12629-01-5 / Human Growth Hormone; 51110-01-1 / Somatostatin
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24. Binder G, Weber S, Ehrismann M, Zaiser N, Meisner C, Ranke MB, Maier L, Wudy SA, Hartmann MF, Heinrich U, Bettendorf M, Doerr HG, Pfaeffle RW, Keller E, South German Working Group for Pediatric Endocrinology: Effects of dehydroepiandrosterone therapy on pubic hair growth and psychological well-being in adolescent girls and young women with central adrenal insufficiency: a double-blind, randomized, placebo-controlled phase III trial. J Clin Endocrinol Metab; 2009 Apr;94(4):1182-90
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  • [Title] Effects of dehydroepiandrosterone therapy on pubic hair growth and psychological well-being in adolescent girls and young women with central adrenal insufficiency: a double-blind, randomized, placebo-controlled phase III trial.
  • CONTEXT AND OBJECTIVE: The efficacy of oral dehydroepiandrosterone (DHEA) in the treatment of atrichia pubis and psychological distress in young females with central adrenal insufficiency is unknown.
  • Our study aimed to evaluate this therapy.
  • Inclusion criteria were ACTH deficiency plus two or more additional pituitary deficiencies, serum DHEA less than 400 ng/ml, and pubertal stage more than B2.
  • Exclusion criteria were cerebral radiation with more than 30 Gy, tumor remission less than 1 yr, amaurosis, hypothalamic obesity, psychiatric disorders, and unstable hormone medication.
  • INTERVENTION: Patients were randomized to placebo (n = 12) or 25 mg HPLC-purified DHEA/d (n = 11) orally for 12 months after stratification into a nontumor (n = 7) and a tumor group (n = 16).
  • MAIN OUTCOME MEASURES: Clinical scoring of pubic hair stage was performed at 0, 6, and 12 months (primary endpoint), and psychometrical evaluation (Symptom Check-List-90-R and the Centre for Epidemiological Studies-Depression Scale) at 0 and 12 months (secondary endpoint).
  • RESULTS: In the placebo group, four patients dropped out because of recurrence of craniopharyngioma, manifestation of type 1 diabetes, and change of residence (n = 2); in the DHEA group, one patient dropped out because of recurrent anxiety attacks.
  • DHEA substitution resulted in normalization of DHEA sulfate and androstanediol glucuronide morning serum levels 2 h after drug intake (P < 0.006), and of its 24 h urinary metabolite levels (P < 0.0001), placebo had no effect.
  • The DHEA group exhibited significant progress in pubic hair growth from Tanner stage I-III to II-V (mean: +1.5 stages), whereas the placebo group did not (relative risk 0.138; 95% confidence interval 0.021-0.914; P = 0.0046).
  • [MeSH-major] Adrenal Insufficiency / drug therapy. Adrenocorticotropic Hormone / deficiency. Dehydroepiandrosterone / therapeutic use. Hair / growth & development. Hypopituitarism / drug therapy
  • [MeSH-minor] Adolescent. Adult. Blood Pressure / drug effects. Blood Pressure / physiology. Brain Neoplasms / epidemiology. Double-Blind Method. Female. Humans. Hydrocortisone / therapeutic use. Obesity / epidemiology. Young Adult

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  • (PMID = 19126625.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase III; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 459AG36T1B / Dehydroepiandrosterone; 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
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25. Rekasi Z, Czompoly T, Schally AV, Boldizsar F, Varga JL, Zarandi M, Berki T, Horvath RA, Nemeth P: Antagonist of growth hormone-releasing hormone induces apoptosis in LNCaP human prostate cancer cells through a Ca2+-dependent pathway. Proc Natl Acad Sci U S A; 2005 Mar 1;102(9):3435-40
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  • JV-1-38 evoked prompt Ca2+ signal in a dose-dependent way (1-10 microM) and induced early stage of apoptosis in LNCaP human prostate cancer cells at a concentration effective in suppression of cell proliferation (10 microM) peaking after 3 h.
  • Unexpectedly, agonist GHRH(1-29)NH2, which elevates cytosolic free Ca2+ concentration in pituitary somatotrophs at nanomolar concentrations, failed to induce Ca2+ signal or apoptosis even at a 10-fold higher concentration (100 microM).
  • EDTA (10 mM) or nifedipine (10 microM) significantly reduced the Ca2+ signal and early stage of apoptosis induced by JV-1-38, supporting the view that the increase in intracellular Ca2+ in response to JV-1-38 occurs primarily through extracellular Ca2+ entry through voltage-operated Ca2+ channels.
  • Treatment with GHRH antagonists may offer a new approach to the therapy of prostate and other hormone-sensitive cancers.
  • [MeSH-major] Apoptosis / drug effects. Calcium / metabolism. Growth Hormone-Releasing Hormone / analogs & derivatives. Growth Hormone-Releasing Hormone / antagonists & inhibitors. Growth Hormone-Releasing Hormone / pharmacology. Prostatic Neoplasms / metabolism
  • [MeSH-minor] Cell Line, Tumor. Edetic Acid / pharmacology. Flow Cytometry. Humans. Male. Nifedipine / pharmacology. Phosphatidylserines / metabolism

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • Hazardous Substances Data Bank. Disodium EDTA .
  • Hazardous Substances Data Bank. Nifedipine .
  • Hazardous Substances Data Bank. ETHYLENEDIAMINE TETRAACETIC ACID .
  • Hazardous Substances Data Bank. DISODIUM CALCIUM EDTA .
  • Hazardous Substances Data Bank. CALCIUM, ELEMENTAL .
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  • [Cites] Expert Opin Investig Drugs. 2003 Aug;12(8):1385-94 [12882623.001]
  • [Cites] Peptides. 2001 Jun;22(6):879-86 [11390017.001]
  • [Cites] Cell Mol Life Sci. 2004 May;61(9):1042-68 [15112052.001]
  • [Cites] Eur J Endocrinol. 2004 Sep;151(3):391-6 [15362970.001]
  • [Cites] Int J Cancer. 2004 Nov 20;112(4):570-6 [15382037.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Oct 19;101(42):15160-5 [15469915.001]
  • [Cites] J Med Chem. 1976 Mar;19(3):423-5 [1255667.001]
  • [Cites] Biochem Biophys Res Commun. 1982 Nov 30;109(2):588-94 [6185122.001]
  • [Cites] Proc Natl Acad Sci U S A. 1988 Mar;85(5):1637-41 [3278323.001]
  • [Cites] J Biol Chem. 1989 May 15;264(14):8171-8 [2498308.001]
  • [Cites] Endocrinology. 1991 Jan;128(1):592-603 [1670926.001]
  • [Cites] Mol Endocrinol. 1992 Oct;6(10):1734-44 [1333056.001]
  • [Cites] Mol Endocrinol. 1993 Jan;7(1):77-84 [7680413.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Dec 6;91(25):12298-302 [7991622.001]
  • [Cites] J Immunol Methods. 1995 Jul 17;184(1):39-51 [7622868.001]
  • [Cites] Endocrinology. 1995 Sep;136(9):4147-50 [7649123.001]
  • [Cites] Ann N Y Acad Sci. 1996 Dec 26;805:184-203 [8993403.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Nov 24;95(24):14373-8 [9826707.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Jan 19;96(2):692-7 [9892695.001]
  • [Cites] Prostate. 2001 Oct 1;49(2):116-21 [11582590.001]
  • [Cites] Front Neuroendocrinol. 2001 Oct;22(4):248-91 [11587553.001]
  • [Cites] Anticancer Drugs. 2001 Oct;12(9):761-8 [11593058.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jan 8;99(1):196-200 [11773624.001]
  • [Cites] Endocrinology. 2002 Apr;143(4):1475-84 [11897706.001]
  • [Cites] Immunol Lett. 2002 Jun 3;82(1-2):159-64 [12008048.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jun 11;99(12):8054-9 [12060752.001]
  • [Cites] Lancet Oncol. 2002 May;3(5):298-302 [12067807.001]
  • [Cites] Prostate. 2002 Aug 1;52(3):173-82 [12111694.001]
  • [Cites] Peptides. 2002 Jun;23(6):1127-33 [12126741.001]
  • [Cites] Peptides. 2002 Jun;23(6):1187-94 [12126750.001]
  • [Cites] Trends Endocrinol Metab. 2002 Sep;13(7):299-303 [12163232.001]
  • [Cites] Endocrine. 2002 Jun;18(1):85-90 [12166629.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Sep 3;99(18):11866-71 [12186980.001]
  • [Cites] Regul Pept. 2002 Oct 15;108(2-3):47-53 [12220726.001]
  • [Cites] Cancer. 2002 Oct 15;95(8):1735-45 [12365022.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Oct;87(10):4707-14 [12364462.001]
  • [Cites] Breast Cancer Res Treat. 2003 Jan;77(1):15-26 [12602901.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Dec 21;96(26):14894-8 [10611309.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Jan 18;97(2):532-4 [10639112.001]
  • [Cites] Endocrinology. 2000 Jun;141(6):2120-8 [10830299.001]
  • [Cites] Breast Cancer Res Treat. 2000 Mar;60(1):71-9 [10845811.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Sep 12;97(19):10555-60 [10962030.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Sep 12;97(19):10561-6 [10962031.001]
  • [Cites] Prostate. 2000 Oct 1;45(2):158-66 [11027415.001]
  • [Cites] Endocr Rev. 2000 Dec;21(6):619-70 [11133067.001]
  • [Cites] J Clin Endocrinol Metab. 2001 May;86(5):2144-52 [11344219.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Aug 5;100(16):9512-7 [12867592.001]
  • (PMID = 15728367.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / JV 1-38; 0 / Phosphatidylserines; 9034-39-3 / Growth Hormone-Releasing Hormone; 9G34HU7RV0 / Edetic Acid; I9ZF7L6G2L / Nifedipine; SY7Q814VUP / Calcium
  • [Other-IDs] NLM/ PMC552899
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