[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 34 of about 34
1. Livadas S, Hadjidakis DJ, Argyropoulou MI, Stamatelatou M, Kelekis D, Raptis SA: Disappearance of a growth hormone secreting macro adenoma during long-term somatostatin analogue administration and recurrence following somatostatin withdrawal. Hormones (Athens); 2006 Jan-Mar;5(1):57-63
MedlinePlus Health Information. consumer health - Pituitary Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Disappearance of a growth hormone secreting macro adenoma during long-term somatostatin analogue administration and recurrence following somatostatin withdrawal.
  • Acromegaly is caused by excessive growth hormone secretion, usually from a pituitary adenoma.
  • The use of somatostatin analogues as primary or adjunctive therapy has been widely applied in the management of acromegaly.
  • We are aware of only three reported cases of complete shrinkage of a pituitary adenoma after long-term analogue administration.
  • We report a patient in whom long term (62 months) lanreotide-L.A.R administration resulted in complete disappearance of a growth hormone secreting pituitary macroadenoma, followed by recurrence of the adenoma six months post therapy discontinuation.
  • [MeSH-major] Adenoma / secretion. Antineoplastic Agents / administration & dosage. Human Growth Hormone / secretion. Neoplasm Recurrence, Local. Peptides, Cyclic / administration & dosage. Pituitary Neoplasms / secretion. Somatostatin / analogs & derivatives
  • [MeSH-minor] Acromegaly / drug therapy. Female. Humans. Magnetic Resonance Imaging. Middle Aged

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16728386.001).
  • [ISSN] 1109-3099
  • [Journal-full-title] Hormones (Athens, Greece)
  • [ISO-abbreviation] Hormones (Athens)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Peptides, Cyclic; 118992-92-0 / lanreotide; 12629-01-5 / Human Growth Hormone; 51110-01-1 / Somatostatin
  •  go-up   go-down


2. Heaney AP, Fernando M, Melmed S: PPAR-gamma receptor ligands: novel therapy for pituitary adenomas. J Clin Invest; 2003 May;111(9):1381-8
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] PPAR-gamma receptor ligands: novel therapy for pituitary adenomas.
  • Pituitary tumors cause considerable morbidity due to local invasion, hypopituitarism, or hormone hypersecretion.
  • In many cases, no suitable drug therapies are available, and surgical excision is currently the only effective treatment.
  • We show here abundant expression of nuclear hormone receptor PPAR-gamma in all of 39 human pituitary tumors.
  • PPAR-gamma activating thiazolidinediones (TZDs) rosiglitazone and troglitazone induced G(0)-G(1) cell-cycle arrest and apoptosis in human, rat somatolactotroph, and murine gonadotroph pituitary tumor cells, and suppressed in vitro hormone secretion.
  • In vivo development and growth of murine somatolactotroph and gonadotroph tumors, generated by subcutaneous injection of prolactin-secreting (PRL-secreting) and growth hormone-secreting (GH-secreting) GH3 cells, luteinizing hormone-secreting (LH-secreting) LbetaT2 cells, and alpha-T3 cells, was markedly suppressed in rosiglitazone-treated mice, and serum GH, PRL, and LH levels were attenuated in all treated animals (P < 0.009).
  • These results demonstrate that PPAR-gamma is an important molecular target in pituitary adenoma cells and PPAR-gamma ligands inhibit tumor cell growth and GH, PRL, and LH secretion in vitro and in vivo.
  • TZDs are proposed as novel oral medications for managing pituitary tumors.

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Biol Chem. 1999 Mar 26;274(13):9116-21 [10085162.001]
  • [Cites] Nat Med. 1998 Sep;4(9):1046-52 [9734398.001]
  • [Cites] N Engl J Med. 1994 Nov 3;331(18):1188-93 [7935656.001]
  • [Cites] Nat Med. 1999 Nov;5(11):1317-21 [10546001.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Nov;84(11):3859-66 [10566620.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Feb;85(2):526-9 [10690849.001]
  • [Cites] Cell Immunol. 2000 May 1;201(2):77-82 [10831316.001]
  • [Cites] J Biol Chem. 2000 Jul 21;275(29):22435-41 [10801895.001]
  • [Cites] J Clin Invest. 2000 Aug;106(4):523-31 [10953027.001]
  • [Cites] Int J Clin Pract. 2000 Jun;54(5):333-7 [10954962.001]
  • [Cites] Cancer Res. 2000 Oct 1;60(19):5558-64 [11034103.001]
  • [Cites] Eur J Endocrinol. 2000 Nov;143(5):615-21 [11078985.001]
  • [Cites] Clin Endocrinol (Oxf). 2001 Feb;54(2):183-8 [11207632.001]
  • [Cites] J Clin Endocrinol Metab. 2001 May;86(5):2170-7 [11344222.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Sep;86(9):4072-7 [11549628.001]
  • [Cites] Nat Med. 2002 Nov;8(11):1281-7 [12379847.001]
  • [Cites] J Endocrinol Invest. 1980 Oct-Dec;3(4):343-7 [7204884.001]
  • [Cites] Clin Endocrinol (Oxf). 1986 Nov;25(5):561-72 [3621623.001]
  • [Cites] Nature. 1990 Oct 18;347(6294):645-50 [2129546.001]
  • [Cites] Nature. 1992 Aug 27;358(6389):771-4 [1324435.001]
  • [Cites] Clin Endocrinol (Oxf). 1993 Jun;38(6):571-8 [8334743.001]
  • [Cites] J Biol Chem. 1994 Jul 8;269(27):18083-9 [8027069.001]
  • [Cites] Genes Dev. 1994 May 15;8(10):1224-34 [7926726.001]
  • [Cites] Cell. 1995 Dec 1;83(5):803-12 [8521497.001]
  • [Cites] Cell. 1995 Dec 1;83(5):813-9 [8521498.001]
  • [Cites] J Clin Endocrinol Metab. 1996 Feb;81(2):443-5 [8636245.001]
  • [Cites] Diabetes. 1996 Dec;45(12):1661-9 [8922349.001]
  • [Cites] Curr Opin Lipidol. 1997 Jun;8(3):159-66 [9211064.001]
  • [Cites] Nature. 1998 Jan 1;391(6662):79-82 [9422508.001]
  • [Cites] Nature. 1998 Jan 1;391(6662):82-6 [9422509.001]
  • [Cites] Diabetes. 1998 Apr;47(4):507-14 [9568680.001]
  • [Cites] Nature. 1998 Jun 25;393(6687):790-3 [9655393.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Jul 7;95(14):8280-5 [9653178.001]
  • [Cites] Mol Cell. 1998 Feb;1(3):465-70 [9660931.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Jul 21;95(15):8806-11 [9671760.001]
  • [Cites] Cancer Res. 1998 Aug 1;58(15):3344-52 [9699665.001]
  • [Cites] Biochem Biophys Res Commun. 1999 Aug 11;261(3):833-7 [10441511.001]
  • (PMID = 12727930.001).
  • [ISSN] 0021-9738
  • [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-75979
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Ligands; 0 / Nuclear Proteins; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Thiazoles; 0 / Thiazolidinediones; 0 / Transcription Factors; 2295-31-0 / 2,4-thiazolidinedione
  • [Other-IDs] NLM/ PMC154441
  •  go-up   go-down


3. Bangaru ML, Woodliff J, Raff H, Kansra S: Growth suppression of mouse pituitary corticotroph tumor AtT20 cells by curcumin: a model for treating Cushing's disease. PLoS One; 2010;5(4):e9893
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Growth suppression of mouse pituitary corticotroph tumor AtT20 cells by curcumin: a model for treating Cushing's disease.
  • BACKGROUND: Pituitary corticotroph tumors secrete excess adrenocorticotrophic hormone (ACTH) resulting in Cushing's disease (CD).
  • Standard treatment includes surgery and, if not successful, radiotherapy, both of which have undesirable side effects and frequent recurrence of the tumor.
  • Pharmacotherapy using PPARgamma agonists, dopamine receptor agonists, retinoic acid or somatostatin analogs is still experimental.
  • Curcumin, a commonly used food additive in South Asian cooking, has potent growth inhibitory effects on cell proliferation.
  • Our laboratory recently demonstrated that curcumin inhibited growth and induced apoptosis in prolactin- and growth hormone-producing tumor cells.
  • Subsequently, Schaaf et.al. confirmed our findings and also showed the in vivo effectiveness of curcumin to suppress pituitary tumorigenesis.
  • PRINCIPAL FINDINGS: Using the mouse corticotroph tumor cells, AtT20 cells, we report that curcumin had a robust, irreversible inhibitory effect on cell proliferation and clonogenic property.
  • The curcumin-induced growth inhibition was accompanied by decreased NFkappaB activity.
  • CONCLUSION: The ability of curcumin to inhibit NFkappaB and induce apoptosis in pituitary corticotroph tumor cells leads us to propose developing it as a novel therapeutic agent for the treatment of CD.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / drug therapy. Cell Proliferation / drug effects. Curcumin / pharmacology. Pituitary ACTH Hypersecretion / drug therapy
  • [MeSH-minor] Adrenocorticotropic Hormone / secretion. Animals. Antineoplastic Agents. Apoptosis / drug effects. Cell Line, Tumor. Dose-Response Relationship, Drug. Mice. NF-kappa B / antagonists & inhibitors

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CURCUMIN .
  • Hazardous Substances Data Bank. Corticotropin .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Synapse. 2000 Mar 1;35(3):228-33 [10657030.001]
  • [Cites] Curr Opin Oncol. 2000 Nov;12(6):543-9 [11085453.001]
  • [Cites] Clin Endocrinol (Oxf). 2001 Feb;54(2):183-8 [11207632.001]
  • [Cites] J Clin Invest. 2001 Oct;108(8):1123-31 [11602619.001]
  • [Cites] Anticancer Res. 2001 Jul-Aug;21(4B):2895-900 [11712783.001]
  • [Cites] Carcinogenesis. 2002 Jan;23(1):143-50 [11756235.001]
  • [Cites] J Biol Chem. 2002 Mar 8;277(10):8329-37 [11756417.001]
  • [Cites] Prostate. 2002 Aug 1;52(3):183-200 [12111695.001]
  • [Cites] Nat Med. 2002 Nov;8(11):1281-7 [12379847.001]
  • [Cites] Tumori. 2003 Jan-Feb;89(1):54-9 [12729363.001]
  • [Cites] Mol Cancer Ther. 2004 Sep;3(9):1101-8 [15367704.001]
  • [Cites] Lancet. 1982 Sep 18;2(8299):646-9 [6125785.001]
  • [Cites] J Cell Physiol. 1992 May;151(2):326-36 [1572907.001]
  • [Cites] J Biol Chem. 1995 Oct 20;270(42):24995-5000 [7559628.001]
  • [Cites] Oncogene. 1996 Aug 1;13(3):609-16 [8760302.001]
  • [Cites] J Clin Invest. 1997 Dec 15;100(12):2952-60 [9399940.001]
  • [Cites] J Clin Invest. 1997 Dec 15;100(12):2961-9 [9399941.001]
  • [Cites] J Invest Dermatol. 1998 Oct;111(4):656-61 [9764849.001]
  • [Cites] Clin Cancer Res. 1999 Jan;5(1):119-27 [9918209.001]
  • [Cites] Biochem Pharmacol. 1999 Oct 1;58(7):1167-72 [10484074.001]
  • [Cites] Carcinogenesis. 2004 Nov;25(11):2183-9 [15256484.001]
  • [Cites] J Endocrinol Invest. 2004 Dec;27(11):1055-9 [15754738.001]
  • [Cites] Mol Cell Endocrinol. 2005 Jul 15;239(1-2):27-36 [15950373.001]
  • [Cites] Biochem Pharmacol. 2005 Sep 1;70(5):700-13 [16023083.001]
  • [Cites] Ann N Y Acad Sci. 2005 Nov;1056:206-17 [16387689.001]
  • [Cites] Mol Cancer Ther. 2006 Oct;5(10):2563-71 [17041101.001]
  • [Cites] Mol Endocrinol. 2006 Nov;20(11):2976-86 [16873443.001]
  • [Cites] Mol Cancer Ther. 2007 Mar;6(3):1022-30 [17363495.001]
  • [Cites] J Pharmacol Exp Ther. 2007 May;321(2):616-25 [17289836.001]
  • [Cites] Cell. 2007 Sep 7;130(5):769-74 [17803898.001]
  • [Cites] Endocrinology. 2008 Aug;149(8):4158-67 [18450960.001]
  • [Cites] J Clin Endocrinol Metab. 2009 Jan;94(1):115-22 [18957506.001]
  • [Cites] Neuroendocrinology. 2009;90(3):292-300 [19684383.001]
  • [Cites] Endocr Relat Cancer. 2009 Dec;16(4):1339-50 [19726538.001]
  • [ErratumIn] PLoS One. 2010;5(4). doi:10.1371/annotation/38a101d6-a1f2-4a74-ab63-bc5c61e5f62b
  • (PMID = 20405005.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / NF-kappa B; 9002-60-2 / Adrenocorticotropic Hormone; IT942ZTH98 / Curcumin
  • [Other-IDs] NLM/ PMC2854133
  •  go-up   go-down


Advertisement
4. 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
Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • Sst2 gene transfer may open new therapeutic strategies in treatment combined with somatostatin analogues.
  • [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

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • Guide to Pharmacology. gene/protein/disease-specific - SST2 receptor - data and references .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19074883.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [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 / RNA, Messenger; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 12629-01-5 / Human Growth Hormone; 9002-62-4 / Prolactin; RWM8CCW8GP / Octreotide
  •  go-up   go-down


5. Becker G, Kocher M, Kortmann RD, Paulsen F, Jeremic B, Müller RP, Bamberg M: Radiation therapy in the multimodal treatment approach of pituitary adenoma. Strahlenther Onkol; 2002 Apr;178(4):173-86
MedlinePlus Health Information. consumer health - Pituitary Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Radiation therapy in the multimodal treatment approach of pituitary adenoma.
  • BACKGROUND: Pituitary tumors are relatively uncommon, comprising 10-12% of all intracranial tumors.
  • The treatment consisting of surgery, radiotherapy and drug therapy or a combination of these modalities is aimed at the control of tumor cell proliferation and--in endocrine active tumors--the reduction of hormone secretion.
  • However, the slow proliferation characteristics of pituitary tumors necessitate long-term studies for the evaluation of the treatment results.
  • In the last decade there has been continuous improvement in surgical procedures, radiotherapy techniques and drug generation.
  • In this paper, literature will be reviewed to assess the role of modern radiotherapy and radiosurgery in the management of pituitary adenomas.
  • MATERIAL AND METHODS: Nowadays, magnetic resonance imaging for the definition of the target volume and a real three-dimensional (3-D) treatment planning with field conformation and the possibility for non-coplanar irradiation has to be recommended.
  • Most groups irradiate these benign tumors with single doses of 1.8-2.0 Gy up to a total dose of 45 Gy or 50.4 Gy in extensive parasellar adenomas.
  • Adenomas are mostly small, well circumscribed lesions, and have, therefore, attracted the use of stereotactically guided high-precision irradiation techniques which allow extreme focussing and provide steep dose gradients with selective treatment of the target and optimal protection of the surrounding brain tissue.
  • RESULTS: Radiation therapy controls tumor growth in 80-98% of patients with non-secreting adenomas and 67-89% for endocrine active tumors.
  • Reviewing the recent literature including endocrine active and non-secreting adenomas, irradiated postoperatively or in case of recurrence the 5-, 10- and 15-year local control rates amount 92%, 89% and 79%.
  • In cases of microprolactinoma primary therapy consists of dopamine agonists.
  • Irradiation should be preferred in patients with macroprolactinomas, when drug therapy and/or surgery failed or for patients medically unsuitable for surgery.
  • After radiotherapy in acromegaly patients somatomedin-C and growth hormone concentrations decrease to normal levels in 70-90%, with a decrease rate of 10-30% per year.
  • Hypopituitarism is the most common side effect of pituitary irradiation with an incidence of 13-56%.
  • Other side effects are rare too, and do also depend on the damage produced by tumor itself or preceding surgery.
  • They include deterioration of vision in 1.7% of all cases, vascular changes in 6.3%, neuropsychological disorders such as dementia in 0.7% and secondary malignancies in 0.8%, if single doses of 2.0 Gy and total doses of 50 Gy are not exceeded.
  • CONCLUSION: Conventional radiation therapy of pituitary adenoma is highly effective.
  • It is recommended after subtotal resection of primary tumors such as macroadenomas, after gross total resection from endocrine active adenomas with postsurgical hormone secretion and for recurrent tumors.
  • Radiosurgery seems to be a possible treatment alternative in experienced centers, and only in patients with adenomas smaller than 25-30 mm with a minimum distance of 2-3 mm to the chiasm.
  • [MeSH-major] Adenoma / radiotherapy. Pituitary Neoplasms / radiotherapy. Prolactinoma / radiotherapy. Radiosurgery
  • [MeSH-minor] Acromegaly / etiology. Adult. Brain Diseases / etiology. Brain Neoplasms / etiology. Brain Neoplasms / secondary. Child. Combined Modality Therapy. Cushing Syndrome / etiology. Dose Fractionation. Female. Follow-Up Studies. Humans. Male. Neoplasm Recurrence, Local. Neoplasms, Radiation-Induced / etiology. Postoperative Care. Radiotherapy / adverse effects. Radiotherapy Dosage. Radiotherapy, Conformal. Stroke / etiology. Time Factors

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12040754.001).
  • [ISSN] 0179-7158
  • [Journal-full-title] Strahlentherapie und Onkologie : Organ der Deutschen Röntgengesellschaft ... [et al]
  • [ISO-abbreviation] Strahlenther Onkol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 103
  •  go-up   go-down


6. Taboada GF, Luque RM, Neto LV, Machado Ede O, Sbaffi BC, Domingues RC, Marcondes JB, Chimelli LM, Fontes R, Niemeyer P, de Carvalho DP, Kineman RD, Gadelha MR: Quantitative analysis of somatostatin receptor subtypes (1-5) gene expression levels in somatotropinomas and correlation to in vivo hormonal and tumor volume responses to treatment with octreotide LAR. Eur J Endocrinol; 2008 Mar;158(3):295-303
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Quantitative analysis of somatostatin receptor subtypes (1-5) gene expression levels in somatotropinomas and correlation to in vivo hormonal and tumor volume responses to treatment with octreotide LAR.
  • OBJECTIVE: To determine whether the somatostatin receptor subtype (SSTR) expression profile correlates with hormonal and tumor volume responses to postsurgical octreotide long acting repeatable (OCT LAR) treatment.
  • DESIGN AND METHODS: Quantitative real-time RT-PCR was used to evaluate the absolute mRNA copy numbers for all five SSTR subtypes in 22 somatotropinomas.
  • Response to OCT LAR was studied by hormone levels (GH and IGF-I) and tumor volume (sella turcica magnetic resonance imaging).
  • A positive correlation was also found between SSTR2 mRNA levels and the percentage decrease in tumor volume after 6 months of OCT LAR (r=0.79, P=0.002, n=12).
  • CONCLUSIONS: Somatostatin receptor subtype 2 mRNA expression levels in somatotropinomas correlate positively with in vivo hormonal and tumor volume responses to OCT LAR.

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18299461.001).
  • [ISSN] 1479-683X
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Grant] United States / PHS HHS / / NIDDK 30677
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Membrane Proteins; 0 / RNA, Messenger; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 0 / somatostatin receptor 3; 0 / somatostatin receptor 5; 0 / somatostatin receptor subtype-4; 0 / somatostatin receptor type 1; 9002-72-6 / Growth Hormone; RWM8CCW8GP / Octreotide
  •  go-up   go-down


7. Neto LV, Machado Ede O, Luque RM, Taboada GF, Marcondes JB, Chimelli LM, Quintella LP, Niemeyer P Jr, de Carvalho DP, Kineman RD, Gadelha MR: Expression analysis of dopamine receptor subtypes in normal human pituitaries, nonfunctioning pituitary adenomas and somatotropinomas, and the association between dopamine and somatostatin receptors with clinical response to octreotide-LAR in acromegaly. J Clin Endocrinol Metab; 2009 Jun;94(6):1931-7
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression analysis of dopamine receptor subtypes in normal human pituitaries, nonfunctioning pituitary adenomas and somatotropinomas, and the association between dopamine and somatostatin receptors with clinical response to octreotide-LAR in acromegaly.
  • CONTEXT: Dopamine receptor (DR) and somatostatin receptor subtype expression in pituitary adenomas may predict the response to postsurgical therapies.
  • OBJECTIVES: Our objectives were to assess and compare the mRNA levels of DR1-5 and somatostatin receptors 1-5 in normal pituitaries (NPs), nonfunctioning pituitary adenomas (NFPAs), and somatotropinomas.
  • DESIGN AND PATIENTS: Eight NPs, 30 NFPAs, and 39 somatotropinomas were analyzed for receptor mRNA levels by real-time RT-PCR.
  • The relationship between expression levels of DR subtypes in NPs and somatotropinomas was DR2T>>>DR4>>DR5>DR1, whereas in NFPAs, DR2T>>>DR4>>DR1>DR5.
  • CONCLUSIONS: DR2 is the predominant DR subtype in NPs, NFPAs, and somatotropinomas.
  • The fact that DR1, DR4, and DR5 are also expressed in many adenomas tested suggests that these receptors might also play a role in the therapeutic impact of postsurgical medical therapies in patients with NFPA and acromegaly.

  • Genetic Alliance. consumer health - Acromegaly.
  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Science. 2000 Apr 7;288(5463):154-7 [10753124.001]
  • [Cites] Rev Endocr Metab Disord. 2009 Jun;10(2):83-90 [18651224.001]
  • [Cites] Clin Endocrinol (Oxf). 2001 Apr;54(4):469-77 [11318782.001]
  • [Cites] Endocrine. 2001 Apr;14(3):329-36 [11444429.001]
  • [Cites] J Neurophysiol. 2002 Apr;87(4):2167-75 [11929934.001]
  • [Cites] Genome Biol. 2002 Jun 18;3(7):RESEARCH0034 [12184808.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Apr;89(4):1674-83 [15070930.001]
  • [Cites] J Biol Chem. 1978 Apr 10;253(7):2244-53 [416027.001]
  • [Cites] J Histochem Cytochem. 1979 Aug;27(8):1205-7 [383827.001]
  • [Cites] Endocrinology. 1983 May;112(5):1567-77 [6832061.001]
  • [Cites] Proc Soc Exp Biol Med. 1984 Feb;175(2):191-5 [6694976.001]
  • [Cites] Brain Res. 1988 Mar 8;443(1-2):77-84 [2896059.001]
  • [Cites] EMBO J. 1989 Dec 20;8(13):4025-34 [2531656.001]
  • [Cites] Nature. 1989 Dec 21-28;342(6252):923-6 [2531847.001]
  • [Cites] FEBS Lett. 1990 Apr 9;263(1):18-22 [2139615.001]
  • [Cites] Biochemistry. 1990 Feb 13;29(6):1367-71 [2139794.001]
  • [Cites] J Neurochem. 1991 Mar;56(3):1024-9 [1825222.001]
  • [Cites] J Neurochem. 1991 Sep;57(3):795-801 [1861151.001]
  • [Cites] Neurosci Lett. 1991 Sep 2;130(1):12-6 [1836253.001]
  • [Cites] Nature. 1992 Jul 9;358(6382):149-52 [1319557.001]
  • [Cites] Mol Endocrinol. 1992 Jun;6(6):920-6 [1323056.001]
  • [Cites] Mol Endocrinol. 1992 Nov;6(11):1815-24 [1282671.001]
  • [Cites] Annu Rev Pharmacol Toxicol. 1993;33:281-307 [8494342.001]
  • [Cites] Neuroendocrinology. 1994 Sep;60(3):314-22 [7969790.001]
  • [Cites] J Neurochem. 1995 Sep;65(3):1157-65 [7643093.001]
  • [Cites] Anal Biochem. 1995 Sep 20;230(2):353-5 [7503432.001]
  • [Cites] Endocrinology. 1997 May;138(5):1871-8 [9112381.001]
  • [Cites] Physiol Rev. 1998 Jan;78(1):189-225 [9457173.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Feb;83(2):374-8 [9467544.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Apr;83(4):1368-75 [9543168.001]
  • [Cites] Brain Res Mol Brain Res. 1998 Apr;55(2):285-92 [9582438.001]
  • [Cites] Endocrinology. 1998 Oct;139(10):4213-21 [9751502.001]
  • [Cites] Biochem Biophys Res Commun. 1999 Mar 5;256(1):33-40 [10066418.001]
  • [Cites] J Mol Endocrinol. 2005 Oct;35(2):333-41 [16216913.001]
  • [Cites] Trends Pharmacol Sci. 2005 Nov;26(11):595-602 [16183138.001]
  • [Cites] Neuroendocrinology. 2006;83(3-4):258-63 [17047391.001]
  • [Cites] Eur J Endocrinol. 2007 Jan;156(1):65-74 [17218727.001]
  • [Cites] Eur J Endocrinol. 2007 Apr;156 Suppl 1:S13-21 [17413183.001]
  • [Cites] Eur J Endocrinol. 2007 Apr;156 Suppl 1:S23-8 [17413184.001]
  • [Cites] Eur J Endocrinol. 2007 Apr;156 Suppl 1:S37-43 [17413187.001]
  • [Cites] Eur J Endocrinol. 2007 Apr;156 Suppl 1:S57-63 [17413190.001]
  • [Cites] Cell Signal. 2007 Nov;19(11):2304-16 [17706924.001]
  • [Cites] J Neuroendocrinol. 2007 Oct;19(10):773-8 [17850459.001]
  • [Cites] Eur J Endocrinol. 2008 Mar;158(3):295-303 [18299461.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Apr;93(4):1412-7 [18211974.001]
  • [Cites] Mol Pharmacol. 2000 Aug;58(2):455-62 [10908315.001]
  • (PMID = 19293270.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] ENG
  • [Grant] United States / PHS HHS / / 30677
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; 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 / Delayed-Action Preparations; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / Receptors, Dopamine; 0 / Receptors, Somatostatin; RWM8CCW8GP / Octreotide
  • [Other-IDs] NLM/ PMC2730344
  •  go-up   go-down


8. 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
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • The effect of drugs was tested in cell cultures at various concentrations.
  • 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.

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • Hazardous Substances Data Bank. DOPAMINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


9. Lania A, Mantovani G, Spada A: Genetic abnormalities of somatostatin receptors in pituitary tumors. Mol Cell Endocrinol; 2008 May 14;286(1-2):180-6
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic abnormalities of somatostatin receptors in pituitary tumors.
  • Normal human pituitary and pituitary adenomas have been shown to express almost all SST subtypes, with the exception of SST4.
  • Consistent with the observation that octreotide and other somatostatin analogs bind to SST2 and SST5 with high affinity, these genes have been screened for quantitative/qualitative abnormalities in tumors removed from patients with poor responsiveness to somatostatin analogs treatment.
  • Data obtained in GH-secreting adenomas suggested that resistance to octreotide was frequently associated with low expression of SST2 mRNA, although other authors failed to confirm this finding.
  • Similarly, loss of heterozygosis at SST5 gene locus in pituitary adenomas has been described in individual tumors.
  • In recent years, molecular studies investigated the possible association of gene polymorphisms and susceptibility to diseases and/or resistance to drugs.
  • [MeSH-major] Adenoma / genetics. Pituitary Neoplasms / genetics. Receptors, Somatostatin / genetics
  • [MeSH-minor] Acromegaly / drug therapy. Acromegaly / genetics. Acromegaly / metabolism. Antineoplastic Agents, Hormonal / therapeutic use. Drug Resistance, Neoplasm. Growth Hormone-Secreting Pituitary Adenoma / drug therapy. Growth Hormone-Secreting Pituitary Adenoma / genetics. Growth Hormone-Secreting Pituitary Adenoma / metabolism. Human Growth Hormone / secretion. Humans. Loss of Heterozygosity. Mutation. Octreotide / therapeutic use. Pituitary Gland / metabolism. Polymorphism, Genetic

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17913341.001).
  • [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] 0 / Antineoplastic Agents, Hormonal; 0 / Receptors, Somatostatin; 12629-01-5 / Human Growth Hormone; RWM8CCW8GP / Octreotide
  • [Number-of-references] 69
  •  go-up   go-down


10. Fernando MA, Heaney AP: Alpha1-adrenergic receptor antagonists: novel therapy for pituitary adenomas. Mol Endocrinol; 2005 Dec;19(12):3085-96
Hazardous Substances Data Bank. Corticotropin .

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

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • Hazardous Substances Data Bank. DOXAZOSIN MESYLATE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16020484.001).
  • [ISSN] 0888-8809
  • [Journal-full-title] Molecular endocrinology (Baltimore, Md.)
  • [ISO-abbreviation] Mol. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenergic alpha-1 Receptor Antagonists; 0 / Adrenergic alpha-Antagonists; 0 / Antineoplastic Agents; 0 / I-kappa B Proteins; 0 / NF-kappa B; 0 / Receptors, Adrenergic, alpha-1; 0 / Tumor Necrosis Factor-alpha; 139874-52-5 / NF-kappaB inhibitor alpha; 66796-54-1 / Pro-Opiomelanocortin; 9002-60-2 / Adrenocorticotropic Hormone; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases; NW1291F1W8 / Doxazosin
  •  go-up   go-down


11. Matrone C, Pivonello R, Colao A, Cappabianca P, Cavallo LM, Del Basso De Caro ML, Taylor JE, Culler MD, Lombardi G, Di Renzo GF, Annunziato L: Expression and function of somatostatin receptor subtype 1 in human growth hormone secreting pituitary tumors deriving from patients partially responsive or resistant to long-term treatment with somatostatin analogs. Neuroendocrinology; 2004 Mar;79(3):142-8
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression and function of somatostatin receptor subtype 1 in human growth hormone secreting pituitary tumors deriving from patients partially responsive or resistant to long-term treatment with somatostatin analogs.
  • The role of somatostatin (SS) receptor subtype 1 (SSTR(1)) in mediating the inhibitory effect of SS on growth hormone (GH) secreting pituitary tumors has been recently demonstrated.
  • In the present study, we evaluated the effect of the selective SSTR(1) agonist BIM-23745 on in vitro GH secretion in GH-secreting pituitary tumor cells, deriving from patients resistant or partially responsive to octreotide long-acting release (octreotide-LAR) or lanreotide therapy in vivo and expressing SSTR(1) mRNA.
  • Our data demonstrate that (1) SSTR(1) receptor was present in 56.25% (9/16) of the GH-secreting adenomas examined;.
  • (2) in all GH-secreting pituitary tumors that expressed SSTR(1), BIM-23745 significantly inhibited GH secretion in vitro, and (3) when SSTR(1) subtype was present in tumors from patients resistant to octreotide-LAR or lanreotide therapy, BIM-23745 was able to inhibit the in vitro GH secretion.
  • In conclusion, the results of the current study suggest that SS analogs selective for the SSTR(1) may represent a further useful approach for the treatment of acromegaly in patients resistant or partially responsive to octreotide-LAR or lanreotide treatment in vivo.
  • [MeSH-major] Acromegaly / metabolism. Adenoma / secretion. Antineoplastic Agents / pharmacology. Human Growth Hormone / secretion. Pituitary Neoplasms / secretion. Receptors, Somatostatin / agonists. Somatostatin / analogs & derivatives. Somatostatin / pharmacology
  • [MeSH-minor] Adult. Drug Resistance, Neoplasm. Female. Humans. In Vitro Techniques. Male. Middle Aged. Octreotide / pharmacology. Octreotide / therapeutic use. Peptides, Cyclic / therapeutic use

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2004 S. Karger AG, Basel
  • (PMID = 15103227.001).
  • [ISSN] 0028-3835
  • [Journal-full-title] Neuroendocrinology
  • [ISO-abbreviation] Neuroendocrinology
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Peptides, Cyclic; 0 / Receptors, Somatostatin; 0 / somatostatin receptor type 1; 118992-92-0 / lanreotide; 12629-01-5 / Human Growth Hormone; 51110-01-1 / Somatostatin; RWM8CCW8GP / Octreotide
  •  go-up   go-down


12. Waśko R, Bolko P, Owecki M, Jaskuła M, Sowiński J: The efficacy of octreotide LAR (long acting release) treatment in patients with somatotropinoma, and mixed pituitary tumours. Pharm World Sci; 2004 Dec;26(6):324-7
MedlinePlus Health Information. consumer health - Pituitary Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The efficacy of octreotide LAR (long acting release) treatment in patients with somatotropinoma, and mixed pituitary tumours.
  • OBJECTIVE: The efficacy of somatostatin analogues in the treatment of acromegaly is not always equal and therefore we wanted to evaluate the efficacy of therapy with octreotide long acting release (LAR) in patients with monohormonal tumours (somatotropinomas) in comparison to individuals with mixed pituitary tumours secreting alpha-subunit.
  • METHOD: The 35 acromegalic patients (18 males and 17 females), aged 41.8 +/- 8.8 years, were divided into 2 groups according to the secreted hormones: 1 with mixed pituitary tumours with elevated growth hormone and alpha-subunit concentrations, the other with isolated growth hormone hypersecretion and normal alpha-subunit levels.
  • RESULTS: The decrease of GH and IGF-I levels after octreotide LAR treatment were observed in both groups.
  • CONCLUSIONS: After octreotide LAR treatment, the decrease of GH level and of mean IGF-I values was greater in patients with mixed pituitary tumours and high alpha-subunit concentrations than in patients with isolated GH hypersecretion and normal alpha-subunit levels.
  • [MeSH-major] Adenoma / drug therapy. Antineoplastic Agents, Hormonal / therapeutic use. Octreotide / therapeutic use. Pituitary Neoplasms / drug therapy
  • [MeSH-minor] Acromegaly / drug therapy. Acromegaly / etiology. Adult. Delayed-Action Preparations. Female. Human Growth Hormone / blood. Humans. Insulin-Like Growth Factor I / metabolism. Male. Middle Aged

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15683101.001).
  • [ISSN] 0928-1231
  • [Journal-full-title] Pharmacy world & science : PWS
  • [ISO-abbreviation] Pharm World Sci
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article
  • [Publication-country] Netherlands
  • [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
  •  go-up   go-down


13. Wasko R, Jankowska A, Kotwicka M, Liebert W, Sowinski J, Warchol JB: Effects of treatment with somatostatin analogues on the occurrence of apoptosis in somatotropinomas. Neuro Endocrinol Lett; 2003 Oct;24(5):334-8
MedlinePlus Health Information. consumer health - Pituitary Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of treatment with somatostatin analogues on the occurrence of apoptosis in somatotropinomas.
  • Present study aimed to examine whether treatment of somatotropinoma types tumours with somatostatine analogue (lanreotide) results in apoptosis.
  • MATERIAL AND METHODS: The studies were performed on 35 patients with somatotropinoma type tumours on whom adenomectomy was performed by transsphenoidal approach.
  • The results of the studies demonstrated the occurrence of lanreotide induced apoptosis in somatotropinoma type tumours.
  • The grade of apoptotic cells in macroadenomas type adenomas, treated with lanreotide, ranged from 4.0% to 17.1% (mean 8.7+/-2.6%).
  • Patients in whom hypophysectomy was not preceded by lanreotide treatment demonstrated low level of apoptotic cells (no more than 3.5%).
  • CONCLUSIONS: The studies showed that treatment with somatostatine analogue-lanreotide induced apoptosis of tumour cell suggesting that the induction of apoptotic cell death may be involved in the anticancer activity of somatostatine analogue.
  • [MeSH-major] Adenoma / drug therapy. Antineoplastic Agents / administration & dosage. Apoptosis / drug effects. Peptides, Cyclic / administration & dosage. Pituitary Neoplasms / drug therapy. Somatostatin / administration & dosage

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 14647007.001).
  • [ISSN] 0172-780X
  • [Journal-full-title] Neuro endocrinology letters
  • [ISO-abbreviation] Neuro Endocrinol. Lett.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Sweden
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Peptides, Cyclic; 118992-92-0 / lanreotide; 51110-01-1 / Somatostatin
  •  go-up   go-down


14. Waśko R, Bolko P, Kostrzewski J, Horst-Sikorska W, Liebert W, Sowiński J: [Estimation of efficacy of the octreotide LAR administration in the patients with somatotropinoma]. Pol Arch Med Wewn; 2001 Aug;106(2):693-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Estimation of efficacy of the octreotide LAR administration in the patients with somatotropinoma].
  • [Transliterated title] Ocena skuteczności stosowania oktreotydu LAR u pacjentów z guzami przysadki typu somatotropinoma.
  • Acromegaly is caused by excessive secretion of growth hormone by a hypophyseal adenoma type of somatotropinoma.
  • Treatment of adenomas, which secrete GH, involves pharmacotherapy followed by surgery.
  • Modern pharmacotherapy leaning is based on somatostatin analogues (factor restrictive secretion GH): octreotide, octreotide LAR and lanreotide.
  • The aim of our study was estimation of efficiency of octreotide LAR in the patients with somatotropinoma prepared to neurosurgery intervention.
  • The presence of pituitary adenoma in all patients was confirmed by MRI.
  • The concentration of GH before octreotide LAR therapy in all patients increased remarkable and ranged from 15.6 to 78.6 ng/ml, mean: 31.20 +/- 16.84 (norm: 0-10 ng/ml), also, in all cases the serum IGF-I level was increased and ranged from 451 to 1107.6 ng/ml, mean: 801.75 +/- 207.82 (norm: 100-400 ng/ml).
  • Long acting somatostatin analogues--octreotide LAR is particular efficient in lowering of growth hormone and IGF-I in patients with somatotropinoma and shows efficiency in normalization of increased prolactin concentration.
  • Because of extreme effectiveness of octreotide LAR, it should be used the routine treatment at the patients suffering from active acromegaly and preparing to neurosurgical treatment.
  • [MeSH-major] Acromegaly / drug therapy. Antineoplastic Agents, Hormonal / administration & dosage. Human Growth Hormone / blood. Insulin-Like Growth Factor I / metabolism. Octreotide / administration & dosage. Peptides, Cyclic / administration & dosage. Prolactin / blood. Somatostatin / administration & dosage
  • [MeSH-minor] Adult. Aged. Female. Hormones / administration & dosage. Humans. Male. Middle Aged. Pituitary Neoplasms / diagnostic imaging. Radiography. Treatment Outcome

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11926144.001).
  • [Journal-full-title] Polskie Archiwum Medycyny Wewnetrznej
  • [ISO-abbreviation] Pol. Arch. Med. Wewn.
  • [Language] pol
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Hormones; 0 / Peptides, Cyclic; 0G3DE8943Y / lanreotide; 12629-01-5 / Human Growth Hormone; 51110-01-1 / Somatostatin; 67763-96-6 / Insulin-Like Growth Factor I; 9002-62-4 / Prolactin; RWM8CCW8GP / Octreotide
  •  go-up   go-down


15. 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
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • Our experience is based on an analysis of 12 patients with GH-secreting tumors and 2 patients with ACTH-secreting adenomas.
  • 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).
  • RESULTS: In none of the cases a total surgical removal of the invasive GH-secreting adenoma was attained (according the following cure criteria: basal serum GH level below 2.5 micrograms/l, OGTT < 1 microgram/l, normal sex- and age-related IGF-I level).
  • 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

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • Hazardous Substances Data Bank. Corticotropin .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


16. Gołkowski F, Buziak-Bereza M, Huszno B: [Evaluation of the efficacy of long-acting somatostatin analog as adjunctive therapy in patients with active acromegaly]. Przegl Lek; 2006;63(3):117-22
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Evaluation of the efficacy of long-acting somatostatin analog as adjunctive therapy in patients with active acromegaly].
  • Transsphenoidal surgery is the first-line therapy for patients with acromegaly, but can achieve biochemical control with normalization of somatomedin C in 40-80% of cases.
  • All patients with continued growth hormone hypersecretion after neurosurgery require adjunctive therapy to prevent morbidity and premature mortality.
  • The aim of our study was to evaluate the efficacy of long-acting somatostatin analog--octreotide LAR (OCT-LAR) as adjunctive therapy for patients with persistent disease.
  • All patients were diagnosed as having growth hormone secreting pituitary tumor and underwent transsphenoidal surgery (TSS).
  • Radiotherapy (RT) was used as adjunctive therapy in 7 of investigated persons.
  • In all subjects elevated level of somatomedin C was found, 9 have increased level of growth hormone (hGH) as well.
  • After 6 months therapy with OCT-LAR we noticed drop in somatomedin C and hGH levels in all patients.
  • We found no significant correlation between decrease in somatomedin C and its level prior to the treatment (p=0.8), but high positive correlation between decrease in hGh level and its initial value (R=0.75, p=0.002).
  • The therapeutic outcome defined as decrease in somatomedin C level was not significantly different between patients with or without adjunctive radiotherapy in the past (p=0.08) and between patients with intensive or weak isotope collection in the pituitary in 99mTc-octreotide scintiscan (p=0.2).
  • Initial values of somatomedin C as well as age and isotopic imaging findings are not valuable predictor factors for therapeutic outcome.
  • [MeSH-major] Acromegaly / drug therapy. Adenoma / drug therapy. Antineoplastic Agents, Hormonal / administration & dosage. Octreotide / administration & dosage. Pituitary Neoplasms / drug therapy
  • [MeSH-minor] Adult. Female. Follow-Up Studies. Growth Hormone / secretion. Humans. Insulin-Like Growth Factor I / secretion. Male. Middle Aged. Treatment Outcome

  • Genetic Alliance. consumer health - Acromegaly.
  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16967698.001).
  • [ISSN] 0033-2240
  • [Journal-full-title] Przegla̧d lekarski
  • [ISO-abbreviation] Prz. Lek.
  • [Language] pol
  • [Publication-type] Clinical Trial; English Abstract; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 67763-96-6 / Insulin-Like Growth Factor I; 9002-72-6 / Growth Hormone; RWM8CCW8GP / Octreotide
  •  go-up   go-down


17. Rozhivanov RV, Kurbatov DG: [Sexual function rehabilitation of men with pituitary tumors]. Urologiia; 2010 Jul-Aug;(4):48, 50-3
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Sexual function rehabilitation of men with pituitary tumors].
  • A prospective trial of the methods of sexual rehabilitation of 31 men with pituitary tumors has shown that therapy with testosterone and chorionic gonadotropin effectively corrects hypogonadism and sexual disorders.
  • Both methods of treatment had no negative effect on the size of the prostatic gland and PSA level except 2 patients with somatotropinoma on testosterone.
  • In the course of chorionic gonadotropin treatment pituitary tumor increased in size in 3 patients.
  • [MeSH-major] Androgens / therapeutic use. Chorionic Gonadotropin / therapeutic use. Erectile Dysfunction / drug therapy. Hormone Replacement Therapy / methods. Pituitary Neoplasms / complications. Testosterone / therapeutic use
  • [MeSH-minor] Adult. Cohort Studies. Humans. Libido / drug effects. Male. Middle Aged. Prospective Studies. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Erectile Dysfunction.
  • MedlinePlus Health Information. consumer health - Hormone Replacement Therapy.
  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • Hazardous Substances Data Bank. TESTOSTERONE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20973135.001).
  • [ISSN] 1728-2985
  • [Journal-full-title] Urologii︠a︡ (Moscow, Russia : 1999)
  • [ISO-abbreviation] Urologiia
  • [Language] rus
  • [Publication-type] Clinical Trial; English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Androgens; 0 / Chorionic Gonadotropin; 3XMK78S47O / Testosterone
  •  go-up   go-down


18. Boulis NM, Noordmans AJ, Barkan A, Hassing J, Chandler WF: Somatotropinoma infarction during octreotide therapy leading to bilateral cavernous sinus syndrome. Pituitary; 2000 Nov;3(3):185-8
MedlinePlus Health Information. consumer health - Pituitary Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Somatotropinoma infarction during octreotide therapy leading to bilateral cavernous sinus syndrome.
  • The cyclic somatostatin analog, octreotide, forms the mainstay of medical treatment for acromegaly.
  • In addition to lowering circulating growth hormone levels and shrinking tumor size, octreotide may provide symptomatic relief of headaches associated with growth hormone secreting tumors.
  • The majority of reported complications of octreotide therapy are gastrointestinal and metabolic.
  • The present case illustrates the development of acute bilateral cavernous sinus syndrome with loss of eye movement bilaterally during octreotide therapy.
  • Serial MRI examination suggest tumor infarction as the etiology.
  • The symptoms resolved over 2 months as the tumor shrunk in size and growth hormone was dramatically reduced.
  • [MeSH-major] Cavernous Sinus. Cerebral Infarction / chemically induced. Cranial Nerve Diseases / chemically induced. Human Growth Hormone / secretion. Octreotide / adverse effects. Ophthalmoplegia / chemically induced. Pituitary Neoplasms / chemically induced. Pituitary Neoplasms / secretion
  • [MeSH-minor] Abducens Nerve / drug effects. Child. Female. Humans. Magnetic Resonance Imaging. Oculomotor Nerve / drug effects. Syndrome

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Metabolism. 1992 Sep;41(9 Suppl 2):22-33 [1355588.001]
  • [Cites] Neurol Med Chir (Tokyo). 1990 May;30(5):350-3 [1699153.001]
  • [Cites] Biol Psychiatry. 1989 May;26(1):97-101 [2541810.001]
  • [Cites] Scand J Gastroenterol. 1998 Dec;33(12):1303-9 [9930395.001]
  • [Cites] Cephalalgia. 1997 Feb;17(1):27-30 [9051332.001]
  • [Cites] N Engl J Med. 1996 Jan 25;334(4):246-54 [8532003.001]
  • [Cites] J Endocrinol. 1997 Oct;155 Suppl 1:S53-5 [9389996.001]
  • [Cites] South Med J. 1988 May;81(5):660-3 [3368818.001]
  • [Cites] Cephalalgia. 1994 Aug;14(4):303-4 [7954762.001]
  • [Cites] J Surg Res. 1993 Oct;55(4):446-50 [7692142.001]
  • [Cites] Endocr Rev. 1988 Nov;9(4):417-36 [2905987.001]
  • [Cites] J Neurosurg. 1983 Oct;59(4):677-9 [6886789.001]
  • [Cites] Pain. 1991 Dec;47(3):341-4 [1664509.001]
  • [Cites] Lab Invest. 1999 Aug;79(8):935-44 [10462031.001]
  • [Cites] N Engl J Med. 1995 Aug 31;333(9):555-60 [7623904.001]
  • [Cites] Lancet. 1993 Jul 31;342(8866):301 [8101320.001]
  • [Cites] Am J Med. 1994 Nov;97(5):468-73 [7977436.001]
  • [Cites] Neurosurgery. 1988 Sep;23(3):395-8 [3226523.001]
  • [Cites] J Endocrinol Invest. 1999 Oct;22(9):698-700 [10595834.001]
  • [Cites] Med Clin (Barc). 1989 Oct 28;93(13):501-2 [2622243.001]
  • [Cites] J Clin Endocrinol Metab. 1988 Nov;67(5):1040-8 [2903168.001]
  • [Cites] Arch Intern Med. 1989 Jun;149(6):1443-5 [2730266.001]
  • (PMID = 11383484.001).
  • [ISSN] 1386-341X
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 12629-01-5 / Human Growth Hormone; RWM8CCW8GP / Octreotide
  •  go-up   go-down


19. Yetkin DO, Boysan SN, Tiryakioglu O, Yalin AS, Kadioglu P: Forty month follow-up of persistent and difficultly controlled acromegalic patients treated with depot long acting somatostatin analog octreotide. Endocr J; 2007 Jun;54(3):459-64

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The objective of the present study was to investigate the effects of octreotide long acting release (S-LAR) preparation on GH and IGF-1 serum concentrations and pituitary tumor size in patients with persistent and difficultly controlled acromegaly even after adjuvant irradiation and/or dopamine agonists.
  • Initially, pituitary adenoma volume was median: 1.18 ml [IQR: 0.08-3.50] and it shrank to 0.21 ml [IQR: 0-2.1] at 40 months (p = 0.08).
  • S-LAR is an effective treatment regimen in reducing GH and IGF-1 concentrations and as well as in shrinking tumor volume in persistent and difficultly controlled acromegalic patients.
  • [MeSH-major] Acromegaly / drug therapy. Adenoma / drug therapy. Growth Hormone-Secreting Pituitary Adenoma / drug therapy. Neoplasm, Residual / drug therapy. Octreotide / administration & dosage. Somatostatin / analogs & derivatives
  • [MeSH-minor] Adult. Comorbidity. Delayed-Action Preparations / adverse effects. Delayed-Action Preparations / therapeutic use. Dose-Response Relationship, Drug. Female. Follow-Up Studies. Glucose Tolerance Test. Human Growth Hormone / blood. Humans. Insulin-Like Growth Factor I / analysis. Male. Middle Aged. Salvage Therapy. Treatment Failure

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17495423.001).
  • [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 / Delayed-Action Preparations; 12629-01-5 / Human Growth Hormone; 51110-01-1 / Somatostatin; 67763-96-6 / Insulin-Like Growth Factor I; RWM8CCW8GP / Octreotide
  •  go-up   go-down


20. Muller AF, Van Der Lely AJ: Pharmacological therapy for acromegaly: a critical review. Drugs; 2004;64(16):1817-38
Genetic Alliance. consumer health - Acromegaly.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pharmacological therapy for acromegaly: a critical review.
  • The treatment of acromegaly has changed considerably over the last few decades.
  • In the late 1970s, the introduction of the dopamine receptor agonists made it possible to reduce growth hormone (GH) secretion by somatotropinomas for the first time.
  • Currently these compounds should be considered in patients with a mixed GH-prolactin secreting pituitary adenoma and/or those in whom pre-treatment insulin-like growth factor (IGF)-I concentrations are below 750 microg/L.
  • These compounds are capable of achieving biochemical control of GH and IGF-I in 50-60% of patients and tumour shrinkage in some 30%.
  • In particular, candidates for treatment with these compounds are those patients who have undergone an unsuccessful transsphenoidal operation or who await the therapeutic effect of external pituitary irradiation.
  • In selected patients primary medical therapy with somatostatin analogues is certainly a feasible option.
  • To date, pegvisomant is the only available member of a new class of drugs that was especially designed to block the GHR.
  • Pegvisomant is the most effective treatment for normalising IGF-I concentrations and appears to have a good safety profile.
  • However, liver function tests should be regularly monitored and tumour size should be closely followed.
  • Finally, we propose a treatment algorithm for acromegaly.
  • [MeSH-major] Acromegaly / drug therapy
  • [MeSH-minor] Adenoma / complications. Animals. Dopamine Agonists / therapeutic use. Hormone Antagonists / therapeutic use. Human Growth Hormone / antagonists & inhibitors. Human Growth Hormone / metabolism. Humans. Pituitary Neoplasms / complications. Receptors, Somatotropin / antagonists & inhibitors. Somatostatin / analogs & derivatives. Somatostatin / pharmacology. Somatostatin / therapeutic use

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Invest. 1997 Nov 1;100(9):2386-92 [9410919.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Oct;83(10):3419-26 [9768641.001]
  • [Cites] Ann Intern Med. 1992 Nov 1;117(9):719-26 [1416573.001]
  • [Cites] Science. 1992 Jun 19;256(5064):1677-80 [1535167.001]
  • [Cites] Clin Endocrinol (Oxf). 1994 Jul;41(1):95-102 [8050136.001]
  • [Cites] N Engl J Med. 1990 Apr 5;322(14):966-77 [2179724.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Mar;88(3):963-8 [12629068.001]
  • [Cites] Cancer Res. 1988 Dec 15;48(24 Pt 1):6977-85 [2903792.001]
  • [Cites] Science. 1978 Oct 27;202(4366):390-402 [212832.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Jul;86(7):2976-81 [11443154.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Nov;83(11):3808-16 [9814451.001]
  • [Cites] Lancet. 2001 Nov 24;358(9295):1754-9 [11734231.001]
  • [Cites] J Clin Endocrinol Metab. 2000 May;85(5):2068-71 [10843197.001]
  • [Cites] J Endocrinol Invest. 1999 Jan;22(1):40-7 [10090136.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Oct;85(10):3779-85 [11061538.001]
  • [Cites] Endocr Rev. 2002 Oct;23 (5):623-46 [12372843.001]
  • [Cites] Br Med J (Clin Res Ed). 1984 Oct 27;289(6452):1101-3 [6435792.001]
  • [Cites] N Engl J Med. 1983 Sep 22;309(12 ):704-9 [6888442.001]
  • [Cites] Ann Surg. 1909 Dec;50(6):1002-17 [17862444.001]
  • [Cites] Endocr Rev. 1998 Dec;19(6):717-97 [9861545.001]
  • [Cites] Clin Endocrinol (Oxf). 2003 Feb;58(2):132-5 [12580925.001]
  • [Cites] Endocr Rev. 1988 Aug;9(3):357-73 [3145190.001]
  • [Cites] Clin Endocrinol (Oxf). 2003 Feb;58(2):128-31 [12580924.001]
  • [Cites] Clin Pharmacokinet. 2002;41(4):261-309 [11978145.001]
  • [Cites] Eur J Endocrinol. 1995 May;132(5):559-64 [7749496.001]
  • [Cites] Endocrinol Metab Clin North Am. 1989 Jun;18(2):277-310 [2663476.001]
  • [Cites] Acta Endocrinol (Copenh). 1993 May;128(5):389-93 [8100375.001]
  • [Cites] Trends Pharmacol Sci. 1995 Mar;16(3):86-8 [7792934.001]
  • [Cites] Endocr J. 1995 Apr;42(2):295-300 [7627275.001]
  • [Cites] Clin Endocrinol (Oxf). 1983 Dec;19(6):711-9 [6652932.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Oct;83(10):3409-10 [9768639.001]
  • [Cites] Clin Endocrinol (Oxf). 2000 Nov;53(5):577-86 [11106918.001]
  • [Cites] Br Med J. 1975 Feb 8;1(5953):299-303 [1111790.001]
  • [Cites] J Clin Endocrinol Metab. 1981 Oct;53(4):752-8 [6793607.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Jul;87(13):5061-5 [2367524.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Jan;86(1):140-5 [11231991.001]
  • [Cites] J Clin Endocrinol Metab. 1994 Sep;79(3):724-9 [7521350.001]
  • [Cites] N Engl J Med. 1996 Jan 25;334(4):246-54 [8532003.001]
  • [Cites] J Clin Endocrinol Metab. 1984 Jun;58(6):988-92 [6725515.001]
  • [Cites] Clin Endocrinol (Oxf). 1985 Feb;22(2):209-17 [4039234.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Aug;82(8):2756 [9253368.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Sep;86(9):4072-7 [11549628.001]
  • [Cites] N Engl J Med. 1981 Jun 11;304(24):1450-4 [7015129.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Apr;87(4):1797-804 [11932320.001]
  • [Cites] Eur J Endocrinol. 1994 Jul;131(1):20-6 [7913650.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Jun;86(6):2779-86 [11397887.001]
  • [Cites] N Engl J Med. 1994 Oct 6;331(14):904-9 [7915824.001]
  • [Cites] AJNR Am J Neuroradiol. 1997 Apr;18(4):765-72 [9127047.001]
  • [Cites] J Clin Endocrinol Metab. 1989 Apr;68(4):844-50 [2537844.001]
  • [Cites] Am J Cardiol. 1995 May 15;75(15):1042-7 [7747686.001]
  • [Cites] Endocrinology. 2002 Oct;143(10):4123-30 [12239124.001]
  • [Cites] Am J Med. 1980 Oct;69(4):571-5 [7424946.001]
  • [Cites] Ann N Y Acad Sci. 1994 Sep 15;733:122-37 [7978860.001]
  • [Cites] Science. 1992 Jan 17;255(5042):306-12 [1549776.001]
  • [Cites] J Mol Biol. 1991 Dec 20;222(4):865-8 [1762154.001]
  • [Cites] J Clin Endocrinol Metab. 1994 Feb;78(2):398-403 [8106629.001]
  • [Cites] Am J Pathol. 1989 Mar;134(3):605-13 [2466405.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Oct;82(10):3308-14 [9329359.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Aug;85(8):2958-61 [10946911.001]
  • [Cites] Br Med J. 1977 Apr 2;1(6065):875-8 [576843.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Feb;82(2):518-23 [9024247.001]
  • [Cites] Ann Endocrinol (Paris). 2002 Apr;63(2 Pt 3):2S19-24 [12037499.001]
  • [Cites] Endocr Rev. 2001 Dec;22(6):724-63 [11739329.001]
  • [Cites] Clin Endocrinol (Oxf). 1988 May;28(5):551-8 [3145820.001]
  • [Cites] Ann Med. 1999 Oct;31 Suppl 2:23-7 [10574151.001]
  • [Cites] J Endocrinol Invest. 1980 Oct-Dec;3(4):405-14 [6782153.001]
  • [Cites] J Endocrinol Invest. 1999 Jun;22(6):409-18 [10435849.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Feb;86(2):478-81 [11157994.001]
  • [Cites] Clin Endocrinol (Oxf). 2000 Dec;53(6):719-24 [11155094.001]
  • [Cites] Am J Respir Crit Care Med. 2001 Sep 1;164(5):852-7 [11549545.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Jul;86(7):3304-10 [11443205.001]
  • [Cites] Pept Res. 1989 Jan-Feb;2(1):128-32 [2577697.001]
  • [Cites] Metabolism. 1996 Aug;45(8 Suppl 1):72-4 [8769388.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Jul;87(7):3013-8 [12107192.001]
  • [Cites] J Clin Endocrinol Metab. 1992 Sep;75(3):812-9 [1517371.001]
  • [Cites] Diabetes. 1999 Jan;48(1):77-85 [9892225.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Jul;85(7):2476-82 [10902796.001]
  • [Cites] Int J Cancer. 1997 Mar 4;70(5):530-7 [9052751.001]
  • [Cites] Acta Endocrinol Suppl (Copenh). 1978;216:207-16 [347863.001]
  • [Cites] J Biol Chem. 1997 Apr 4;272(14):9189-96 [9083050.001]
  • [Cites] Clin Endocrinol (Oxf). 1995 Jun;42(6):593-9 [7634499.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Oct;82(10):3187-91 [9329336.001]
  • [Cites] Ann Intern Med. 1986 Dec;105(6):856-61 [2877605.001]
  • [Cites] J Clin Endocrinol Metab. 1994 Jul;79(1):145-51 [8027218.001]
  • [Cites] Acta Endocrinol (Copenh). 1989 Aug;121(2):286-9 [2773624.001]
  • [Cites] Laryngoscope. 1994 Apr;104(4):484-7 [8164490.001]
  • [Cites] N Engl J Med. 2000 Apr 20;342(16):1210-1 [10770989.001]
  • [Cites] Clin Endocrinol (Oxf). 1990 Jun;32(6):719-28 [2200621.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Jan;82(1):18-22 [8989225.001]
  • [Cites] Mol Endocrinol. 1995 Mar;9(3):292-302 [7539887.001]
  • [Cites] J Clin Endocrinol Metab. 1993 Mar;76(3):721-7 [8095269.001]
  • [Cites] Ann Intern Med. 1984 Jan;100(1):78-91 [6229205.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Aug;82(8):2755-6 [9253367.001]
  • [Cites] Annu Rev Med. 1976;27:379-88 [779605.001]
  • [Cites] J Clin Endocrinol Metab. 1985 Jun;60(6):1161-5 [2860119.001]
  • [Cites] Mol Endocrinol. 1997 Mar;11(3):265-73 [9058373.001]
  • [Cites] Recent Prog Horm Res. 1999;54:397-438; discussion 438-9 [10548885.001]
  • [Cites] Pituitary. 1999;1(2):105-14 [11081188.001]
  • [Cites] Clin Endocrinol (Oxf). 1988 Oct;29(4):411-20 [3251673.001]
  • [Cites] Eur J Endocrinol. 1999 Sep;141(3):267-71 [10474124.001]
  • [Cites] J Clin Invest. 1982 Nov;70(5):965-77 [6290540.001]
  • [Cites] Am J Cardiol. 1993 Jul 15;72 (2):205-10 [8328385.001]
  • [Cites] Endocrinology. 1994 Jan;134(1):301-6 [7903931.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Feb;85(2):781-92 [10690891.001]
  • [Cites] Acta Neurochir (Wien). 1999;141(4):399-405 [10352750.001]
  • [Cites] Endocr Rev. 1991 Nov;12(4):450-82 [1684746.001]
  • [Cites] Ann Intern Med. 1990 Feb 1;112(3):173-81 [2404445.001]
  • [Cites] Clin Endocrinol (Oxf). 1989 Oct;31(4):401-10 [2627746.001]
  • [Cites] Science. 1991 Nov 8;254(5033):821-5 [1948064.001]
  • [Cites] Hosp Med. 2002 Mar;63(3):162-5 [11933820.001]
  • [Cites] J Clin Endocrinol Metab. 1995 Nov;80(11):3267-72 [7593436.001]
  • [Cites] Eur J Clin Invest. 1997 Apr;27(4):277-84 [9134375.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Feb;83(2):374-8 [9467544.001]
  • [Cites] J Clin Endocrinol Metab. 1988 Nov;67(5):958-63 [2903171.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Apr;86(4):1716-23 [11297608.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Feb;85(2):526-9 [10690849.001]
  • [Cites] Eur J Endocrinol. 2000 Nov;143(5):577-84 [11078980.001]
  • [Cites] J Clin Endocrinol Metab. 1974 May;38(5):910-2 [4823928.001]
  • [Cites] Endocrinology. 1994 Dec;135(6):2814-7 [7988476.001]
  • [Cites] Endocr Rev. 1995 Feb;16(1):3-34 [7758431.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Sep;87(9):4054-8 [12213843.001]
  • [Cites] Ann Intern Med. 1992 Nov 1;117(9):711-8 [1416572.001]
  • [Cites] Eur J Endocrinol. 2002 May;146(5):707-16 [11980628.001]
  • [Cites] Lancet. 1999 Mar 13;353(9156):895 [10093984.001]
  • [Cites] Clin Endocrinol (Oxf). 1996 Oct;45(4):415-21 [8959079.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Nov;85(11):4099-103 [11095439.001]
  • [Cites] J Biol Chem. 1994 Aug 12;269(32):20806 [8051183.001]
  • [Cites] Eur J Endocrinol. 1996 Apr;134(4):454-6 [8640297.001]
  • [Cites] Front Neuroendocrinol. 1999 Jul;20(3):157-98 [10433861.001]
  • [Cites] Metabolism. 1996 Aug;45(8 Suppl 1):27-30 [8769375.001]
  • [Cites] Horm Metab Res. 2000 Jun;32(6):224-9 [10898551.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Jan;84(1):17-23 [9920056.001]
  • [Cites] Endocr Rev. 2004 Feb;25(1):102-52 [14769829.001]
  • [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] Endocrinology. 1991 Sep;129(3):1402-8 [1874179.001]
  • [Cites] Acta Endocrinol (Copenh). 1977 Jun;85(2):235-48 [405832.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Oct;82(10):3185-6 [9329335.001]
  • [Cites] Ann Intern Med. 1994 Oct 1;121(7):478-83 [8067645.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Sep;83(9):3034-40 [9745397.001]
  • [Cites] J Endocrinol. 1991 Mar;128(3):347-57 [1707433.001]
  • [Cites] J Biol Chem. 1991 Feb 5;266(4):2252-8 [1989980.001]
  • [Cites] Endocr Rev. 1995 Aug;16(4):427-42 [8521788.001]
  • [Cites] Endocrinol Metab Clin North Am. 1992 Sep;21(3):713-35 [1355728.001]
  • [Cites] J Biol Chem. 1990 Feb 25;265(6):3111-5 [2406245.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Sep;85(9):3132-40 [10999798.001]
  • [Cites] Clin Endocrinol (Oxf). 2003 Feb;58(2):136-7 [12580926.001]
  • [Cites] J Clin Endocrinol Metab. 1990 Aug;71(2):391-7 [2199479.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Oct;87(10):4554-63 [12364434.001]
  • [Cites] Neurobiol Aging. 1989 May-Jun;10(3):227-31 [2664540.001]
  • [Cites] Metabolism. 1992 Sep;41(9 Suppl 2):51-8 [1518434.001]
  • [Cites] Drugs. 1995 Feb;49(2):255-79 [7729332.001]
  • [Cites] Am J Cardiol. 1999 May 15;83(10 ):1506-9, A8 [10335774.001]
  • [Cites] Clin Endocrinol (Oxf). 1998 Mar;48(3):311-6 [9578821.001]
  • [Cites] Life Sci. 1995;56(5):333-42 [7530798.001]
  • [Cites] J Clin Endocrinol Metab. 1988 Nov;67(5):1040-8 [2903168.001]
  • [Cites] Endocr Rev. 2003 Feb;24(1):28-47 [12588807.001]
  • [Cites] Pituitary. 1999 Nov;2(3):205-10 [11081155.001]
  • [Cites] Pituitary. 2000 May;2(4):269-76 [11081148.001]
  • [Cites] N Engl J Med. 2000 Apr 20;342(16):1171-7 [10770982.001]
  • [Cites] Trends Endocrinol Metab. 2001 May-Jun;12(4):173-8 [11295574.001]
  • [Cites] Pituitary. 2000 Oct;3(2):61-5 [11141697.001]
  • [Cites] Endocrinol Metab Clin North Am. 1992 Sep;21(3):669-92 [1521518.001]
  • [Cites] Anesthesiology. 2000 Jul;93(1):110-4 [10861153.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Aug;83(8):2730-4 [9709939.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Apr;86(4):1551-7 [11297582.001]
  • [Cites] J Clin Invest. 1997 Feb 15;99(4):789-98 [9045884.001]
  • [Cites] Metabolism. 1996 Aug;45(8 Suppl 1):67-71 [8769387.001]
  • [Cites] J Clin Endocrinol Metab. 1995 Sep;80(9):2768-75 [7673422.001]
  • [Cites] Q J Med. 1993 May;86(5):293-9 [8327647.001]
  • [Cites] J Clin Endocrinol Metab. 1978 Feb;46(2):196-202 [108287.001]
  • [Cites] J Clin Endocrinol Metab. 1996 Jun;81(6):2089-97 [8964833.001]
  • [Cites] Br J Anaesth. 2000 Feb;84(2):179-82 [10743450.001]
  • [Cites] J Neurosurg. 1994 Jul;81(1):10-4 [8207509.001]
  • [Cites] J Clin Endocrinol Metab. 1974 Feb;38(2):200-6 [4812616.001]
  • [Cites] Postgrad Med J. 1976;52suppl 1:71-4 [959128.001]
  • [Cites] J Endocrinol Invest. 1997 Jun;20(6):348-67 [9294784.001]
  • [Cites] Arch Intern Med. 1991 Aug;151(8):1573-8 [1872661.001]
  • [Cites] Acta Endocrinol (Copenh). 1977 Nov;86(3):464-72 [335755.001]
  • [Cites] Clin Endocrinol (Oxf). 1999 Mar;50(3):295-9 [10435053.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Feb;89(2):638-45 [14764775.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Dec;87(12 ):5737-45 [12466380.001]
  • [Cites] Acta Endocrinol (Copenh). 1978 Apr;87(4):687-700 [417539.001]
  • (PMID = 15301564.001).
  • [ISSN] 0012-6667
  • [Journal-full-title] Drugs
  • [ISO-abbreviation] Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Dopamine Agonists; 0 / Hormone Antagonists; 0 / Receptors, Somatotropin; 12629-01-5 / Human Growth Hormone; 51110-01-1 / Somatostatin
  • [Number-of-references] 197
  •  go-up   go-down


21. Theodoropoulou M, Tichomirowa MA, Sievers C, Yassouridis A, Arzberger T, Hougrand O, Deprez M, Daly AF, Petrossians P, Pagotto U, Beckers A, Stalla GK: Tumor ZAC1 expression is associated with the response to somatostatin analog therapy in patients with acromegaly. Int J Cancer; 2009 Nov 1;125(9):2122-6
ORBi (University of Liege). Free full Text at ORBi .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumor ZAC1 expression is associated with the response to somatostatin analog therapy in patients with acromegaly.
  • Somatostatin analogs (SSA) with their potent antisecretory and antiproliferative effects are the main medical treatment option for patients with neuroendocrine tumors, such as gastroenteropancreatic and acromegaly-associated growth hormone secreting pituitary tumors.
  • Although a good portion of acromegalic patients gets normalized after SSA treatment, strict hormonal control is not achieved in a sizeable proportion of these patients.
  • The reasons for this incomplete response to SSA treatment are unclear.
  • We have found that the tumor suppressor ZAC1 (LOT1/PLAGL1) is essential for the antiproliferative effect of SSA in pituitary tumor cells.
  • The aim of the present retrospective cohort study was to determine whether ZAC1 immunoreactivity in archival somatotrophinoma tissue derived from 45 patients with acromegaly routinely pretreated with SSA before surgery, was associated with response to SSA (normalization of GH, IGF-I and presence of tumor shrinkage).
  • A significant positive correlation was found between strong ZAC1 immunoreactivity and IGF-I normalization and presence of tumor shrinkage after SSA treatment, which was not affected by age at diagnosis, gender or duration of SSA treatment.
  • These in vivo data combined with the antiproliferative properties of ZAC1/Zac1 provide evidence of a mechanistic role for this transcription factor on SSA induced tumor shrinkage and hormone normalization.
  • [MeSH-major] Acromegaly / drug therapy. Cell Cycle Proteins / analysis. Octreotide / therapeutic use. Peptides, Cyclic / therapeutic use. Pituitary Neoplasms / drug therapy. Somatostatin / analogs & derivatives. Transcription Factors / analysis. Tumor Suppressor Proteins / analysis
  • [MeSH-minor] Adolescent. Adult. Aged. Cohort Studies. Female. Human Growth Hormone / blood. Humans. Insulin-Like Growth Factor I / analysis. Male. Middle Aged. Retrospective Studies

  • Genetic Alliance. consumer health - Acromegaly.
  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2009 UICC.
  • (PMID = 19637311.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / PLAGL1 protein, human; 0 / Peptides, Cyclic; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 118992-92-0 / lanreotide; 12629-01-5 / Human Growth Hormone; 51110-01-1 / Somatostatin; 67763-96-6 / Insulin-Like Growth Factor I; RWM8CCW8GP / Octreotide
  •  go-up   go-down


22. Casarini AP, Jallad RS, Pinto EM, Soares IC, Nonogaki S, Giannella-Neto D, Musolino NR, Alves VA, Bronstein MD: Acromegaly: correlation between expression of somatostatin receptor subtypes and response to octreotide-lar treatment. Pituitary; 2009;12(4):297-303
Genetic Alliance. consumer health - Acromegaly.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acromegaly: correlation between expression of somatostatin receptor subtypes and response to octreotide-lar treatment.
  • This study analyzes SSTR's expression in somatotrophinomas, comparing to SA response, hormonal levels, and tumor volume.
  • We analyzed 39 somatotrophinomas; 49% were treated with SA.
  • SSTR3 was more expressed in patients with tumor reduction.
  • There was a positive correlation between the percentage of tumor reduction and SSTR1, SSTR2 and SSTR3 expression.
  • [MeSH-major] Acromegaly / drug therapy. Acromegaly / metabolism. Octreotide / therapeutic use. Receptors, Somatostatin / metabolism
  • [MeSH-minor] Antineoplastic Agents, Hormonal / therapeutic use. Human Growth Hormone / metabolism. Humans. Immunohistochemistry. Insulin-Like Growth Factor I / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Somatostatin / analogs & derivatives

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Endocrinol Metab. 2005 Mar;90(3):1856-63 [15613435.001]
  • [Cites] Clin Endocrinol (Oxf). 2005 Aug;63(2):168-75 [16060910.001]
  • [Cites] Neuroendocrinology. 2004 Mar;79(3):142-8 [15103227.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Jul;86(7):2976-81 [11443154.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Aug;84(8):2759-65 [10443675.001]
  • [Cites] Clin Endocrinol (Oxf). 1992 Aug;37(2):181-5 [1395069.001]
  • [Cites] BMC Biotechnol. 2003 Oct 13;3:18 [14552656.001]
  • [Cites] Eur J Endocrinol. 2002 May;146(5):701-5 [11980627.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Jan;86(1):140-5 [11231991.001]
  • [Cites] J Clin Endocrinol Metab. 1994 Sep;79(3):724-9 [7521350.001]
  • [Cites] N Engl J Med. 1996 Jan 25;334(4):246-54 [8532003.001]
  • [Cites] Clin Endocrinol (Oxf). 2000 Jan;52(1):35-42 [10651751.001]
  • [Cites] Mol Endocrinol. 2002 Nov;16(11):2502-14 [12403839.001]
  • [Cites] J Neurochem. 2004 Jun;89(5):1057-91 [15147500.001]
  • [Cites] J Biol Chem. 1978 Sep 25;253(18):6473-83 [210185.001]
  • [Cites] Cell Physiol Biochem. 2002;12 (1):31-8 [11914546.001]
  • [Cites] J Clin Endocrinol Metab. 1994 Feb;78(2):398-403 [8106629.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Jun;88(6):2797-802 [12788890.001]
  • [Cites] Front Horm Res. 2006;35:129-34 [16809928.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Aug;90(8):4465-73 [15886238.001]
  • [Cites] Neuropeptides. 2001 Feb;35(1):1-23 [11346306.001]
  • [Cites] Clin Endocrinol (Oxf). 2005 Nov;63(5):514-9 [16268802.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Jul;87(7):3013-8 [12107192.001]
  • [Cites] Clin Endocrinol (Oxf). 2007 Aug;67(2):310-5 [17555503.001]
  • [Cites] J Clin Endocrinol Metab. 2007 May;92(5):1592-9 [17311860.001]
  • [Cites] Eur J Endocrinol. 1995 Dec;133(6):686-90 [8548053.001]
  • [Cites] J Endocrinol Invest. 2006 Oct;29(9):826-30 [17114915.001]
  • [Cites] Eur J Endocrinol. 2005 Jul;153(1):135-41 [15994755.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Aug;86(8):3809-14 [11502816.001]
  • [Cites] Lab Invest. 2005 Aug;85(8):1040-50 [15951835.001]
  • [Cites] Eur J Endocrinol. 2007 Jan;156(1):65-74 [17218727.001]
  • [Cites] J Endocrinol Invest. 1993 Mar;16(3):181-7 [8514973.001]
  • [Cites] Endocrinology. 2002 Jul;143(7):2626-34 [12072395.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Feb;85(2):781-92 [10690891.001]
  • [Cites] Endocr Rev. 1991 Nov;12(4):450-82 [1684746.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Dec;87(12):5545-52 [12466351.001]
  • [Cites] Clin Endocrinol (Oxf). 2003 Jul;59(1):115-28 [12807513.001]
  • [Cites] Front Horm Res. 2004;32:235-52 [15281350.001]
  • [Cites] J Clin Pathol. 2006 Mar;59(3):274-9 [16505278.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Apr;89(4):1577-85 [15070915.001]
  • [Cites] Biochim Biophys Acta. 2003 Sep 22;1616(1):1-84 [14507421.001]
  • [Cites] Endocr Rev. 2004 Feb;25(1):102-52 [14769829.001]
  • [Cites] J Clin Endocrinol Metab. 1995 Apr;80(4):1386-92 [7714115.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Sep;83(9):3034-40 [9745397.001]
  • [Cites] Endocr Rev. 1995 Aug;16(4):427-42 [8521788.001]
  • [Cites] Horm Res. 2000;53 Suppl 3:65-70 [10971108.001]
  • [Cites] Clin Endocrinol (Oxf). 1995 Mar;42(3):295-301 [7758235.001]
  • [Cites] Life Sci. 1995;56(5):333-42 [7530798.001]
  • [Cites] Endocr Rev. 2003 Feb;24(1):28-47 [12588807.001]
  • [Cites] Science. 1973 Jan 5;179(4068):77-9 [4682131.001]
  • [Cites] Endocr J. 2004 Apr;51(2):227-36 [15118275.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Jul;88(7):3090-8 [12843148.001]
  • (PMID = 19330452.001).
  • [ISSN] 1573-7403
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 0 / somatostatin receptor 3; 0 / somatostatin receptor 5; 0 / somatostatin receptor subtype-4; 0 / somatostatin receptor type 1; 12629-01-5 / Human Growth Hormone; 51110-01-1 / Somatostatin; 67763-96-6 / Insulin-Like Growth Factor I; RWM8CCW8GP / Octreotide
  •  go-up   go-down


23. Saveanu A, Jaquet P: Somatostatin-dopamine ligands in the treatment of pituitary adenomas. Rev Endocr Metab Disord; 2009 Jun;10(2):83-90
MedlinePlus Health Information. consumer health - Pituitary Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Somatostatin-dopamine ligands in the treatment of pituitary adenomas.
  • Somatostatin receptors (sst1-5) and dopamine receptor 2 (D2DR) are well expressed and co-localized in several human pituitary adenomas, suggesting possible functional interactions in the control of hormonal hypersecretion and tumor cell growth.
  • The present review describes the expression and functionality of these receptors in the different classes of human pituitary adenomas.
  • The sst2 agonists, octreotide and lanreotide, control GH hypersecretion and tumor growth in about 65% of somatotropinomas.
  • Such drugs are much less effective in the control of the others pituitary adenomas also expressing ssts and D2DR receptors.
  • Such ligands bearing distinct ssts and DRD2 pharmacophores may synergistically produce an increased control of secretion and/or of proliferation in the different types of pituitary adenomas.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Pituitary Neoplasms / drug therapy. Receptors, Dopamine D2 / agonists. Receptors, Somatostatin / agonists

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Invest. 1997 Nov 1;100(9):2386-92 [9410919.001]
  • [Cites] J Biol Chem. 2003 Nov 21;278(47):46741-9 [12933819.001]
  • [Cites] Eur J Endocrinol. 2005 Apr;152(4):645-54 [15817922.001]
  • [Cites] J Biol Chem. 2001 Jun 22;276(25):22621-9 [11278324.001]
  • [Cites] Pituitary. 2001 Aug;4(3):173-8 [12138990.001]
  • [Cites] Eur J Endocrinol. 1998 Nov;139(5):516-21 [9849816.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Apr;89(4):1674-83 [15070930.001]
  • [Cites] J Med Chem. 1998 Jun 18;41(13):2175-9 [9632348.001]
  • [Cites] J Nucl Med. 2003 Aug;44(8):1315-21 [12902423.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Jan;86(1):140-5 [11231991.001]
  • [Cites] Am J Physiol Endocrinol Metab. 2005 Aug;289(2):E278-87 [15769796.001]
  • [Cites] Endocr Rev. 1992 May;13(2):220-40 [1352243.001]
  • [Cites] Nat Rev Drug Discov. 2002 Oct;1(10):808-20 [12360258.001]
  • [Cites] Mol Endocrinol. 2007 Oct;21(10):2565-78 [17609435.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Sep;84(9):3268-76 [10487698.001]
  • [Cites] Cell Signal. 2007 Nov;19(11):2304-16 [17706924.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Nov;88(11):5414-21 [14602782.001]
  • [Cites] Eur J Endocrinol. 1994 Jan;130(1):80-91 [8124483.001]
  • [Cites] Biochem Biophys Res Commun. 1996 Oct 3;227(1):200-4 [8858125.001]
  • [Cites] J Clin Endocrinol Metab. 1992 Aug;75(2):540-6 [1353505.001]
  • [Cites] J Clin Endocrinol Metab. 1994 Feb;78(2):398-403 [8106629.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Jun;88(6):2797-802 [12788890.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Nov;91(11):4482-8 [16940446.001]
  • [Cites] Br J Clin Pharmacol. 2004 Apr;57(4):373-87 [15025734.001]
  • [Cites] J Clin Endocrinol Metab. 2004 May;89(5):2452-62 [15126577.001]
  • [Cites] Neuroendocrinology. 2006;83(3-4):258-63 [17047391.001]
  • [Cites] J Pharmacol Exp Ther. 2000 Aug;294(2):407-12 [10900212.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Jul;87(7):3013-8 [12107192.001]
  • [Cites] Int J Cancer. 1997 Mar 4;70(5):530-7 [9052751.001]
  • [Cites] Horm Res. 1997;47(4-6):227-34 [9167956.001]
  • [Cites] Eur J Endocrinol. 2005 Jul;153(1):135-41 [15994755.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Apr;93(4):1412-7 [18211974.001]
  • [Cites] Am J Physiol Endocrinol Metab. 2005 Dec;289(6):E1044-50 [16046458.001]
  • [Cites] Eur J Endocrinol. 2007 Jan;156(1):65-74 [17218727.001]
  • [Cites] Endocrine. 2001 Apr;14(3):329-36 [11444429.001]
  • [Cites] J Clin Endocrinol Metab. 1972 Dec;35(6):941-3 [4634493.001]
  • [Cites] Eur J Endocrinol. 2001 Jul;145(1):35-41 [11415850.001]
  • [Cites] J Biol Chem. 2004 May 14;279(20):21374-82 [15001578.001]
  • [Cites] Eur J Endocrinol. 2008 May;158(5):595-603 [18426817.001]
  • [Cites] Eur J Nucl Med. 2001 Jul;28(7):836-46 [11504080.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Oct;89(10):5181-8 [15472224.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Feb;85(2):781-92 [10690891.001]
  • [Cites] J Biol Chem. 2002 May 31;277(22):19762-72 [11896051.001]
  • [Cites] Endocr Rev. 2003 Aug;24(4):389-427 [12920149.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Dec;87(12):5545-52 [12466351.001]
  • [Cites] J Biol Chem. 2001 Apr 27;276(17):14027-36 [11134004.001]
  • [Cites] EMBO Rep. 2004 Jan;5(1):30-4 [14710183.001]
  • [Cites] Clin Endocrinol (Oxf). 2000 Apr;52(4):437-45 [10762286.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Feb;83(2):374-8 [9467544.001]
  • [Cites] J Biol Chem. 2000 Mar 17;275(11):7862-9 [10713101.001]
  • [Cites] Mol Endocrinol. 2003 Jan;17(1):93-106 [12511609.001]
  • [Cites] J Clin Endocrinol Metab. 1992 Nov;75(5):1318-25 [1358910.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Apr;93(4):1203-10 [18198230.001]
  • [Cites] Life Sci. 2006 Jan 11;78(7):689-93 [16115652.001]
  • [Cites] Eur J Endocrinol. 2003 Apr;148(4):433-42 [12656664.001]
  • [Cites] J Pharmacol Exp Ther. 2005 Aug;314(2):485-94 [15805429.001]
  • [Cites] Science. 2000 Apr 7;288(5463):154-7 [10753124.001]
  • [Cites] Front Neuroendocrinol. 1999 Jul;20(3):157-98 [10433861.001]
  • [Cites] Trends Pharmacol Sci. 2005 Mar;26(3):131-7 [15749158.001]
  • [Cites] Clin Endocrinol (Oxf). 2005 Jul;63(1):39-44 [15963059.001]
  • [Cites] Cancer Cell Int. 2006 Mar 06;6:5 [16519802.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Sep;88(9):4239-45 [12970293.001]
  • [Cites] J Clin Endocrinol Metab. 1989 Sep;69(3):500-9 [2760167.001]
  • [Cites] J Clin Endocrinol Metab. 1992 Nov;75(5):1310-7 [1430093.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Mar 5;99(5):3294-9 [11880655.001]
  • [Cites] J Biol Chem. 2004 Sep 10;279(37):38636-43 [15247250.001]
  • [Cites] Pituitary. 1999;1(2):115-20 [11081189.001]
  • [Cites] Eur J Endocrinol. 1999 Oct;141(4):396-408 [10526255.001]
  • [Cites] Endocr Rev. 2003 Feb;24(1):28-47 [12588807.001]
  • [Cites] FEBS Lett. 2003 Aug 28;550(1-3):11-7 [12935878.001]
  • [Cites] Regul Pept. 2007 Oct 4;143(1-3):109-17 [17531331.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Feb;89(2):638-45 [14764775.001]
  • (PMID = 18651224.001).
  • [ISSN] 1573-2606
  • [Journal-full-title] Reviews in endocrine & metabolic disorders
  • [ISO-abbreviation] Rev Endocr Metab Disord
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Receptors, Dopamine D2; 0 / Receptors, Somatostatin
  • [Number-of-references] 72
  •  go-up   go-down


24. Sathyapalan T, Lowry M, Turnbull LW, Rowland-Hill C, Atkin SL: Mechanism of action of octreotide in acromegalic tumours in vivo using dynamic contrast-enhanced magnetic resonance imaging. Pituitary; 2007;10(3):233-6
Hazardous Substances Data Bank. GADOPENTETATE DIMEGLUMINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • CONTEXT: Octreotide causes significant tumour shrinkage in patients with acromegaly but the exact mechanism of action is unclear in vivo.
  • DESIGN: Five patients with acromegaly were treated with octreotide as primary medical therapy.
  • MAIN OUTCOME MEASURES: Amplitude of contrast intake, exchange rate and maximum enhancement index of tumour tissue was compared before and after treatment.
  • RESULTS: Amplitude of contrast intake (9.87 +/- 3.52 vs. 4.97 +/- 1.96 P < or = 0.05) and exchange rate (6.27 +/- 1.57 vs. 1.63 +/- 0.76 P value < or = 0.01) were significantly higher at baseline in adenoma compared to normal pituitary tissue but was comparable to normal pituitary tissue after treatment.
  • There was a significant decrease in amplitude of contrast intake and exchange rate which relates to functional vascularity of adenoma at 24 weeks compared to baseline (P-values 0.026 and 0.002 respectively) but there were no significant changes in the normal pituitary tissue.
  • CONCLUSION: DCE-MRI in acromegalic tumours treated with octreotide showed a significant reduction in functional vascularity after octreotide therapy compared to baseline in pituitary adenomas.
  • This supports the antiangiogenic action of somatostatin analogue therapy in vitro, but it remains unclear if this mechanism is important clinically in analogue pre-treatment reducing the effect of radiotherapy on these pituitary tumours.
  • [MeSH-major] Acromegaly / drug therapy. Adenoma / drug therapy. Angiogenesis Inhibitors / therapeutic use. Antineoplastic Agents, Hormonal / therapeutic use. Growth Hormone-Secreting Pituitary Adenoma / drug therapy. Octreotide / therapeutic use
  • [MeSH-minor] Adult. Aged. Contrast Media. Drug Resistance, Neoplasm. Female. Gadolinium DTPA. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Regional Blood Flow / drug effects. Somatostatin / analogs & derivatives. Somatostatin / therapeutic use

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Endocrinol Metab. 2005 Mar;90(3):1856-63 [15613435.001]
  • [Cites] Clin Endocrinol (Oxf). 2002 Oct;57(4):425-41 [12354124.001]
  • [Cites] Semin Oncol. 1994 Oct;21(5 Suppl 13):61-4 [7992085.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Jul;88(7):3105-12 [12843150.001]
  • [Cites] J Comput Assist Tomogr. 1991 Jul-Aug;15(4):621-8 [2061479.001]
  • [Cites] Technol Cancer Res Treat. 2006 Apr;5(2):127-34 [16551132.001]
  • [Cites] Eur J Endocrinol. 2001 Dec;145(6):717-26 [11720896.001]
  • [Cites] Magn Reson Med. 1991 Feb;17(2):357-67 [2062210.001]
  • [Cites] Magn Reson Med. 1992 Mar;24(1):174-6 [1556924.001]
  • [Cites] J Neurosurg. 2002 Sep;97(3):525-30 [12296634.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Mar;85(3):1287-9 [10720077.001]
  • [Cites] Magn Reson Imaging. 1996;14(4):373-80 [8782175.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Feb 28;92(5):1580-4 [7878022.001]
  • [Cites] Br J Cancer. 2005 Apr 25;92(8):1493-8 [15812556.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Nov;86(11):5194-200 [11701676.001]
  • [Cites] J Physiol Paris. 2000 May-Aug;94(3-4):205-10 [11087998.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Aug;90(8):4483-8 [15899958.001]
  • [Cites] Pharmacol Ther. 2004 Apr;102(1):61-85 [15056499.001]
  • [Cites] Int J Clin Pharmacol Ther. 2002 Dec;40(12):573-4 [12503819.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Oct;87(10):4554-63 [12364434.001]
  • [Cites] Int J Clin Pharmacol Ther. 2003 Dec;41(12):600-2 [14692711.001]
  • (PMID = 17541750.001).
  • [ISSN] 1386-341X
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents, Hormonal; 0 / Contrast Media; 51110-01-1 / Somatostatin; K2I13DR72L / Gadolinium DTPA; RWM8CCW8GP / Octreotide
  •  go-up   go-down


25. Pawlikowski M, Melen-Mucha G: Perspectives of new potential therapeutic applications of somatostatin analogs. Neuro Endocrinol Lett; 2003 Feb-Apr;24(1-2):21-7
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Perspectives of new potential therapeutic applications of somatostatin analogs.
  • At the present time only two long-acting somatostatin (SS) analogs, octreotide and lanreotide, are commonly used in the routine therapy.
  • The established indications for SS analogs treatment include acromegaly, neuroendocrine tumors of the pancreas and gastrointestinal tract, and some gastro-enterologic diseases (pancreatitis, gastrointestinal bleedings, refractory diarrheas, pancreatic and intestinal fistulas).
  • The recent investigations allow to predict the enlargement of therapeutic applications of SS analogs.
  • It concerns pituitary tumors other than somatotropinoma, tumors of other endocrine glands like thyroid and adrenal gland, as well as some non-endocrine tumors.
  • The pre- or postoperative in vivo imaging of SS receptors by means of the receptor scintigraphy, as well as the post-operative identification of SS receptor subtypes in the excised tumor tissues using immunohistochemistry, should play an important role in the prediction of the effects of SS analog treatment.
  • Beside oncology, new therapeutic applications of SS analogs could be presumed among others in ophthalmology; it concerns the treatment of progressive Graves-Basedow ophtalmopathy, diabetic retinopathy, glaucoma and corneal diseases connected with corneal vascularization.
  • [MeSH-major] Hormone Antagonists / therapeutic use. Somatostatin / analogs & derivatives. Somatostatin / therapeutic use
  • [MeSH-minor] Acromegaly / drug therapy. Animals. Antineoplastic Agents, Hormonal / therapeutic use. Endocrine Gland Neoplasms / drug therapy. Humans. Receptors, Somatostatin / drug effects

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12743527.001).
  • [ISSN] 0172-780X
  • [Journal-full-title] Neuro endocrinology letters
  • [ISO-abbreviation] Neuro Endocrinol. Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Sweden
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Hormone Antagonists; 0 / Receptors, Somatostatin; 51110-01-1 / Somatostatin
  • [Number-of-references] 72
  •  go-up   go-down


26. Fusco A, Gunz G, Jaquet P, Dufour H, Germanetti AL, Culler MD, Barlier A, Saveanu A: Somatostatinergic ligands in dopamine-sensitive and -resistant prolactinomas. Eur J Endocrinol; 2008 May;158(5):595-603
Hazardous Substances Data Bank. DOPAMINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: Ten percent of patients with prolactinoma fail to respond with normalization of prolactin (PRL) and tumor shrinkage under dopamine agonist (DA) therapy.
  • The resistance to treatment is linked to a loss of dopamine receptor 2 (D2DR).
  • D2DR remains the primary target for effective treatment of prolactinomas.

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18426817.001).
  • [ISSN] 1479-683X
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / BIM 23926; 0 / Ergolines; 0 / Ligands; 0 / RNA, Messenger; 0 / Receptors, Dopamine D2; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 0 / somatostatin receptor 5; 0 / somatostatin receptor type 1; 51110-01-1 / Somatostatin; 98H1T17066 / pasireotide; LL60K9J05T / cabergoline; VTD58H1Z2X / Dopamine
  •  go-up   go-down


27. Donangelo I, Rodacki M, Peixoto MC, Vaisman M, Caldas NR, Gadelha MR: Dependency and analgesia related to treatment with subcutaneous octreotide in patients with growth hormone-secreting tumors. Endocr Pract; 2004 Mar-Apr;10(2):107-11
MedlinePlus Health Information. consumer health - Pituitary Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dependency and analgesia related to treatment with subcutaneous octreotide in patients with growth hormone-secreting tumors.
  • OBJECTIVE: To describe three patients diagnosed with somatotropinomas in whom the analgesic effect of octreotide was observed, along with dependency to the drug.
  • METHODS: These patients had pituitary macroadenomas treated with transphenoidal surgery and pituitary radiotherapy, and received high daily doses (>900 microg/day) of subcutaneous octreotide because of persistent high levels of growth hormone and insulin-like growth factor I (IGF-I).
  • RESULTS: Headache occurred prior to drug administration in all three cases, with relief soon after.
  • We also observed tolerance to octreotide's analgesic and anti-secretory actions (one patient), craving for the drug (two patients), withdrawal syndrome (one patient), and drug abuse (one patient).
  • CONCLUSION: Dependency syndrome may occur when high doses of octreotide are used, sometimes leading to drug abuse.
  • Tolerance to the growth hormone anti-secretory effect of the drug may encourage physicians to increase doses to levels at which drug dependency has been observed.
  • [MeSH-major] Adenoma / drug therapy. Adenoma / secretion. Antineoplastic Agents, Hormonal / adverse effects. Human Growth Hormone / secretion. Octreotide / adverse effects. Pituitary Neoplasms / drug therapy. Pituitary Neoplasms / secretion. Substance-Related Disorders
  • [MeSH-minor] Adolescent. Adult. Combined Modality Therapy. Drug Tolerance. Female. Humans. Middle Aged

  • MedlinePlus Health Information. consumer health - Drug Abuse.
  • MedlinePlus Health Information. consumer health - Drugs and Young People.
  • MedlinePlus Health Information. consumer health - Opioid Abuse and Addiction.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15256326.001).
  • [ISSN] 1530-891X
  • [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
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 12629-01-5 / Human Growth Hormone; RWM8CCW8GP / Octreotide
  •  go-up   go-down


28. Wasko R, Sawicka J, Stachowiak C, Kozak W, Junik R, Sowinski J: [Effect of lanreotide on prolactin level in patients with pituitary mixed tumors]. Ann Endocrinol (Paris); 2002 Dec;63(6 Pt 1):532-5
MedlinePlus Health Information. consumer health - Pituitary Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Effect of lanreotide on prolactin level in patients with pituitary mixed tumors].
  • [Transliterated title] Influence du lanréotide sur la concentration sérique de prolactine chez les patients atteints de tumeurs somato-lactotropes.
  • Acromegaly is a disease caused by a pituitary tumor (somatotropinoma) or by ectopic secretion of GH or IGF-1.
  • Last time a lanreotide and an octreotide (the somatostatine analogues) are useful in the therapy of acromegaly.
  • We noticed that the lanreotide caused not only serum level reduction of a growth hormone but also prolactine in patients with mixed pituitary tumors.
  • [MeSH-major] Acromegaly / etiology. Antineoplastic Agents / therapeutic use. Peptides, Cyclic / therapeutic use. Pituitary Neoplasms / blood. Pituitary Neoplasms / drug therapy. Prolactin / blood. Somatostatin / analogs & derivatives. Somatostatin / therapeutic use
  • [MeSH-minor] Adult. Female. Follow-Up Studies. Growth Hormone / secretion. Human Growth Hormone / blood. Humans. Male. Middle Aged. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12527855.001).
  • [ISSN] 0003-4266
  • [Journal-full-title] Annales d'endocrinologie
  • [ISO-abbreviation] Ann. Endocrinol. (Paris)
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Peptides, Cyclic; 118992-92-0 / lanreotide; 12629-01-5 / Human Growth Hormone; 51110-01-1 / Somatostatin; 9002-62-4 / Prolactin; 9002-72-6 / Growth Hormone
  •  go-up   go-down


29. Jallad RS, Musolino NR, Kodaira S, Cescato VA, Bronstein MD: Does partial surgical tumour removal influence the response to octreotide-LAR in acromegalic patients previously resistant to the somatostatin analogue? Clin Endocrinol (Oxf); 2007 Aug;67(2):310-5
MedlinePlus Health Information. consumer health - Pituitary Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Does partial surgical tumour removal influence the response to octreotide-LAR in acromegalic patients previously resistant to the somatostatin analogue?
  • OBJECTIVE: To compare the intrapatient response to the same dose of slow-release octreotide (OCT-LAR) before and after noncurative surgery in acromegalic patients who did not attain disease control after primary treatment with OCT-LAR.
  • PATIENTS: Eleven acromegalic patients (eight men, aged 42.45 +/- 11.15 years, 10 macroadenomas) received OCT-LAR (20 mg, n = 1; 30 mg, n = 10) every 28 days as the primary treatment (1stOCT-LAR) for 11.3 +/- 4.2 months, without IGF-I normalization.
  • MEASUREMENTS: GH and IGF-I serum concentrations were obtained under basal conditions as well as during treatment.
  • Pituitary tumour volume was assessed by magnetic resonance imaging (MRI) of the sella.
  • Tumour shrinkage was observed in eight of 10 patients with macroadenomas (median 63.7%, range 24.5-75.5%).
  • MRI confirmed surgical tumour removal (median 64%, range 4.9-96.6%) in eight of the 10 patients.
  • The degree of surgical tumour reduction did not correlate with IGF-I normalization (P = 0.794).
  • CONCLUSIONS: Using strict criteria (same patient, same drug, same dose) our results strongly suggest that the surgical reduction of tumour mass can improve the outcome of OCT-LAR treatment in acromegalic patients resistant to primary therapy with SA.
  • [MeSH-major] Acromegaly / drug therapy. Antineoplastic Agents, Hormonal / therapeutic use. Growth Hormone-Secreting Pituitary Adenoma / surgery. Octreotide / therapeutic use. Pituitary Neoplasms / surgery. Somatostatin / metabolism
  • [MeSH-minor] Adult. Aged. Delayed-Action Preparations. Drug Resistance, Neoplasm. Female. Growth Hormone / blood. Humans. Insulin-Like Growth Factor I / analysis. Magnetic Resonance Imaging. Male. Middle Aged. Multivariate Analysis. Prospective Studies. Treatment Outcome

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17555503.001).
  • [ISSN] 0300-0664
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Delayed-Action Preparations; 51110-01-1 / Somatostatin; 67763-96-6 / Insulin-Like Growth Factor I; 9002-72-6 / Growth Hormone; RWM8CCW8GP / Octreotide
  •  go-up   go-down


30. Bronstein MD: Acromegaly: molecular expression of somatostatin receptor subtypes and treatment outcome. Front Horm Res; 2006;35:129-34
Genetic Alliance. consumer health - Acromegaly.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acromegaly: molecular expression of somatostatin receptor subtypes and treatment outcome.
  • SSTR2 and SSTR5 are usually expressed in GH-secreting pituitary tumors, and both octreotide and lanreotide bind preferentially to SSTR2 and, to a lesser extent, to SSTR5.
  • SA inhibitory effects on GH secretion and tumor cell proliferation can occur together or be dissociated events, depending on the tumor expression of SSTR subtypes involved in each mechanism.
  • The development of specific somatostatin subtypes analogs, mainly for SSTR5, of a SSTR2-SSTR5 bispecific compound, and of a "universal" analog with high affinity to SSTR1, 2, 3, and 5 showed preliminary, albeit promising results for the treatment of resistant somatotropic adenomas.
  • [MeSH-major] Acromegaly / drug therapy. Acromegaly / metabolism. Protein Isoforms / metabolism. Receptors, Somatostatin / metabolism
  • [MeSH-minor] Dopamine Agonists / therapeutic use. Drug Design. Drug Resistance, Neoplasm. Drug Therapy, Combination. Gene Expression. Growth Hormone / antagonists & inhibitors. Humans. Octreotide / therapeutic use. Peptides, Cyclic / therapeutic use. Pituitary Neoplasms / drug therapy. Somatostatin / analogs & derivatives. Somatostatin / therapeutic use. Treatment Outcome

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16809928.001).
  • [ISSN] 0301-3073
  • [Journal-full-title] Frontiers of hormone research
  • [ISO-abbreviation] Front Horm Res
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Dopamine Agonists; 0 / Peptides, Cyclic; 0 / Protein Isoforms; 0 / Receptors, Somatostatin; 118992-92-0 / lanreotide; 51110-01-1 / Somatostatin; 9002-72-6 / Growth Hormone; RWM8CCW8GP / Octreotide
  • [Number-of-references] 19
  •  go-up   go-down


31. 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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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, the alpha-subunit of the heterotrimeric GTP-binding protein, is coded from the GNAS gene, which is imprinted in a tissue-specific manner.
  • Gs alpha is paternally silenced in normal pituitary, but Gs alpha imprinting relaxation is found in some tumoral tissue.
  • The paternal and maternal transcripts were quantified using allele-specific real-time PCR and FokI polymorphism.
  • As is the case for the gsp oncogene, high Gs alpha expression in gsp- tumors was associated with smaller tumor size and better octreotide sensitivity.
  • [MeSH-major] Adenoma / genetics. Drug Resistance, Neoplasm / genetics. GTP-Binding Protein alpha Subunits, Gs / genetics. Genomic Imprinting. Growth Hormone-Secreting Pituitary Adenoma / genetics
  • [MeSH-minor] Antineoplastic Agents, Hormonal / therapeutic use. Blotting, Western. DNA Methylation. Humans. Octreotide / therapeutic use. Prolactinoma / drug therapy. Prolactinoma / genetics. Prolactinoma / pathology. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


32. Heaney AP: PPAR-gamma in Cushing's disease. Pituitary; 2004;7(4):265-9
Hazardous Substances Data Bank. Corticotropin .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The majority of pituitary tumors that cause Cushing's disease are small (<1 cm diameter), and most disease morbidity is due to the effects of elevated, non-suppressible, ACTH levels that these tumors secrete.
  • Tumor-derived ACTH leads to adrenal-derived steroid hypersecretion and results in many disabling and sometimes life-threatening symptoms including abnormal fat deposition, skin thinning, psychological disturbances, hypertension, diabetes, osteoporosis and muscle weakness.
  • In experienced specialized centers, 70% of corticotroph microadenomas can be successfully resected by transsphenoidal pituitary surgery.
  • However, surgical "cure" rates for larger ACTH-secreting pituitary tumors are achieved in only 30% of cases, and recent reports highlight a significant recurrence rate after longer term follow-up even in smaller tumors.
  • Post-surgical persistence of ACTH hypersecretion may require pituitary-directed radiation, but this treatment may take some time to be effective, and like extensive surgical pituitary tumor resection, ultimately leads to partial- or total hypopituitarism in approximately 80% of cases.
  • Although hypercortisolism may be completely resolved by adrenalectomy, this procedure does not suppress, and may act as a stimulus to pituitary tumor growth, and is associated with other co-morbidity.
  • Although some currently available drug-based treatments for Cushing's disease effectively control hypercortisolism, their drawback has been that they do not impact on pituitary tumor growth.
  • Recent studies have identified the potential utility of peroxisome-proliferator activating receptor-gamma (PPAR-gamma) novel ligands in in vitro, and in vivo Cushing's disease models, and have paved the way for early clinical studies to develop novel therapeutic approaches in Cushing's disease.
  • [MeSH-major] PPAR gamma / metabolism. Pituitary ACTH Hypersecretion / drug therapy
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / drug therapy. ACTH-Secreting Pituitary Adenoma / pathology. Adrenocorticotropic Hormone / metabolism. Cushing Syndrome / drug therapy. Cushing Syndrome / metabolism. Humans. Ligands. Neoplasm Invasiveness. Pituitary Neoplasms / drug therapy. Pituitary Neoplasms / pathology. Thiazolidinediones / therapeutic use

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Eur J Endocrinol. 2004 Jun;150(6):863-75 [15191358.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Mar;90(3):1340-6 [15585550.001]
  • [Cites] Neuro Endocrinol Lett. 2005 Feb;26(1):51-4 [15726020.001]
  • [Cites] J Clin Invest. 2003 May;111(9):1381-8 [12727930.001]
  • [Cites] Clin Endocrinol (Oxf). 1991 Jan;34(1):63-9 [2004474.001]
  • [Cites] Diabetes. 1996 Dec;45(12):1661-9 [8922349.001]
  • [Cites] Nature. 1990 Oct 18;347(6294):645-50 [2129546.001]
  • [Cites] Clin Endocrinol (Oxf). 2005 Feb;62(2):259-61 [15670207.001]
  • [Cites] Acta Neurochir (Wien). 2001;143(5):477-81; discussion 481-2 [11482698.001]
  • [Cites] Nat Rev Cancer. 2004 Apr;4(4):285-95 [15057288.001]
  • [Cites] Nat Med. 1998 Sep;4(9):1046-52 [9734398.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Nov;84(11):3859-66 [10566620.001]
  • [Cites] Ann Intern Med. 1988 Sep 15;109(6):487-93 [2843068.001]
  • [Cites] Neuro Oncol. 2001 Jul;3(3):141-51 [11465394.001]
  • [Cites] Lancet. 1987 Mar 7;1(8532):573 [2881126.001]
  • [Cites] J Clin Endocrinol Metab. 1985 Oct;61(4):718-22 [4031015.001]
  • [Cites] Nat Med. 2002 Nov;8(11):1281-7 [12379847.001]
  • [Cites] Ann N Y Acad Sci. 2002 Sep;970:119-33 [12381547.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Feb;85(2):526-9 [10690849.001]
  • [Cites] N Engl J Med. 1995 Mar 23;332(12):791-803 [7862184.001]
  • [Cites] Nature. 1998 Jan 1;391(6662):79-82 [9422508.001]
  • [Cites] Clin Ther. 2002 Mar;24(3):378-96 [11952022.001]
  • [Cites] Int J Epidemiol. 2000 Apr;29(2):197-207 [10817114.001]
  • [Cites] Pituitary. 2002;5(2):77-82 [12675504.001]
  • [Cites] Diabetes. 1998 Apr;47(4):507-14 [9568680.001]
  • [Cites] Clin Endocrinol (Oxf). 2002 Apr;56(4):541-51 [11966748.001]
  • [Cites] Clin Endocrinol (Oxf). 1991 Aug;35(2):169-78 [1657460.001]
  • [Cites] Nature. 1992 Aug 27;358(6389):771-4 [1324435.001]
  • [Cites] J Neurosurg. 2001 Jul;95(1):1-8 [11453376.001]
  • [Cites] Clin Cancer Res. 2003 Jan;9(1):1-9 [12538445.001]
  • (PMID = 16416039.001).
  • [ISSN] 1386-341X
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ligands; 0 / PPAR gamma; 0 / Thiazolidinediones; 9002-60-2 / Adrenocorticotropic Hormone; AA68LXK93C / 2,4-thiazolidinedione
  • [Number-of-references] 35
  •  go-up   go-down


33. Park C, Yang I, Woo J, Kim S, Kim J, Kim Y, Sohn S, Kim E, Lee M, Park H, Jung J, Park S: Somatostatin (SRIF) receptor subtype 2 and 5 gene expression in growth hormone-secreting pituitary adenomas: the relationship with endogenous srif activity and response to octreotide. Endocr J; 2004 Apr;51(2):227-36
MedlinePlus Health Information. consumer health - Pituitary Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Somatostatin (SRIF) receptor subtype 2 and 5 gene expression in growth hormone-secreting pituitary adenomas: the relationship with endogenous srif activity and response to octreotide.
  • To investigate the potential pathophysiologic role of human SRIF receptor gene expression in GH-secreting adenomas in acromegalic patients, we studied the relationship between the SRIF receptor gene expression, endogenous SRIF activity and exogenous response to octreotide in 16 acromagalic patients.
  • Pituitary tumor SRIF receptor subtype 2 and 5 (sst2 and sst5) mRNA levels were measured by real-time RT-PCR.
  • These results suggest common transcriptional and/or post-transcriptonal regulatory mechanisms for these SRIF receptor subtypes within GH-secreting pituitary adenomas.
  • The functional observations suggest that the degree (or level) of sst2 and sst5 expression is critical for the ultimate GH response of somatotropinomas to endogenous SRIF tone and exogenous SRIF analogue therapy.
  • [MeSH-major] Adenoma / drug therapy. Adenoma / metabolism. Antineoplastic Agents, Hormonal / therapeutic use. Octreotide / therapeutic use. Pituitary Neoplasms / drug therapy. Pituitary Neoplasms / metabolism. Receptors, Somatostatin / metabolism
  • [MeSH-minor] Acromegaly / drug therapy. Adult. Female. Gene Expression. Human Growth Hormone / secretion. Humans. Male. Middle Aged. Treatment Outcome

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15118275.001).
  • [ISSN] 0918-8959
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 0 / somatostatin receptor 5; 12629-01-5 / Human Growth Hormone; RWM8CCW8GP / Octreotide
  •  go-up   go-down


34. Pisarek H, Pawlikowski M, Kunert-Radek J, Winczyk K: Does the response of GH-secreting pituitary adenomas to octreotide depend on the cellular localization of the somatostatin receptor subtypes SSTR2 and SSTR5? Endokrynol Pol; 2010 Mar-Apr;61(2):178-81
MedlinePlus Health Information. consumer health - Pituitary Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Does the response of GH-secreting pituitary adenomas to octreotide depend on the cellular localization of the somatostatin receptor subtypes SSTR2 and SSTR5?
  • INTRODUCTION: The immunohistochemical examination of somatostatin receptor (SSTR) subtypes expression in different endocrine tumours, including pituitary adenomas, revealed membranous or cytoplasmic distribution of SSTR1-5.
  • In an earlier study a positive correlation between the summarized score of SSTR2A + SSTR2B expressions and growth hormone (GH) response to octreotide administration was found, independently of receptor distribution within the cell.
  • The pituitary adenomas from these patients were immunostained to determine the hormonal phenotype and expression of SSTR subtypes.
  • The cytoplasmic but not the membranous localization is connected with the higher responsiveness to the octreotide in somatotropinomas.
  • [MeSH-major] Adenoma / drug therapy. Adenoma / pathology. Octreotide / pharmacology. Pituitary Neoplasms / drug therapy. Pituitary Neoplasms / pathology. Receptors, Somatostatin / analysis
  • [MeSH-minor] Adult. Aged. Antineoplastic Agents, Hormonal / pharmacology. Chemotherapy, Adjuvant. Cytoplasm / pathology. Female. Growth Hormone / secretion. Humans. Immunohistochemistry. Male. Middle Aged. Tissue Distribution

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20464704.001).
  • [ISSN] 0423-104X
  • [Journal-full-title] Endokrynologia Polska
  • [ISO-abbreviation] Endokrynol Pol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 0 / somatostatin receptor 5; 9002-72-6 / Growth Hormone; RWM8CCW8GP / Octreotide
  •  go-up   go-down






Advertisement