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1. Biermasz NR, Smit JW, Pereira AM, Frölich M, Romijn JA, Roelfsema F: Acromegaly caused by growth hormone-releasing hormone-producing tumors: long-term observational studies in three patients. Pituitary; 2007;10(3):237-49
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  • [Title] Acromegaly caused by growth hormone-releasing hormone-producing tumors: long-term observational studies in three patients.
  • During medical treatment basal GH secretion remained (slightly) elevated and secretory regularity was decreased in 24 h blood sampling studies.
  • We did not observe development of tachyphylaxis towards the drug or radiological evidence of (growing) metastases.
  • We propose life-long suppressive therapy with somatostatin analogs in cases with persisting elevated serum GHRH concentrations after removal of the primary tumor.
  • [MeSH-major] Acromegaly / etiology. Adenoma / secretion. Carcinoid Tumor / secretion. Human Growth Hormone / secretion. Lung Neoplasms / secretion. Pancreatic Neoplasms / secretion. Paraneoplastic Endocrine Syndromes / metabolism. Parathyroid Neoplasms / secretion
  • [MeSH-minor] Adult. Entropy. Female. Hormones / blood. Humans. Longitudinal Studies. Magnetic Resonance Imaging. Male. Middle Aged. Octreotide. Pituitary Gland / pathology. Positron-Emission Tomography. Tomography, X-Ray Computed. Treatment Outcome

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  • (PMID = 17541749.001).
  • [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] 0 / Hormones; 12629-01-5 / Human Growth Hormone; RWM8CCW8GP / Octreotide
  • [Other-IDs] NLM/ PMC2045692
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2. Sasaki M, Funayama H, Asano T, Kasono K, Namai K, Tamemoto H, Ueno S, Ota M, Kawakami M, Shinoda S, Ishikawa SE: Full-blown Cushing's disease after an episode of pituitary apoplexy. Endocr J; 2003 Oct;50(5):501-6
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  • [Title] Full-blown Cushing's disease after an episode of pituitary apoplexy.
  • The present study reports a rare case of full-blown Cushing's disease several years after an episode of pituitary apoplexy.
  • Ten years ago she had an episode of pituitary apoplexy.
  • Diabetes mellitus was diagnosed at age 56, and thereafter she had been controlled her plasma glucose with diet therapy and oral hypoglycemic agents.
  • Dexamethasone suppression test showed that a large dose of 8 mg dexamethasone, but not a small dose of 2 mg, suppressed the pituitary-adrenocortical axis.
  • Brain T(1)-weighted magnetic resonance imaging depicted a low signal of pituitary tumor, which was not enhanced by gadolinium.
  • The pituitary tumor was removed by transsphenoidal adenomectomy, and immunohistochemistry revealed an ACTH-producing adenoma.
  • The evidence suggested the possibility that the two pituitary tumors with dormant period of several years were a recurrence of ACTH-producing tumors in the present patient.
  • [MeSH-major] Cushing Syndrome / etiology. Pituitary Apoplexy / complications
  • [MeSH-minor] Adenoma / complications. Adenoma / diagnosis. Adenoma / secretion. Adenoma / surgery. Administration, Oral. Adrenocorticotropic Hormone / secretion. Diabetes Complications. Diabetes Mellitus / diet therapy. Diabetes Mellitus / drug therapy. Female. Humans. Hypoglycemic Agents / administration & dosage. Magnetic Resonance Imaging. Middle Aged. Neoplasm Recurrence, Local. Obesity / complications. Pituitary Neoplasms / complications. Pituitary Neoplasms / diagnosis. Pituitary Neoplasms / secretion. Pituitary Neoplasms / surgery

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  • (PMID = 14614205.001).
  • [ISSN] 0918-8959
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Hypoglycemic Agents; 9002-60-2 / Adrenocorticotropic Hormone
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3. Ahtiainen P, Sharp V, Rulli SB, Rivero-Müller A, Mamaeva V, Röyttä M, Huhtaniemi I: Enhanced LH action in transgenic female mice expressing hCGbeta-subunit induces pituitary prolactinomas; the role of high progesterone levels. Endocr Relat Cancer; 2010 Sep;17(3):611-21
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  • [Title] Enhanced LH action in transgenic female mice expressing hCGbeta-subunit induces pituitary prolactinomas; the role of high progesterone levels.
  • The etiology of pituitary adenomas remains largely unknown, with the exception of involvement of estrogens in the formation of prolactinomas.
  • We have examined the molecular pathogenesis of prolactin-producing pituitary adenomas in transgenic female mice expressing the human choriongonadotropin (hCG) beta-subunit.
  • Curiously, despite normal estrogen levels, large prolactinomas developed in these mice, and we provide here several lines of evidence that the elevated P(4) levels are involved in the growth of these estrogen-dependent tumors.
  • The antiprogestin mifepristone inhibited tumor growth, and combined postgonadectomy estradiol/P(4) treatment was more effective than estrogen alone in inducing tumor growth.
  • Evidence for direct growth-promoting effect of P(4) was obtained from cultures of primary mouse pituitary cells and rat somatomammotroph GH3 cells.
  • The mouse tumors and cultured cells revealed stimulation of the cyclin D1/cyclin-dependent kinase 4/retinoblastoma protein/transcription factor E2F1 pathway in the growth response to P(4).
  • If extrapolated to humans, and given the importance of endogenous P(4) and synthetic progestins in female reproductive functions and their pharmacotherapy, it is relevant to revisit the potential role of these hormones in the origin and growth of prolactinomas.

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  • (PMID = 20453081.001).
  • [ISSN] 1479-6821
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] ENG
  • [Grant] United Kingdom / Wellcome Trust / / 063552; United Kingdom / Wellcome Trust / / 082101
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Chorionic Gonadotropin, beta Subunit, Human; 4G7DS2Q64Y / Progesterone; 9002-62-4 / Prolactin; 9002-67-9 / Luteinizing Hormone; EC 2.7.11.22 / Cyclin-Dependent Kinase 4
  • [Other-IDs] NLM/ PMC2881531
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4. Bangaru ML, Woodliff J, Raff H, Kansra S: Growth suppression of mouse pituitary corticotroph tumor AtT20 cells by curcumin: a model for treating Cushing's disease. PLoS One; 2010;5(4):e9893
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  • [Title] Growth suppression of mouse pituitary corticotroph tumor AtT20 cells by curcumin: a model for treating Cushing's disease.
  • BACKGROUND: Pituitary corticotroph tumors secrete excess adrenocorticotrophic hormone (ACTH) resulting in Cushing's disease (CD).
  • Standard treatment includes surgery and, if not successful, radiotherapy, both of which have undesirable side effects and frequent recurrence of the tumor.
  • Pharmacotherapy using PPARgamma agonists, dopamine receptor agonists, retinoic acid or somatostatin analogs is still experimental.
  • 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.
  • CONCLUSION: The ability of curcumin to inhibit NFkappaB and induce apoptosis in pituitary corticotroph tumor cells leads us to propose developing it as a novel therapeutic agent for the treatment of CD.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / drug therapy. Cell Proliferation / drug effects. Curcumin / pharmacology. Pituitary ACTH Hypersecretion / drug therapy
  • [MeSH-minor] Adrenocorticotropic Hormone / secretion. Animals. Antineoplastic Agents. Apoptosis / drug effects. Cell Line, Tumor. Dose-Response Relationship, Drug. Mice. NF-kappa B / antagonists & inhibitors

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  • [ErratumIn] PLoS One. 2010;5(4). doi:10.1371/annotation/38a101d6-a1f2-4a74-ab63-bc5c61e5f62b
  • (PMID = 20405005.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / NF-kappa B; 9002-60-2 / Adrenocorticotropic Hormone; IT942ZTH98 / Curcumin
  • [Other-IDs] NLM/ PMC2854133
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5. Kovacs K, Horvath E: Effects of medical therapy on pituitary tumors. Ultrastruct Pathol; 2005 May-Aug;29(3-4):163-7
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  • [Title] Effects of medical therapy on pituitary tumors.
  • Previously surgery and irradiation were the only available procedures to treat patients with pituitary tumors.
  • During the last few decades, novel drugs such as dopamine agonists and long-acting somatostatin analogs were developed and, an alternative medical therapy emerged.
  • This paper summarizes the effect of medical therapy on the morphologic features of pituitary tumors and illustrates the ultrastructural alterations on electron micrographs.
  • Currently drugs can be used in the management of pituitary tumors secreting GH, PRL, and/or TSH in excess.
  • No medical therapy is available so far for ACTH-, FSH-, LH-, or alpha-subunit-secreting tumors as well as non-hormone-secreting pituitary tumors.
  • Dopamine agonists are effective in the management of PRL-secreting tumors; they cause marked reversible tumor shrinkage in the substantial majority of patients.
  • Long-acting somatostatin analogs are useful in the management of GH- and TSH-secreting pituitary tumors; they lead to mild to moderate tumor shrinkage in approximately 50% of cases.
  • In patients treated with these drugs reduction of elevated blood hormone levels and amelioration of clinical symptoms ensue.
  • Blood hormone levels increase and the clinical symptoms reappear after discontinuation of treatment.
  • Recently GH receptor blockers (pegvisomant) were introduced in the treatment of GH-producing pituitary adenomas.
  • To the authors' knowledge the effect of these drugs on the morphology of pituitary tumors has not been revealed so far.
  • [MeSH-major] Dopamine Agonists / therapeutic use. Human Growth Hormone / analogs & derivatives. Octreotide / therapeutic use. Pituitary Neoplasms / drug therapy
  • [MeSH-minor] Humans. Microscopy, Electron, Transmission. Prolactin / secretion. Thyrotropin / secretion. Treatment Outcome

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  • (PMID = 16036872.001).
  • [ISSN] 0191-3123
  • [Journal-full-title] Ultrastructural pathology
  • [ISO-abbreviation] Ultrastruct Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dopamine Agonists; 0 / pegvisomant; 12629-01-5 / Human Growth Hormone; 9002-62-4 / Prolactin; 9002-71-5 / Thyrotropin; RWM8CCW8GP / Octreotide
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6. Kobayashi T, Mori Y, Uchiyama Y, Kida Y, Fujitani S: Long-term results of gamma knife surgery for growth hormone-producing pituitary adenoma: is the disease difficult to cure? J Neurosurg; 2005 Jan;102(s_supplement):119-123

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  • [Title] Long-term results of gamma knife surgery for growth hormone-producing pituitary adenoma: is the disease difficult to cure?
  • OBJECT: The authors conducted a study to determine the long-term results of gamma knife surgery for residual or recurrent growth hormine (GH)-producing pituitary adenomas and to compare the results with those after treatment of other pituitary adenomas.
  • The mean maximum dose was 35.3 Gy and the mean margin dose was 18.9 Gy.
  • Growth hormone normalization (GH < 1.0 ng/ml) was found in 4.8%, nearly normal (< 2.0 ng/ml) in 11.9%, significantly decreased (< 5.0 ng/ml) in 23.8%, decreased in 21.4%, unchanged in 21.4%, and increased in 16.7%.
  • CONCLUSIONS: Gamma knife surgery was effective and safe for the control of tumors; however, normalization of GH and IGF-1 secretion was difficult to achieve in cases with large tumors and low-dose radiation.
  • Gamma knife radiosurgery is thus indicated for small tumors after surgery or medication therapy when a relatively high-dose radiation is required.

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  • (PMID = 28306435.001).
  • [ISSN] 1933-0693
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Keywords] NOTNLM ; gamma knife surgery / growth hormone—producing pituitary adenoma / insulin-like growth factor
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7. Kobayashi T, Mori Y, Uchiyama Y, Kida Y, Fujitani S: Long-term results of gamma knife surgery for growth hormone-producing pituitary adenoma: is the disease difficult to cure? J Neurosurg; 2005 Jan;102 Suppl:119-23
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term results of gamma knife surgery for growth hormone-producing pituitary adenoma: is the disease difficult to cure?
  • OBJECT: The authors conducted a study to determine the long-term results of gamma knife surgery for residual or recurrent growth hormine (GH)-producing pituitary adenomas and to compare the results with those after treatment of other pituitary adenomas.
  • The mean maximum dose was 35.3 Gy and the mean margin dose was 18.9 Gy.
  • Growth hormone normalization (GH < 1.0 ng/ml) was found in 4.8%, nearly normal (< 2.0 ng/ml) in 11.9%, significantly decreased (< 5.0 ng/ml) in 23.8%, decreased in 21.4%, unchanged in 21.4%, and increased in 16.7%.
  • CONCLUSIONS: Gamma knife surgery was effective and safe for the control of tumors; however, normalization of GH and IGF-1 secretion was difficult to achieve in cases with large tumors and low-dose radiation.
  • Gamma knife radiosurgery is thus indicated for small tumors after surgery or medication therapy when a relatively high-dose radiation is required.
  • [MeSH-major] Adenoma / secretion. Adenoma / surgery. Human Growth Hormone / secretion. Pituitary Neoplasms / secretion. Pituitary Neoplasms / surgery. Radiosurgery / instrumentation
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Follow-Up Studies. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Neoplasm Recurrence, Local. Outcome Assessment (Health Care). Pituitary ACTH Hypersecretion / pathology. Pituitary ACTH Hypersecretion / surgery. Prolactinoma / pathology. Prolactinoma / surgery

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  • (PMID = 15662793.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 12629-01-5 / Human Growth Hormone
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8. Petrossians P, Thonnard AS, Beckers A: Medical treatment in Cushing's syndrome: dopamine agonists and cabergoline. Neuroendocrinology; 2010;92 Suppl 1:116-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Medical treatment in Cushing's syndrome: dopamine agonists and cabergoline.
  • Dopamine (DA) is a catecholamine with a wide range of functions and whose five subtype receptors are found in different organs where they exert a mainly inhibitory action.
  • Since this action may also appear in a number of secretory tumors in various locations, DA agonists have elicited some interest as a medical treatment for hypercorticism.
  • Non-iatrogenic Cushing's syndromes are due in 70% of the cases to a pituitary adrenocorticotropic hormone (ACTH)-producing adenoma, and, less frequently, to an adrenal adenoma or an ectopic ACTH secretion by a neuroendocrine tumor.
  • First-line treatment in Cushing's syndrome consists of the surgical removal of the secreting tumor.
  • However, surgery may not achieve a complete cure in a number of cases, hence emphasizing the potential benefit of a medical complementary treatment, which could also benefit patients as an alternative approach, either when waiting for, or when the patient is not eligible for surgery.
  • Studies of corticotropic adenomas have shown that 80% of these tumors express D2 receptors.
  • Clinical trials of DA agonists in Cushing's disease have shown an inhibitory effect of these drugs with an inhibition of ACTH secretion and/or a decrease of tumor size.
  • There are only a few cases of documented use of DA agonists in ectopic ACTH secretion, but when the tumor expresses DA receptors, DA agonists may represent a useful complementary treatment.
  • DA receptors are also expressed in normal and tumoral adrenals, suggesting a potential use of DA agonists in Cushing's syndrome secondary to adrenal tumors.
  • In conclusion, DA agonists represent a potential preparatory or complementary treatment for endogenous Cushing's syndrome, especially in Cushing's disease.
  • In the future, association of these drugs with somatostatin analogs may also prove beneficial.
  • [MeSH-major] Cushing Syndrome / drug therapy. Dopamine Agonists / therapeutic use. Ergolines / therapeutic use

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  • [Copyright] Copyright © 2010 S. Karger AG, Basel.
  • (PMID = 20829631.001).
  • [ISSN] 1423-0194
  • [Journal-full-title] Neuroendocrinology
  • [ISO-abbreviation] Neuroendocrinology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Dopamine Agonists; 0 / Ergolines; LL60K9J05T / cabergoline
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9. Shomali ME, Katznelson L: Medical therapy of gonadotropin-producing and nonfunctioning pituitary adenomas. Pituitary; 2002;5(2):89-98
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Medical therapy of gonadotropin-producing and nonfunctioning pituitary adenomas.
  • Clinically nonfunctioning pituitary adenomas are one of the most common types of pituitary tumors.
  • Unless they present with symptoms related to local mass effect, most tumors are detected incidentally when imaging studies are performed for other reasons.
  • Although clinically nonfunctioning, most of these tumors have evidence, in vitro, of gonadotropin hormone or glycoprotein subunit production.
  • When these tumors present as macroadenomas, often with associated mass effect and hypopituitarism, primary therapy is neurosurgery.
  • The role for medical therapy will be reviewed here.
  • [MeSH-major] Adenoma / drug therapy. Adenoma / secretion. Gonadotropins / secretion. Pituitary Neoplasms / drug therapy. Pituitary Neoplasms / secretion
  • [MeSH-minor] Dopamine Agonists / therapeutic use. Gonadotropin-Releasing Hormone / analogs & derivatives. Humans. Somatostatin / analogs & derivatives

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  • (PMID = 12675506.001).
  • [ISSN] 1386-341X
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / M01 RR01066; United States / NIA NIH HHS / AG / R29 AG15882
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dopamine Agonists; 0 / Gonadotropins; 33515-09-2 / Gonadotropin-Releasing Hormone; 51110-01-1 / Somatostatin
  • [Number-of-references] 100
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10. Vance ML: Medical treatment of functional pituitary tumors. Neurosurg Clin N Am; 2003 Jan;14(1):81-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Medical treatment of functional pituitary tumors.
  • Medical therapy with a dopamine agonist is the most effective for treatment of a prolactin-producing adenoma and is considered as primary treatment.
  • Surgery and pituitary radiation are reserved for patients who either do not tolerate or do not respond to a dopamine agonist drug.
  • A somatostatin analogue is effective medical therapy for patients with acromegaly, and this is usually administered if there is persistent GH hypersecretion after surgical resection.
  • Medical treatment for patients with Cushing's disease is directed at the adrenal glands to reduce cortisol hypersecretion.
  • Unfortunately, there is no effective medical therapy to reduce pituitary corticotropin production.
  • Medical therapy for a gonadotrope adenoma with a dopamine agonist or somatostatin analogue has limited utility but is employed in patients who are unable to undergo surgery and may delay or prevent additional tumor growth.
  • Many patients with a pituitary adenoma can be successfully treated with one treatment, either a dopamine agonist for a prolactinoma or surgery for other types of tumors.
  • A substantial number of patients require multimodality therapy, however, including medical therapy, surgery, and pituitary radiation.
  • Because the biologic behavior of pituitary adenomas varies considerably, a patient with a pituitary adenoma requires lifelong regular monitoring for hormone hypersecretion, tumor recurrence, and development of new pituitary hormone deficiency.
  • [MeSH-major] Adenoma / drug therapy. Pituitary Neoplasms / drug therapy

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  • (PMID = 12690980.001).
  • [ISSN] 1042-3680
  • [Journal-full-title] Neurosurgery clinics of North America
  • [ISO-abbreviation] Neurosurg. Clin. N. Am.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 53
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11. Wiesner TD, Trantakis C, Meixensberger J, Koch CA, Zimmer C, Paschke R: [Structure of an interdisciplinary pituitary outpatient care unit at the University Hospital of Leipzig and results for treatment of prolactin and growth hormone secreting pituitary tumors]. Med Klin (Munich); 2005 Apr 15;100(4):173-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Structure of an interdisciplinary pituitary outpatient care unit at the University Hospital of Leipzig and results for treatment of prolactin and growth hormone secreting pituitary tumors].
  • [Transliterated title] Arbeitsweise einer interdisziplinären neurochirurgisch-endokrinologischen Sprechstunde für Hypophysentumoren am Universitätsklinikum Leipzig und Ergebnisse der Behandlung von hormonaktiven Hypophysenadenomen.
  • BACKGROUND: Treatment of patients with pituitary adenomas is complex and involves several medical specialties.
  • At the Medical Center of the University of Leipzig, Germany, an interdisciplinary pituitary outpatient care unit has been established for 6 years.
  • METHODS: The interdisciplinary collaboration and the outcome of patients with growth hormone-(GH-) and prolactin-secreting pituitary adenomas are described.
  • Moreover, therapeutic strategies for patients with hormonally active pituitary adenomas are presented and discussed.
  • RESULTS: In patients suffering from GH-producing adenomas, a remission could be achieved in 80% (microadenomas) and 40% (macroadenomas) of the cases, respectively.
  • Furthermore, prolactinomas decreased in size during treatment in at least 75% of all cases depending on the initial size of the lesion which is also comparable to data from other groups.
  • CONCLUSION: Taken together, an interdisciplinary approach improves outcome and quality of care of patients with hormonally active pituitary adenomas.
  • [MeSH-major] Adenoma / therapy. Pituitary Neoplasms / therapy. Prolactinoma / therapy
  • [MeSH-minor] Acromegaly / drug therapy. Acromegaly / surgery. Acromegaly / therapy. Adult. Age Factors. Combined Modality Therapy. Dopamine Agonists / therapeutic use. Female. Follow-Up Studies. Germany. Growth Hormone / blood. Growth Hormone / secretion. Hospital Units. Humans. Interdisciplinary Communication. Male. Middle Aged. Outpatients. Patient Care Team. Prolactin / blood. Prolactin / secretion. Sex Factors. Time Factors

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  • (PMID = 15834525.001).
  • [ISSN] 0723-5003
  • [Journal-full-title] Medizinische Klinik (Munich, Germany : 1983)
  • [ISO-abbreviation] Med. Klin. (Munich)
  • [Language] ger
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Dopamine Agonists; 9002-62-4 / Prolactin; 9002-72-6 / Growth Hormone
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12. Gola M, Doga M, Bonadonna S, Mazziotti G, Vescovi PP, Giustina A: Neuroendocrine tumors secreting growth hormone-releasing hormone: Pathophysiological and clinical aspects. Pituitary; 2006;9(3):221-9
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  • [Title] Neuroendocrine tumors secreting growth hormone-releasing hormone: Pathophysiological and clinical aspects.
  • Hypothalamic GHRH is secreted into the portal system, binds to specific surface receptors of the somatotroph cell and elicits intracellular signals that modulate pituitary GH synthesis and/or secretion.
  • Moreover, GHRH is synthesized and expressed in multiple extrapituitary tissues.
  • Excessive peripheral production of GHRH by a tumor source would therefore be expected to cause somatotroph cell hyperstimulation, increased GH secretion and eventually pituitary acromegaly.
  • Immunoreactive GHRH is present in several tumors, including carcinoid tumors, pancreatic cell tumors, small cell lung cancers, endometrial tumors, adrenal adenomas, and pheochromocytomas which have been reported to secrete GHRH.
  • The distinction of pituitary vs. extrapituitary acromegaly is extremely important in planning effective management.
  • Dynamic pituitary tests are not helpful in distinguishing acromegalic patients with pituitary tumors from those harbouring extrapituitary tumors.
  • Plasma GHRH levels are usually elevated in patients with peripheral GHRH-secreting tumors, and are normal or low in patients with pituitary acromegaly.
  • Unique and unexpected clinical features in an acromegalic patient, including respiratory wheezing or dyspnea, facial flushing, peptic ulcers, or renal stones sometimes are helpful in alerting the physician to diagnosing non pituitary endocrine tumors.
  • If no facility to measure plasma GHRH is available, and in the absence of MRI evidence of pituitary adenoma, a CT scan of the thorax and abdominal ultrasound could be performed to exclude with good approximation the possibility of an ectopic GHRH syndrome.
  • Surgical resection of the tumor secreting ectopic GHRH should be the logical approach to a patient with ectopic GHRH syndrome.
  • Standard chemotherapy directed at GHRH-producing carcinoid tumors is generally unsuccessful in controlling the activated GH axis.
  • Therefore, although cytotoxic chemotherapy, pituitary surgery, or irradiation still remain available therapeutic options, long-acting somatostatin analogs are now preferred as a second-line therapy in patients with carcinoid tumors and ectopic GHRH-syndrome.
  • [MeSH-major] Acromegaly / etiology. Adenoma / secretion. Carcinoid Tumor / secretion. Growth Hormone-Releasing Hormone / secretion. Growth Hormone-Secreting Pituitary Adenoma / secretion. Neuroendocrine Tumors / secretion. Paraneoplastic Endocrine Syndromes / etiology
  • [MeSH-minor] Animals. Biomarkers, Tumor / blood. Diagnosis, Differential. Human Growth Hormone / blood. Humans. Insulin-Like Growth Factor I / metabolism. Treatment Outcome. Up-Regulation

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  • (PMID = 17036195.001).
  • [ISSN] 1573-7403
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I; 9034-39-3 / Growth Hormone-Releasing Hormone
  • [Number-of-references] 101
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13. Nasr C, Mason A, Mayberg M, Staugaitis SM, Asa SL: Acromegaly and somatotroph hyperplasia with adenomatous transformation due to pituitary metastasis of a growth hormone-releasing hormone-secreting pulmonary endocrine carcinoma. J Clin Endocrinol Metab; 2006 Dec;91(12):4776-80
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  • [Title] Acromegaly and somatotroph hyperplasia with adenomatous transformation due to pituitary metastasis of a growth hormone-releasing hormone-secreting pulmonary endocrine carcinoma.
  • CONTEXT: GHRH excess from extracranial endocrine tumors is known to cause somatotroph hyperplasia and acromegaly.
  • Hypothalamic gangliocytomas producing GHRH are also known to be associated with pituitary adenomas causing acromegaly.
  • OBJECTIVES: The objective of this study was to describe a case of acromegaly due to a pulmonary GHRH-secreting endocrine carcinoma with metastasis to the pituitary gland and to look at the peculiar histological features of this case.
  • After delivery, she underwent radiation and chemotherapy for pulmonary and skeletal metastases.
  • Her disease was clinically stable for 7 yr until she developed bitemporal hemianopia.
  • Histological examination confirmed metastatic endocrine carcinoma to the pituitary, and immunohistochemistry localized GHRH to the tumor cells.
  • The adjacent pituitary exhibited somatotroph hyperplasia with abundant reactivity for GH and alpha-subunit.
  • CONCLUSION: This is the first report of a GHRH-producing endocrine tumor metastasizing to the pituitary and causing local hyperstimulation with somatotroph hyperplasia and adenomatous transformation.
  • [MeSH-major] Acromegaly / complications. Acromegaly / etiology. Adenoma / etiology. Carcinoma / complications. Growth Hormone-Releasing Hormone / secretion. Lung Neoplasms / complications. Paraneoplastic Endocrine Syndromes / complications. Pituitary Neoplasms / secondary. Somatotrophs / pathology

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  • (PMID = 16968791.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hormones, Ectopic; 0 / Indium Radioisotopes; 9034-39-3 / Growth Hormone-Releasing Hormone
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14. Mezosi E, Nemes O: [Treatment of pituitary adenomas]. Orv Hetil; 2009 Sep 27;150(39):1803-10
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Treatment of pituitary adenomas].
  • According to epidemiological studies, the prevalence of pituitary adenomas is 16.5% and the majority of them are "incidentalomas".
  • The symptoms of pituitary disorders are often non-specific; disturbances of pituitary function, compression symptoms, hypophysis apoplexy or accidental findings may help the diagnosis.
  • The hormonal evaluation of pituitary adenomas is different from the algorithm used in the disorders of peripheral endocrine organs.
  • The first-line therapy of prolactinomas are the dopamine agonists, and the aims of the treatment are to normalize the prolactin level, restore fertility in child-bearing age, decrease tumor mass, save or improve the residual pituitary function and inhibit the relapse of the disease.
  • In case of tumors with good therapeutic response, medical therapy can be withdrawn after 3-5 years; hyperprolactinemia will not recur in 2/3 of these patients.
  • Neurosurgery is the primary therapy of GH-, ACTH-, TSH-producing and inactive adenomas.
  • Acromegalic patients with unresectable tumors have a great benefit from somatostatin analog treatment.
  • The growth hormone receptor antagonist pegvisomant is the newest modality for the treatment of acromegaly.
  • The medical therapy of Cushing's disease is still based on the inhibition of steroid production.
  • The rare TSH-producing tumor can respond to both dopamine agonist and somatostatin analog therapy.
  • The application of conventional radiotherapy has decreased; radiotherapy is mainly used in the treatment of invasive, incurable or malignant tumors.
  • Further studies are needed to elucidate the exact role of radiosurgery and fractionated stereotaxic irradiation in the treatment of pituitary tumors.
  • [MeSH-major] Adenoma / therapy. Pituitary Hormones / blood. Pituitary Neoplasms / therapy
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / therapy. Acromegaly / drug therapy. Acromegaly / etiology. Adrenocorticotropic Hormone / blood. Aminoquinolines / therapeutic use. Bromocriptine / therapeutic use. Cushing Syndrome / drug therapy. Cushing Syndrome / etiology. Dopamine Agonists / therapeutic use. Female. Growth Hormone-Secreting Pituitary Adenoma / therapy. Human Growth Hormone / analogs & derivatives. Human Growth Hormone / blood. Human Growth Hormone / therapeutic use. Humans. Hypophysectomy. Incidental Findings. Male. Pregnancy. Pregnancy Complications, Neoplastic / therapy. Prolactinoma / therapy. Radiosurgery. Receptors, Somatotropin / antagonists & inhibitors. Somatostatin / analogs & derivatives. Somatostatin / therapeutic use. Thyrotropin / blood

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  • (PMID = 19758960.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / Aminoquinolines; 0 / Dopamine Agonists; 0 / Pituitary Hormones; 0 / Receptors, Somatotropin; 0 / pegvisomant; 12629-01-5 / Human Growth Hormone; 3A64E3G5ZO / Bromocriptine; 51110-01-1 / Somatostatin; 80Q9QWN15M / quinagolide; 9002-60-2 / Adrenocorticotropic Hormone; 9002-71-5 / Thyrotropin; 98H1T17066 / pasireotide
  • [Number-of-references] 28
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15. Ragel BT, Couldwell WT: Pituitary carcinoma: a review of the literature. Neurosurg Focus; 2004 Apr 15;16(4):E7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pituitary carcinoma: a review of the literature.
  • Pituitary carcinomas, defined as distant metastases of a pituitary neoplasm, are rare; fewer than 140 reports exist in the English literature.
  • The initial presenting pituitary tumor is usually a secreting, invasive macroadenoma, with adrenocorticotropic hormone (ACTH)--and prolactin (PRL)--secreting tumors being the most common.
  • The latency period between the diagnosis of a pituitary tumor and the diagnosis of a pituitary carcinoma is 9.5 years for ACTH-producing lesions and 4.7 years for PRL-secreting tumors.
  • Treatment options include additional surgery, radiotherapy, and chemotherapy, all of which are associated with poor results.
  • Future studies will focus on identifying those invasive pituitary tumors most likely to metastasize and treating them aggressively before they progress to pituitary carcinomas.
  • [MeSH-major] Carcinoma / diagnosis. Carcinoma / therapy. Pituitary Neoplasms / diagnosis. Pituitary Neoplasms / therapy
  • [MeSH-minor] Adrenocorticotropic Hormone / secretion. Biomarkers, Tumor / analysis. Gene Expression Regulation, Neoplastic. Genes, p53. Genes, ras / genetics. Humans. Pituitary Gland / pathology. Pituitary Gland / ultrastructure. Point Mutation. Prolactin / secretion

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  • [CommentIn] Neurosurg Focus. 2005 Sep 15;19(3):E11; author reply E11 [16196164.001]
  • (PMID = 15191336.001).
  • [ISSN] 1092-0684
  • [Journal-full-title] Neurosurgical focus
  • [ISO-abbreviation] Neurosurg Focus
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 9002-60-2 / Adrenocorticotropic Hormone; 9002-62-4 / Prolactin
  • [Number-of-references] 122
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16. Lee EJ, Jameson JL: Cell-specific Cre-mediated activation of the diphtheria toxin gene in pituitary tumor cells: potential for cytotoxic gene therapy. Hum Gene Ther; 2002 Mar 1;13(4):533-42
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  • [Title] Cell-specific Cre-mediated activation of the diphtheria toxin gene in pituitary tumor cells: potential for cytotoxic gene therapy.
  • Diphtheria toxin has been suggested for the treatment of malignant cancer.
  • In this paper, we describe a strategy for targeting the expression of the diphtheria toxin gene to growth hormone (GH)-producing pituitary tumor cells using adenoviral vectors.
  • We generated adenoviral vectors in which a stuffer DNA fragment, flanked by two loxP sequences, was placed between the GH or cytomegalovirus (CMV) promoters and the diphtheria toxin gene (GH-loxP-DT, and CMV-loxP-DT) or the beta-Gal gene (GH-loxP-Gal, and CMV-loxP-Gal).
  • Co-infection of GH-loxP-DT with either CMV-Cre or GH-Cre induced cytotoxicity that was limited to GH4 cells.
  • Intratumoral co-injection of adenoviruses carrying diphtheria toxin (GH-loxP-DT, and CMV-loxP-DT) and Cre recombinase (GH-Cre, and CMV-Cre) caused rapid regression of the transplanted GH4 tumors.
  • These results indicate that Cre-mediated activation of a loxP-repressed form of the DT gene provides a useful strategy for targeted suicide gene therapy.
  • This approach may be useful for GH-secreting adenomas and should be applicable to other neoplastic disorders.
  • [MeSH-major] Diphtheria Toxin / genetics. Integrases / genetics. Pituitary Neoplasms / genetics. Viral Proteins / genetics
  • [MeSH-minor] Adenoviridae. Animals. Cell Death / genetics. Gene Expression Regulation, Neoplastic. Gene Transfer Techniques. Genetic Therapy. Genetic Vectors. Growth Hormone / biosynthesis. Growth Hormone / genetics. Mice. Mice, Nude. Mice, Transgenic. Promoter Regions, Genetic. Tumor Cells, Cultured

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  • (PMID = 11874631.001).
  • [ISSN] 1043-0342
  • [Journal-full-title] Human gene therapy
  • [ISO-abbreviation] Hum. Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Diphtheria Toxin; 0 / Viral Proteins; 9002-72-6 / Growth Hormone; EC 2.7.7.- / Cre recombinase; EC 2.7.7.- / Integrases
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17. Janson ET: Treatment of neuroendocrine tumors with somatostatin analogs. Pituitary; 2006;9(3):249-56
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of neuroendocrine tumors with somatostatin analogs.
  • Neuroendocrine tumors constitute a group of hormone producing tumors originating from neuroendocrine cells in different organs.
  • Most tumors have a low proliferation index measured by Ki67 and the progression of the tumor is slow.
  • For some patients these symptoms can be life- threatening as in midgut carcinoid patients suffering from carcinoid crises with extensive flushes and hypotension or in patients with severe diarrhea induced by tumors producing vasointestinal polypeptide.
  • In many other patients the hormone-induced symptoms interfere with the ability to carry out ordinary daily activities.
  • The introduction of somatostatin analogs in the treatment of these hormone related symptoms has made it possible to control most of them and has added significantly to the quality of life for this group of patients.
  • [MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Neuroendocrine Tumors / drug therapy. Somatostatin / therapeutic use
  • [MeSH-minor] Activities of Daily Living. Animals. Cell Proliferation / drug effects. Humans. Quality of Life. Receptors, Somatostatin / drug effects. Receptors, Somatostatin / metabolism. Treatment Outcome

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  • (PMID = 17001461.001).
  • [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; 51110-01-1 / Somatostatin
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18. Zangeneh F, Young WF Jr, Lloyd RV, Chiang M, Kurczynski E, Zangeneh F: Cushing's syndrome due to ectopic production of corticotropin-releasing hormone in an infant with ganglioneuroblastoma. Endocr Pract; 2003 Sep-Oct;9(5):394-9
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  • [Title] Cushing's syndrome due to ectopic production of corticotropin-releasing hormone in an infant with ganglioneuroblastoma.
  • OBJECTIVE: To report the first recognized case of Cushing's syndrome due to a corticotropin-releasing hormone (CRH)-secreting ganglioneuroblastoma, which was found in an 18-month-old boy with hypertensive encephalopathy.
  • The serum adrenocorticotropic hormone (ACTH) concentration was 7 pg/mL (normal, 10 to 60), and the CRH level was 439 pg/mL (normal, 24 to 40).
  • Despite discordant dynamic endocrine testing and negative somatostatin receptor scintigraphy, computed tomography showed a right 3.6- by 3.0-cm extra-adrenal retroperitoneal mass with central calcification extending 7 cm cephalocaudally.
  • The patient underwent exploratory laparotomy, followed by chemotherapy.
  • Because most CRH-producing tumors also secrete ACTH, the ectopic production may represent a paracrine phenomenon in addition to an endocrine phenomenon.
  • The ectopic CRH may also indirectly provoke pituitary ACTH secretion.
  • This dual mechanism may explain the resistance of the tumor to feedback inhibition and a CRH-stimulation response indistinguishable from that observed in pituitary-dependent Cushing's syndrome.
  • [MeSH-major] Corticotropin-Releasing Hormone / metabolism. Cushing Syndrome / etiology. Ganglioneuroblastoma / complications. Retroperitoneal Neoplasms / complications
  • [MeSH-minor] Humans. Immunohistochemistry. Infant. Male. Tomography, X-Ray Computed

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  • (PMID = 14583423.001).
  • [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] 9015-71-8 / Corticotropin-Releasing Hormone
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19. Clemmons DR, Chihara K, Freda PU, Ho KK, Klibanski A, Melmed S, Shalet SM, Strasburger CJ, Trainer PJ, Thorner MO: Optimizing control of acromegaly: integrating a growth hormone receptor antagonist into the treatment algorithm. J Clin Endocrinol Metab; 2003 Oct;88(10):4759-67
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  • [Title] Optimizing control of acromegaly: integrating a growth hormone receptor antagonist into the treatment algorithm.
  • Current guidelines for the treatment of acromegaly have not considered recent advances in medical therapy, in particular, the place of pegvisomant, a GH receptor antagonist.
  • Treatment goals include normalizing biochemical markers, controlling tumor mass, preserving pituitary function, and relieving signs and symptoms.
  • Surgery reduces tumor volume and is considered first-line therapy.
  • Therefore, pharmacotherapy is often used following surgery or as first-line therapy for nonresectable tumors.
  • Dopamine agonists can be considered in patients exhibiting minimal disease or those with GH-prolactin-cosecreting tumors but will not achieve hormone normalization in most patients.
  • Pegvisomant, the newest therapeutic option, blocks GH action at peripheral receptors, normalizes IGF-I levels, reduces signs and symptoms, and corrects metabolic defects.
  • Pegvisomant is the most effective drug treatment for acromegaly in normalizing IGF-I and producing a clinical response; it is the preferred agent in patients resistant to or intolerant of somatostatin analogs.
  • [MeSH-major] Acromegaly / drug therapy. Growth Hormone / antagonists & inhibitors. Human Growth Hormone / therapeutic use
  • [MeSH-minor] Algorithms. Dopamine Agonists / therapeutic use. Humans

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  • (PMID = 14557452.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dopamine Agonists; 0 / pegvisomant; 12629-01-5 / Human Growth Hormone; 9002-72-6 / Growth Hormone
  • [Number-of-references] 92
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20. Schoof E, Dörr HG, Kiess W, Lüdecke DK, Freitag E, Zindel V, Rascher W, Dötsch J: Five-year follow-up of a 13-year-old boy with a pituitary adenoma causing gigantism--effect of octreotide therapy. Horm Res; 2004;61(4):184-9
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  • [Title] Five-year follow-up of a 13-year-old boy with a pituitary adenoma causing gigantism--effect of octreotide therapy.
  • BACKGROUND/AIM: In children, there is little experience with octreotide therapy for pituitary tumors, especially growth hormone (GH) producing adenomas.
  • We report on a 13-year-old boy with gigantism due to a GH-producing pituitary adenoma caused by a Gsalpha mutation on the basis of McCune-Albright syndrome.
  • METHODS: At the age of 6.5 years a GH- and prolactin-producing pituitary adenoma was diagnosed.
  • RESULTS: During therapy with octreotide, the growth rate dropped to normal values; however, rose again after 2 years of treatment.
  • After 5 years of octreotide therapy, GH (6.9 microg/l), IGF-I (620 microg/l), IGF-binding protein 3 (5.4 mg/l), and prolactin (17.0 ng/ml) levels were still elevated.
  • A magnetic resonance imaging scan showed an unchanged residual 4-mm rim of adenoma at the pituitary site.
  • Side effects from octreotide therapy were not reported by the patient or his family.
  • The therapy was changed to the long-acting release octreotide analog octreotide-LAR.
  • After 1 year of treatment with octreotide-LAR, the GH level was 1.0 microg/l, and the prospective final height dropped by 10 cm.
  • CONCLUSIONS: This case demonstrates that combined surgical and medical treatment can influence the prognosis of childhood gigantism; however, the prognosis of this rare condition remains uncertain.
  • [MeSH-major] Adenoma / complications. Adenoma / drug therapy. Antineoplastic Agents, Hormonal / therapeutic use. Gigantism / etiology. Octreotide / therapeutic use. Pituitary Neoplasms / complications. Pituitary Neoplasms / drug therapy
  • [MeSH-minor] Adolescent. GTP-Binding Protein alpha Subunits, Gs / genetics. Human Growth Hormone / secretion. Humans. Magnetic Resonance Imaging. Male. Neoplasm, Residual / drug therapy

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  • [Copyright] Copyright 2004 S. Karger AG, Basel
  • (PMID = 14739526.001).
  • [ISSN] 0301-0163
  • [Journal-full-title] Hormone research
  • [ISO-abbreviation] Horm. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 12629-01-5 / Human Growth Hormone; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs; RWM8CCW8GP / Octreotide
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21. Perrini S, Carreira MC, Conserva A, Laviola L, Giorgino F: Metabolic implications of growth hormone therapy. J Endocrinol Invest; 2008 Sep;31(9 Suppl):79-84
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  • [Title] Metabolic implications of growth hormone therapy.
  • GH deficiency and GH replacement therapy exert opposite effects on body composition and fat accumulation, suggesting that GH may directly regulate adipocyte functions.
  • Multiple studies have shown that in tissues previously deprived of GH, short-term stimulation with GH is able to mimic the actions of insulin, including stimulation of amino-acid and glucose transport, and lipogenesis.
  • However, the antagonistic effects of GH on insulin-mediated metabolic responses are well-documented: GH excess in patients with GH-producing pituitary tumors causes hyperinsulinemia, insulin resistance, and even clinical diabetes mellitus.
  • [MeSH-major] Human Growth Hormone / adverse effects. Human Growth Hormone / therapeutic use. Hypopituitarism / drug therapy. Metabolic Diseases / etiology
  • [MeSH-minor] Humans. Hypoglycemic Agents / therapeutic use. Insulin / pharmacology. Insulin Resistance / physiology. Intra-Abdominal Fat / drug effects. Intra-Abdominal Fat / metabolism. Models, Biological. Receptor Cross-Talk / drug effects. Receptor Cross-Talk / physiology

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  • (PMID = 19020393.001).
  • [ISSN] 0391-4097
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Hypoglycemic Agents; 0 / Insulin; 12629-01-5 / Human Growth Hormone
  • [Number-of-references] 32
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22. Kellner O, Voigt W, Schneyer U, Dempke W, Schmoll HJ: HCG induced hyperthyreosis in germ cell cancer. Anticancer Res; 2000 Nov-Dec;20(6D):5135-8
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  • Human germ cell tumors have the unique capacity for totipotential differentiation.
  • AFP (the product of normal yolk sac) and HCG (produced by trophoblastic tissues) are frequently produced by germ cell tumors.
  • The a-subunit of the glycoprotein HCG is identical to that of several pituitary glycoprotein hormones (e.g.
  • However, the role of TSH within this hormone superfamily is still not yet established.
  • An ultrasound examination of the thyroid gland showed no abnormalities and no iodine exposure had occurred during the last months.
  • The patient was then entered in our phase-II-study for relapsing germ cell carcinomas using a high-dose chemotherapy regime (paclitaxel 175 mg/m2, ifosfamide 9.000 mg/m2, carboplatin 900 mg/m2, etoposide 900 mg/m2) with subsequent retransfusion of collected stem cells.
  • In this case report we have demonstrated a clear positive correlation between HCG levels and thyroidal hormones in a patient with germ cell tumor suggesting a direct stimulation of hormone producing thyroidal cells by HCG, however, this was not associated with clinical symptoms of hyperthyreosis.
  • [MeSH-major] Chorionic Gonadotropin / adverse effects. Hyperthyroidism / chemically induced. Neoplasms, Germ Cell and Embryonal / physiopathology
  • [MeSH-minor] Adult. Humans. Male. Thyroid Gland / drug effects

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  • (PMID = 11326684.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Chorionic Gonadotropin
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23. Nieman LK, Ilias I: Evaluation and treatment of Cushing's syndrome. Am J Med; 2005 Dec;118(12):1340-6
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  • [Title] Evaluation and treatment of Cushing's syndrome.
  • Cushing's syndrome results from sustained pathologic hypercortisolism caused by excessive corticotropin (ACTH) secretion by tumors in the pituitary gland (Cushing's disease, 70%) or elsewhere (15%), or by ACTH-independent cortisol secretion from adrenal tumors (15%).
  • In ACTH-dependent patients, bilateral inferior petrosal sinus sampling with measurement of ACTH before and after administration of ACTH-releasing hormone most accurately distinguishes pituitary from ectopic ACTH secretion.
  • Surgical resection of tumor is the optimal treatment for all forms of Cushing's syndrome; bilateral adrenalectomy, medical treatment, or radiotherapy are sought in inoperable or recurrent cases.
  • The medical treatment of choice is ketoconazole.
  • The prognosis is better for Cushing's disease and benign adrenal causes of Cushing's syndrome than adrenocortical cancer and malignant ACTH-producing tumors.
  • [MeSH-major] Adrenocorticotropic Hormone / blood. Cushing Syndrome / diagnosis. Cushing Syndrome / drug therapy
  • [MeSH-minor] Adrenalectomy. Adult. Antifungal Agents / therapeutic use. Child. Diagnosis, Differential. Humans. Ketoconazole / therapeutic use. Prognosis. Recurrence. Survival Analysis

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  • (PMID = 16378774.001).
  • [ISSN] 1555-7162
  • [Journal-full-title] The American journal of medicine
  • [ISO-abbreviation] Am. J. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antifungal Agents; 9002-60-2 / Adrenocorticotropic Hormone; R9400W927I / Ketoconazole
  • [Number-of-references] 100
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24. Imai A, Tamaya T: GnRH receptor and apoptotic signaling. Vitam Horm; 2000;59:1-33
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  • In addition to its hypophysiotropic action, gonadotropin-releasing hormone (GnRH) can modify activity in extrapituitary organs and peripheral tumors.
  • GnRH analogs are the preferred treatment for advanced and even metastatic or recurring carcinomas in vivo and in vitro.
  • Hormone-responsive tumors undergo apoptosis with the appropriate stimulus; GnRH-induced tumor growth arrest may result from stimulated apoptotic cell death.
  • The sensitivity of tumors and normal tissue to GnRH is strongly associated with the possession of receptors for GnRH as well as other hormonal control.
  • GnRH receptors in tumors differ from those in pituitary gonadotrophs in some aspects, in particular with regard to the transmembrane signaling cascade.
  • The intramembranous phenomena that occur independently of the contribution of other organelles upon tumoral GnRH receptor engagement include (i) activation of phosphotyrosine phosphatase and loss of phosphotyrosine from the endogenous membrane protein and (ii) phosphoinositide and perhaps sphingomyelin cleavage producing lipid-originated second messengers.
  • GnRH has also been demonstrated to increase Fas ligand expression within plasma membrane, which is known to promote apoptotic cell death through attack on Fas-positive cells within tumors.
  • The Fas-Fas ligand complex might, at least in part, account for the antiproliferative action of the hormone.
  • An understanding of the relationship between the extracellular (hormonal) stimuli that leads to cell death and the intracellular events regulating growth arrest on GnRH action may fundamentally help clarify the therapeutic approach to all hormone-dependent carcinomas that respond to stimuli that lead to apoptosis.
  • [MeSH-major] Apoptosis / physiology. Fertility Agents, Female / therapeutic use. Gonadotropin-Releasing Hormone / physiology. Neoplasms, Hormone-Dependent / drug therapy. Receptors, LHRH / physiology

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  • (PMID = 10714235.001).
  • [ISSN] 0083-6729
  • [Journal-full-title] Vitamins and hormones
  • [ISO-abbreviation] Vitam. Horm.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / Fertility Agents, Female; 0 / Phosphatidylinositols; 0 / Receptors, LHRH; 33515-09-2 / Gonadotropin-Releasing Hormone; EC 3.1.3.48 / Protein Tyrosine Phosphatases
  • [Number-of-references] 184
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25. Ning S, Knox SJ, Harsh GR, Culler MD, Katznelson L: Lanreotide promotes apoptosis and is not radioprotective in GH3 cells. Endocr Relat Cancer; 2009 Sep;16(3):1045-55
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  • Somatostatin analogs are a mainstay of medical therapy in patients with GH producing human pituitary tumors, and it has been suggested that somatostatin analogs may be radioprotective.
  • We utilized GH secreting rat GH3 cells to investigate whether a somatostatin analog may limit the effects of radiation on proliferation and apoptosis in vitro and on tumor growth in vivo.
  • Treatment with lanreotide alone at doses of either 100 or 1000 nM for 48 h reduced clonogenic survival by 5-10%.
  • In a mouse GH3 tumor xenograft model, lanreotide 10 mg/kg moderately inhibited the growth of GH3 tumors, with a 4x tumor growth delay (TGD) time that ranged from 4.5 to 8.3 days.
  • The combination of lanreotide, either antecedent to or concurrent, with radiation of 250, 200 or 150 cGy/fraction for 5 days inhibited tumor growth and produced the TGD times that were similar to radiation alone (P>0.05).
  • [MeSH-major] Adenoma / pathology. Apoptosis / drug effects. Growth Hormone-Secreting Pituitary Adenoma / pathology. Peptides, Cyclic / pharmacology. Radiation Tolerance / drug effects. Somatostatin / analogs & derivatives. Somatotrophs / pathology
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Cell Line, Tumor. Cell Survival / drug effects. Cell Survival / radiation effects. Dose-Response Relationship, Drug. Gamma Rays. Male. Mice. Mice, Nude. Radiation Dosage. Radiation-Protective Agents / pharmacology. Rats. Xenograft Model Antitumor Assays

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  • (PMID = 19528243.001).
  • [ISSN] 1479-6821
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Peptides, Cyclic; 0 / Radiation-Protective Agents; 118992-92-0 / lanreotide; 51110-01-1 / Somatostatin
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26. Schally AV, Comaru-Schally AM, Nagy A, Kovacs M, Szepeshazi K, Plonowski A, Varga JL, Halmos G: Hypothalamic hormones and cancer. Front Neuroendocrinol; 2001 Oct;22(4):248-91
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  • The use of peptide analogs for the therapy of various cancers is reviewed.
  • Inhibition of the pituitary-gonadal axis forms the basis for oncological applications of luteinizing hormone-releasing hormone (LH-RH) agonists and antagonists, but direct effects on tumors may also play a role.
  • Analogs of somatostatin are likewise used for treatment of various tumors.
  • Radiolabeled somatostatin analogs have been successfully applied for the localization of tumors expressing somatostatin receptors.
  • Studies on the role of tumoral LH-RH, growth hormone-releasing hormone (GH-RH), and bombesin/GRP and their receptors in the proliferation of various tumors are summarized, but the complete elucidation of all the mechanisms involved will require much additional work.
  • Human tumors producing hypothalamic hormones are also discussed.
  • Treatment of many cancers remains a major challenge, but new therapeutic modalities are being developed based on antagonists of GH-RH and bombesin, which inhibit growth factors or their receptors.
  • These new classes of peptide analogs should lead to a more effective treatment for various cancers.
  • [MeSH-major] Hypothalamic Hormones / physiology. Neoplasms / drug therapy
  • [MeSH-minor] Animals. Bombesin / antagonists & inhibitors. Bombesin / physiology. Breast Neoplasms / drug therapy. Female. Gastrin-Releasing Peptide / antagonists & inhibitors. Gastrin-Releasing Peptide / physiology. Gonadotropin-Releasing Hormone / analogs & derivatives. Gonadotropin-Releasing Hormone / antagonists & inhibitors. Gonadotropin-Releasing Hormone / physiology. Growth Hormone-Releasing Hormone / physiology. Humans. Male. Ovarian Neoplasms / drug therapy. Prostatic Neoplasms / drug therapy. Somatostatin / analogs & derivatives. Somatostatin / physiology

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  • [Copyright] Copyright 2001 Academic Press.
  • (PMID = 11587553.001).
  • [ISSN] 0091-3022
  • [Journal-full-title] Frontiers in neuroendocrinology
  • [ISO-abbreviation] Front Neuroendocrinol
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-40003; United States / NCI NIH HHS / CA / CA-40004; United States / NCI NIH HHS / CA / CA-40077
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hypothalamic Hormones; 33515-09-2 / Gonadotropin-Releasing Hormone; 51110-01-1 / Somatostatin; 80043-53-4 / Gastrin-Releasing Peptide; 9034-39-3 / Growth Hormone-Releasing Hormone; PX9AZU7QPK / Bombesin
  • [Number-of-references] 160
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