[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 100 of about 624
1. Castro DG, Cecílio SA, Canteras MM: Radiosurgery for pituitary adenomas: evaluation of its efficacy and safety. Radiat Oncol; 2010;5:109
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Radiosurgery for pituitary adenomas: evaluation of its efficacy and safety.
  • OBJECT: To assess the effects of radiosurgery (RS) on the radiological and hormonal control and its toxicity in the treatment of pituitary adenomas.
  • METHODS: Retrospective analysis of 42 patients out of the first 48 consecutive patients with pituitary adenomas treated with RS between 1999 and 2008 with a 6 months minimum follow-up.
  • There were 14 patients with non-secretory adenomas and, among functioning adenomas, 9 were prolactinomas, 9 were adrenocorticotropic hormone-secreting and 10 were growth hormone-secreting tumors.
  • The median dose was 12,5 Gy (9 - 15 Gy) and 20 Gy (12 - 28 Gy) for non-secretory and secretory adenomas, respectively.
  • CONCLUSIONS: RS is an effective and safe therapeutic option in the management of selected patients with pituitary adenomas.
  • [MeSH-major] Adenoma / surgery. Pituitary Neoplasms / surgery. Radiosurgery / adverse effects

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Neurosurgery. 2000 Mar;46(3):531-43 [10719848.001]
  • [Cites] J Neurosurg. 2011 Feb;114(2):303-9 [20540596.001]
  • [Cites] J Neurooncol. 2001 Sep;54(2):197-203 [11761436.001]
  • [Cites] J Neurosurg. 2002 Feb;96(2):195-208 [11838791.001]
  • [Cites] J Neurosurg. 2002 Sep;97(3):525-30 [12296634.001]
  • [Cites] Neurosurgery. 2003 Jul;53(1):51-9; discussion 59-61 [12823873.001]
  • [Cites] Yonsei Med J. 2003 Aug 30;44(4):602-7 [12950114.001]
  • [Cites] J Neurosurg. 1989 Oct;71(4):520-7 [2552045.001]
  • [Cites] Clin Endocrinol (Oxf). 1993 Jun;38(6):571-8 [8334743.001]
  • [Cites] Radiother Oncol. 1996 Oct;41(1):45-53 [8961367.001]
  • [Cites] J Neurosurg. 1998 Jun;88(6):1002-8 [9609294.001]
  • [Cites] Clin Endocrinol (Oxf). 2004 Nov;61(5):531-43 [15521954.001]
  • [Cites] Curr Opin Neurol. 2004 Dec;17(6):693-703 [15542978.001]
  • [Cites] J Neurosurg. 2005 Apr;102(4):678-91 [15871511.001]
  • [Cites] Neurosurg Clin N Am. 2006 Apr;17(2):129-41, vi [16793505.001]
  • [Cites] Arq Bras Endocrinol Metabol. 2006 Dec;50(6):996-1004 [17221104.001]
  • [Cites] J Neurosurg. 2000 Dec;93 Suppl 3:19-22 [11143245.001]
  • (PMID = 21083925.001).
  • [ISSN] 1748-717X
  • [Journal-full-title] Radiation oncology (London, England)
  • [ISO-abbreviation] Radiat Oncol
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2994872
  •  go-up   go-down


2. Kreutzer J, Buslei R, Wallaschofski H, Hofmann B, Nimsky C, Fahlbusch R, Buchfelder M: Operative treatment of prolactinomas: indications and results in a current consecutive series of 212 patients. Eur J Endocrinol; 2008 Jan;158(1):11-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Operative treatment of prolactinomas: indications and results in a current consecutive series of 212 patients.
  • OBJECTIVE: Medical therapy with dopamine agonists (DA) is the primary treatment of choice in most patients with prolactinomas.
  • Focusing on a possible shift of recent indications, we retrospectively analyzed our results of surgical treatment in prolactinomas.
  • PATIENTS AND METHODS: Between 1990 and 2005, we have operated on 212 consecutive patients with prolactinomas.
  • Surgical indications were divided into 'classical' indications and 'modern' indications defined as cystic prolactinomas or patients with microprolactinomas who individually decided on a primary surgical treatment.
  • RESULTS: Initial overall remission was accomplished in 53.2% including giant prolactinomas.
  • Overall remission at the latest follow-up was 42.7%, but 72.5% in intrasellar tumors, 80% in cystic prolactinomas, and 84.8% in microprolactinomas.
  • CONCLUSION: Remission rates after surgical treatment of prolactinomas remain excellent, particularly in microadenoma and intrasellar macroadenomas, whereas morbidity of transsphenoidal surgery is low in the hands of experienced pituitary surgeons.

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18166812.001).
  • [ISSN] 1479-683X
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Dopamine Agonists; 9002-62-4 / Prolactin
  •  go-up   go-down


3. Yang QH, Xu JN, Zhang R, Gao L, Xu RK: [Melatonin suppressing the proliferation of E2-induced pituitary prolactin-secreting tumor in rat involves the effects of estrogen receptor]. Zhongguo Ying Yong Sheng Li Xue Za Zhi; 2006 May;22(2):174-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Melatonin suppressing the proliferation of E2-induced pituitary prolactin-secreting tumor in rat involves the effects of estrogen receptor].
  • AIM: To investigate effects of melatonin on estrogen receptor at the primary stage of melatonin (MLT) inhibiting the proliferation of 17-beta-estradiol (E2)-induced pituitary prolactin-secreting tumor (prolactinoma) and its mechanisms in the rat.
  • METHODS: MLT inhibiting the proliferation of 17-beta-E2-induced prolactinoma was created by administrating different concentration of melatonin subcutaneously at 18:00 in every group of SD rat in vivo.
  • We also examined the expression of MLT receptor in prolactinoma cells and the effects of MLT on the expression of estrogen receptor (ER) by in situ hybridization and the effects of MLT on the binding of ER to estrogen response element (ERE) by electrophoretic mobility shift assay (EMSA)in primary culture cells iv vitro.
  • RESULTS: The results showed that the weights of prolactinomas in MLT groups, in which 0.25 mg or 0.50 mg/day/rat melatonin was administrated subcutaneously at 18:00, were decreased significantly (P < 0.01 and P < 0.05).
  • The expression of MLT1a and MLT1b were shown in pituitary prolactinoma cells.
  • Compared with the prolactinoma, the expression of ER and the bind of ER to ERE in prolactinoma treated with 0.25 mg/day/rat or 0.50 mg/day/rat MLT was decreased (P < 0.01 and P < 0.01).
  • CONCLUSION: These data indicate that some dosage of MLT inhibit the development of E2-induced prolactinoma in SD rat.
  • [MeSH-major] Estradiol / pharmacology. Melatonin / pharmacology. Pituitary Neoplasms / pathology. Prolactinoma / pathology

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • Hazardous Substances Data Bank. ESTRADIOL .
  • Hazardous Substances Data Bank. MELATONIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21162234.001).
  • [ISSN] 1000-6834
  • [Journal-full-title] Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology
  • [ISO-abbreviation] Zhongguo Ying Yong Sheng Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Receptors, Estrogen; 4TI98Z838E / Estradiol; JL5DK93RCL / Melatonin
  •  go-up   go-down


Advertisement
4. Dekkers OM, Lagro J, Burman P, Jørgensen JO, Romijn JA, Pereira AM: Recurrence of hyperprolactinemia after withdrawal of dopamine agonists: systematic review and meta-analysis. J Clin Endocrinol Metab; 2010 Jan;95(1):43-51
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • CONTEXT: Dopamine agonists are the treatment of choice for prolactinomas and symptomatic idiopathic hyperprolactinemia.
  • OBJECTIVE: The aim of the study was to assess the effect of dopamine agonist withdrawal in patients with idiopathic hyperprolactinemia and prolactinomas.
  • [MeSH-minor] Humans. Pituitary Neoplasms / complications. Pituitary Neoplasms / drug therapy. Prolactinoma / complications. Prolactinoma / drug therapy. Recurrence. Treatment Outcome. Withholding Treatment


5. Lourenço DM Jr, Toledo RA, Mackowiak II, Coutinho FL, Cavalcanti MG, Correia-Deur JE, Montenegro F, Siqueira SA, Margarido LC, Machado MC, Toledo SP: Multiple endocrine neoplasia type 1 in Brazil: MEN1 founding mutation, clinical features, and bone mineral density profile. Eur J Endocrinol; 2008 Sep;159(3):259-74
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Here, we aimed to investigate the clinical features of a seven-generation Brazilian pedigree, which included 715 at-risk family members.
  • Very high frequencies of functioning and non-functioning MEN1-related tumors were documented and the prevalence of prolactinoma (29.6%) was similar to that previously described in prolactinoma-variant Burin (32%).


6. Borodkin K, Ayalon L, Kanety H, Dagan Y: Dysregulation of circadian rhythms following prolactin-secreting pituitary microadenoma. Chronobiol Int; 2005;22(1):145-56
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dysregulation of circadian rhythms following prolactin-secreting pituitary microadenoma.
  • A patient who developed an irregular sleep-wake pattern following prolactin-secreting pituitary microadenoma is described.
  • The dysregulation of circadian rhythms occurred concomitantly, but not beforehand, with the onset of pituitary disease, thus suggesting an association between the two phenomena.
  • This case also highlights the need to raise the awareness to circadian rhythm sleep disorders and to consider disruptions of sleep-wake cycle in patients with pituitary adenoma.
  • [MeSH-major] Adenoma / complications. Adenoma / metabolism. Circadian Rhythm. Pituitary Neoplasms / complications. Pituitary Neoplasms / metabolism. Prolactin / secretion. Sleep Disorders, Circadian Rhythm / complications

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • Hazardous Substances Data Bank. MELATONIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15865328.001).
  • [ISSN] 0742-0528
  • [Journal-full-title] Chronobiology international
  • [ISO-abbreviation] Chronobiol. Int.
  • [Language] eng
  • [Grant] United States / NIMH NIH HHS / MH / 5T32 MH18399-17
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 9002-62-4 / Prolactin; JL5DK93RCL / Melatonin
  •  go-up   go-down


7. Drutel A, Caron P, Archambeaud F: [New medical treatments in pituitary adenomas]. Ann Endocrinol (Paris); 2008 Sep;69 Suppl 1:S16-28
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [New medical treatments in pituitary adenomas].
  • [Transliterated title] Actualités thérapeutiques dans la prise en charge médicale des adénomes hypophysaires.
  • Currently, the role of dopaminergic and somatostatinergic agonists in the treatment of pituitary adenomas is quite well established.
  • Nevertheless, a clearer understanding of the expression of dopaminergic and somatostatinergic receptors at the cellular level of pituitary adenomas as well as the development of newer analogues compounds may drastically change current therapeutic modalities.
  • In the midst of GH-secreting pituitary adenomas, a positive correlation exists between the expression of Sst2 mRNA and the inhibition of GH release by somatostatin analogues.
  • The involvement of Sst5 subtype in adenomas resistant to preferential Sst2 agonists has recently been proved.
  • Besides, the use of a chimeric molecule presenting a binding affinity to both Sst2 and D2 subtypes (BIM-23A287) inhibits the secretion of GH in ways similar to the Sst2 or D2 agonists used alone or concurrently but however in a concentration 50 times lower than that of the latter.
  • The discovery of Sst5 and D2 subtypes at the level of corticotropic adenomas reveals newer therapeutic perspectives with promising preliminary results with the use of SOM-230 ; these finding lead to a rise in interest in cabergoline.
  • In the midst of non-functioning pituitary adenomas, the expression of Sst2, Sst3 and D2 receptors will perhaps allow the use of combined therapies associating the new somatostatin analogues to the dopaminergic agonists or even use dopastatin (BIM-23A760, chimeric molecule Sst2-Sst5-D2).
  • Finally, concerning prolactinomas the discovery of Sst5 receptors lead to consider the use of somatostatinergic agonists specific to the Sst5 receptor, SOM-230 in particular.
  • Nevertheless, it seems that adenomas resistant to dopaminergic agonist due to a lack of expression of D2 receptor fail to express Sst5 receptors as well.
  • On the other hand, dopastatin appears to be more efficient than cabergoline in the management of this type of adenomas.
  • Therefore, the growing awareness concerning the mechanisms involved in the control of pituitary secretions as well as cellular proliferation will perhaps allow physicians to treat the pathology of pituitary adenomas, macroadenomas in particular, using solely pharmacological means instead of invasive surgical procedures and/or radiotherapy.
  • [MeSH-major] Adenoma / drug therapy. Pituitary Neoplasms / drug therapy

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18954854.001).
  • [ISSN] 0003-4266
  • [Journal-full-title] Annales d'endocrinologie
  • [ISO-abbreviation] Ann. Endocrinol. (Paris)
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Dopamine Agonists; 0 / Peptides, Cyclic; 0 / Receptors, Dopamine; 0 / Receptors, Somatostatin; 118992-92-0 / lanreotide; 51110-01-1 / Somatostatin; RWM8CCW8GP / Octreotide
  • [Number-of-references] 49
  •  go-up   go-down


8. Gallagher J, Lynch FW, Barragry J: A prolactinoma masked by a herbal remedy. Eur J Obstet Gynecol Reprod Biol; 2008 Apr;137(2):257-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A prolactinoma masked by a herbal remedy.
  • [MeSH-major] Materia Medica / adverse effects. Pituitary Neoplasms / diagnosis. Prolactinoma / diagnosis
  • [MeSH-minor] Adolescent. Diagnosis, Differential. Female. Galactorrhea / chemically induced. Galactorrhea / diagnosis. Humans. Hyperprolactinemia / blood. Hyperprolactinemia / complications. Hyperprolactinemia / diagnosis. Magnetic Resonance Imaging. Plant Extracts / adverse effects. Plant Extracts / pharmacology. Prolactin / blood. Vitex

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17298863.001).
  • [ISSN] 0301-2115
  • [Journal-full-title] European journal of obstetrics, gynecology, and reproductive biology
  • [ISO-abbreviation] Eur. J. Obstet. Gynecol. Reprod. Biol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Materia Medica; 0 / Plant Extracts; 9002-62-4 / Prolactin
  •  go-up   go-down


9. Naliato EC, Farias ML, Violante AH: [Prolactinomas and bone mineral density in men]. Arq Bras Endocrinol Metabol; 2005 Apr;49(2):183-95
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Prolactinomas and bone mineral density in men].
  • [Transliterated title] Prolactinomas e densidade mineral óssea em homens.
  • In this paper, we analyze aspects related to bone loss in men with hyperprolactinemia due to prolactinomas: prevalence, clinical relevance, physiopathology, diagnosis and the consequences of the treatment of hyperprolactinemia and hypogonadism on bone mineral density.
  • [MeSH-major] Bone Density. Hyperprolactinemia / complications. Osteoporosis / etiology. Pituitary Neoplasms / complications. Prolactinoma / complications

  • MedlinePlus Health Information. consumer health - Bone Density.
  • MedlinePlus Health Information. consumer health - Osteoporosis.
  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16184246.001).
  • [ISSN] 0004-2730
  • [Journal-full-title] Arquivos brasileiros de endocrinologia e metabologia
  • [ISO-abbreviation] Arq Bras Endocrinol Metabol
  • [Language] por
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Brazil
  • [Number-of-references] 83
  •  go-up   go-down


10. Kimata-Hayashi N, Takano K, Yasufuku-Takano J, Teramoto A, Fujita T: Mechanism of adrenomedullin-induced prolactin release from human prolactin-releasing adenoma cells. Endocr J; 2005 Dec;52(6):769-73
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mechanism of adrenomedullin-induced prolactin release from human prolactin-releasing adenoma cells.
  • The mechanism of adrenomedullin-induced prolactin release was investigated in prolactin-secreting human pituitary adenoma cells by intracellular calcium measurement and static incubation study.
  • Adrenomedullin stimulated prolactin release in a concentration-dependent manner.
  • PKA inhibitor attenuated adrenomedullin-induced prolactin release.
  • These data indicate that adrenomedullin stimulates prolactin release by modulating calcium influx through voltage-gated calcium channels dependently on extracellular sodium.
  • [MeSH-major] Peptides / pharmacology. Pituitary Neoplasms / secretion. Prolactin / secretion. Prolactinoma / secretion

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • Hazardous Substances Data Bank. SODIUM .
  • Hazardous Substances Data Bank. CALCIUM, ELEMENTAL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16410671.001).
  • [ISSN] 0918-8959
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Calcium Channels; 0 / Intracellular Signaling Peptides and Proteins; 0 / Peptides; 0 / protein kinase modulator; 148498-78-6 / Adrenomedullin; 9002-62-4 / Prolactin; 9NEZ333N27 / Sodium; SY7Q814VUP / Calcium; TSN3DL106G / Fura-2
  •  go-up   go-down


11. Jane JA Jr: Management of pediatric sellar tumors. Pediatr Endocrinol Rev; 2008 Feb;5 Suppl 2:720-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Craniopharyngiomas and pituitary adenomas are the most common forms of sellar tumors in children.
  • First-line treatment usually consists of surgical resection of the tumor, although dopamine agonist therapy may be considered as first-line therapy in most patients with prolactin-secreting adenomas.
  • Transsphenoidal resection has become increasingly widespread and represents the mainstay of surgical therapy for pituitary adenomas and selected craniopharyngiomas.
  • [MeSH-major] Pituitary Neoplasms / therapy
  • [MeSH-minor] Adenoma / diagnosis. Adenoma / epidemiology. Adenoma / therapy. Adolescent. Adult. Child. Craniopharyngioma / diagnosis. Craniopharyngioma / epidemiology. Craniopharyngioma / therapy. Female. Human Growth Hormone / secretion. Humans. Male. Pituitary ACTH Hypersecretion / therapy. Prolactinoma / therapy. Radiosurgery. Radiotherapy. Surgical Procedures, Operative / methods

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18317443.001).
  • [ISSN] 1565-4753
  • [Journal-full-title] Pediatric endocrinology reviews : PER
  • [ISO-abbreviation] Pediatr Endocrinol Rev
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Israel
  • [Chemical-registry-number] 12629-01-5 / Human Growth Hormone
  • [Number-of-references] 57
  •  go-up   go-down


12. Yan G, Hou R, Zhuang D, Chen L, Pang Q, Zhu J: Proteomic analysis of prolactinoma cells by immuno-laser capture microdissection combined with online two-dimensional nano-scale liquid chromatography/mass spectrometry. Proteome Sci; 2010 Jan 29;8:2
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Proteomic analysis of prolactinoma cells by immuno-laser capture microdissection combined with online two-dimensional nano-scale liquid chromatography/mass spectrometry.
  • BACKGROUND: Pituitary adenomas, the third most common intracranial tumor, comprise nearly 16.7% of intracranial neoplasm and 25%-44% of pituitary adenomas are prolactinomas.
  • Prolactinoma represents a complex heterogeneous mixture of cells including prolactin (PRL), endothelial cells, fibroblasts, and other stromal cells, making it difficult to dissect the molecular and cellular mechanisms of prolactin cells in pituitary tumorigenesis through high-throughout-omics analysis.
  • Our newly developed immuno-laser capture microdissection (LCM) method would permit rapid and reliable procurement of prolactin cells from this heterogeneous tissue.
  • Thus, prolactin cell specific molecular events involved in pituitary tumorigenesis and cell signaling can be approached by proteomic analysis.
  • RESULTS: Proteins from immuno-LCM captured prolactin cells were digested; resulting peptides were separated by two dimensional-nanoscale liquid chromatography (2D-nanoLC/MS) and characterized by tandem mass spectrometry.
  • All MS/MS spectrums were analyzed by SEQUEST against the human International Protein Index database and a specific prolactinoma proteome consisting of 2243 proteins was identified.
  • This collection of identified proteins by far represents the largest and the most comprehensive database of proteome for prolactinoma.
  • CONCLUSIONS: This manuscript described a more comprehensive proteomic profile of prolactinomas compared to other previous published reports.
  • Thanks to the application of immuno-LCM combined with online two-dimensional nano-scale liquid chromatography here permitted identification of more proteins and, to our best knowledge, generated the largest prolactinoma proteome.
  • This enlarged proteome would contribute significantly to further understanding of prolactinoma tumorigenesis which is crucial to the management of prolactinomas.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Colloids Surf B Biointerfaces. 2009 Jul 1;71(2):187-93 [19286358.001]
  • [Cites] Mod Pathol. 2002 Nov;15(11):1205-12 [12429800.001]
  • [Cites] Am J Pathol. 1999 Jan;154(1):61-6 [9916919.001]
  • [Cites] Cell. 1996 May 31;85(5):707-20 [8646779.001]
  • [Cites] Neurochem Res. 2003 Aug;28(8):1265-73 [12834267.001]
  • [Cites] Anal Chem. 2002 Oct 15;74(20):5383-92 [12403597.001]
  • [Cites] Nat Biotechnol. 1999 Jul;17(7):676-82 [10404161.001]
  • [Cites] Neurosurgery. 1996 Apr;38(4):765-70; discussion 770-1 [8692397.001]
  • [Cites] Front Horm Res. 2004;32:146-74 [15281345.001]
  • [Cites] Nat Protoc. 2006;1(2):586-603 [17406286.001]
  • [Cites] Endocrinology. 2001 May;142(5):1703-9 [11316732.001]
  • [Cites] Electrophoresis. 1995 Jun;16(6):1034-59 [7498127.001]
  • [Cites] J Histochem Cytochem. 2001 Sep;49(9):1193-4 [11511691.001]
  • [Cites] J Chromatogr A. 2006 Nov 24;1135(1):43-51 [17027011.001]
  • [Cites] Electrophoresis. 2008 Jun;29(12):2689-95 [18481836.001]
  • [Cites] Electrophoresis. 2000 Apr;21(6):1104-15 [10786884.001]
  • [Cites] Mol Cell Proteomics. 2002 Aug;1(8):553-60 [12376570.001]
  • [Cites] Proteome Sci. 2009;7:32 [19719850.001]
  • [Cites] Neurosurgery. 1996 Jan;38(1):99-106; discussion 106-7 [8747957.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jul 13;101(28):10296-301 [15240878.001]
  • [Cites] Chem Rev. 2007 Aug;107(8):3654-86 [17649983.001]
  • [Cites] Cancer. 2004 Aug 1;101(3):613-9 [15274075.001]
  • [Cites] Dev Cell. 2002 May;2(5):518-9 [12015958.001]
  • [Cites] Science. 1996 Nov 8;274(5289):998-1001 [8875945.001]
  • [Cites] Electrophoresis. 2003 Jan;24(1-2):296-302 [12652601.001]
  • [Cites] J Cell Sci. 2004 Apr 15;117(Pt 10):1875-84 [15090593.001]
  • [Cites] Int J Clin Exp Pathol. 2008;1(6):475-88 [18787684.001]
  • [Cites] Nature. 2008 Oct 30;455(7217):1251-4 [18820680.001]
  • [Cites] Nat Biotechnol. 1998 Aug;16(8):737-42 [9702771.001]
  • [Cites] Proteome Sci. 2008 Mar 17;6:11 [18346272.001]
  • [Cites] Clin Endocrinol (Oxf). 2000 Sep;53(3):337-44 [10971451.001]
  • [Cites] Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2009 Jul;34(7):569-75 [19648665.001]
  • [Cites] Genome Biol. 2003;4(5):P3 [12734009.001]
  • [Cites] Mass Spectrom Rev. 2005 Nov-Dec;24(6):783-813 [15495141.001]
  • [Cites] Biochem Biophys Res Commun. 2003 Jan 17;300(3):679-85 [12507503.001]
  • [Cites] Proteomics. 2002 Jan;2(1):3-10 [11788986.001]
  • [Cites] Cell Mol Biol (Noisy-le-grand). 2003 Jul;49(5):689-712 [14528906.001]
  • [Cites] Pituitary. 2003;6(4):189-202 [15237930.001]
  • [Cites] Oncogene. 2001 May 31;20(25):3290-300 [11423978.001]
  • [Cites] J Chromatogr A. 2004 Jun 4;1038(1-2):247-65 [15233540.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Jun;87(6):2635-43 [12050228.001]
  • [Cites] Cancer Res. 2005 Nov 15;65(22):10214-22 [16288009.001]
  • [Cites] Am J Pathol. 2002 Mar;160(3):815-22 [11891180.001]
  • [Cites] J Neuroendocrinol. 2007 Nov;19(11):913-22 [17927670.001]
  • [Cites] Anal Chem. 2003 Sep 1;75(17):4646-58 [14632076.001]
  • [Cites] J Proteome Res. 2004 May-Jun;3(3):604-12 [15253443.001]
  • [Cites] Endocrine. 2005 Oct;28(1):43-7 [16311409.001]
  • [Cites] Nature. 1992 Sep 24;359(6393):295-300 [1406933.001]
  • [Cites] Proteomics. 2003 May;3(5):699-713 [12748949.001]
  • [Cites] Anal Chem. 2008 Sep 1;80(17):6715-23 [18680313.001]
  • [Cites] J Mol Endocrinol. 2009 Feb;42(2):75-86 [18987159.001]
  • [Cites] Eur J Endocrinol. 2000 Jul;143(1):R1-6 [10870044.001]
  • [Cites] Methods Mol Biol. 2008;428:159-78 [18287773.001]
  • [Cites] Proteome Sci. 2008;6:6 [18234112.001]
  • [Cites] Am J Pathol. 1999 Feb;154(2):313-23 [10027389.001]
  • [Cites] Pituitary. 2008;11(3):231-45 [18183490.001]
  • (PMID = 20205839.001).
  • [ISSN] 1477-5956
  • [Journal-full-title] Proteome science
  • [ISO-abbreviation] Proteome Sci
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2825229
  •  go-up   go-down


13. Sadideen H, Swaminathan R: Macroprolactin: what is it and what is its importance? Int J Clin Pract; 2006 Apr;60(4):457-61
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Monomeric prolactin (PRL) of molecular weight 23 kDa constitutes up to 95% of adult serum PRL.
  • Macroprolactin is a large antigen-antibody complex of molecular weight greater than 100 kDa and constitutes less than 1% of circulating PRL.
  • Thus, in most cases, hyperprolactinaemia is usually a result of high levels of monomeric PRL, which may be due to excess production as with a prolactinoma or due to disinhibition by compression of the pituitary stalk.
  • The presence of macroprolactin should always be suspected when a patient's clinical history and/or radiological data are incompatible with his/her PRL value.
  • Thus, it may be useful to screen all patients with high sera PRL levels in order to prevent unnecessary investigations into the cause for hyperprolactinaemia.
  • It is hoped that macroprolactinaemia is included in the differential diagnosis of hyperprolactinaemia.
  • [MeSH-major] Hyperprolactinemia / etiology. Prolactin / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16620360.001).
  • [ISSN] 1368-5031
  • [Journal-full-title] International journal of clinical practice
  • [ISO-abbreviation] Int. J. Clin. Pract.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / prolactin, polymeric; 9002-62-4 / Prolactin
  • [Number-of-references] 33
  •  go-up   go-down


14. Schaller B: Gender-related differences in prolactinomas. A clinicopathological study. Neuro Endocrinol Lett; 2005 Apr;26(2):152-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gender-related differences in prolactinomas. A clinicopathological study.
  • BACKGROUND/AIMS: Prolactinomas are the most common tumors of the pituitary gland.
  • PATIENTS & METHODS: Twenty-six patients with prolactinomas, that met strict immunohistochemical and electron microscopic criteria and were surgically treated between January 1990 and June 1997, were retrospectively reviewed.
  • Men were significantly older, both at diagnosis and surgery.
  • Men had a significantly shorter preoperative duration of symptoms and higher preoperative serum prolactin levels than women.
  • The preoperative prolactin levels and proliferative activities (mitotic index, MIB-1 labeling index) were lower in women compared to men and showed a direct correlation to postoperative outcome.
  • CONCLUSION: The biology and the clinical course of prolactinomas seem to differ in women and men.
  • Our findings may justify a more aggressive therapeutic approach to prolactinomas in men than in women.
  • [MeSH-major] Pituitary Neoplasms / pathology. Prolactinoma / pathology. Sex Characteristics

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • 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
  • [ErratumIn] Neuro Endocrinol Lett. 2005 Dec;26(6):628
  • (PMID = 15855888.001).
  • [ISSN] 0172-780X
  • [Journal-full-title] Neuro endocrinology letters
  • [ISO-abbreviation] Neuro Endocrinol. Lett.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Sweden
  •  go-up   go-down


15. Pesatori AC, Baccarelli A, Consonni D, Lania A, Beck-Peccoz P, Bertazzi PA, Spada A: Aryl hydrocarbon receptor-interacting protein and pituitary adenomas: a population-based study on subjects exposed to dioxin after the Seveso, Italy, accident. Eur J Endocrinol; 2008 Dec;159(6):699-703
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aryl hydrocarbon receptor-interacting protein and pituitary adenomas: a population-based study on subjects exposed to dioxin after the Seveso, Italy, accident.
  • OBJECTIVE: The pathogenesis of sporadic pituitary tumors is unknown.
  • Loss-of-function mutations of aryl hydrocarbon receptor-interacting protein (AIP) have been identified in patients with familial pituitary tumors.
  • DESIGN: We investigated the incidence of pituitary tumors in the Seveso population exposed to 2,3,7,8-tetrachlorodibenzo-para-dioxin following an industrial accident in 1976.
  • METHODS: Through the hospital discharge registration system of Lombardy Region, we identified incident cases of pituitary adenomas between 1976 and 1996 in the Seveso population, subdivided in zone A (n=804), B (n=5.941), and R (n=38.624) according to high, intermediate, and low exposure to dioxin respectively, and in the surrounding non-contaminated area, as reference (n=232 745).
  • RESULTS: We identified 42 pituitary adenomas in the reference area, 1 prolactinoma in zone A (rate ratio (RR) 6.2; 95% CI 0.9-45.5, P=0.07), 2 nonfuctioning pituitary tumors (NFPAs) in zone B (RR 1.9; 95% CI 0.5-7.7, P=0.39), and 3 prolactinomas and 2 NFPAs in zone R (RR 0.7; 95% CI 0.3-1.8, P=0.48).
  • The study indicates no statistically significant increase of incident pituitary tumors in this area, although the tendency toward a higher risk (three cases in zones A and B) of pituitary tumors in subjects exposed to high-intermediate dioxin concentrations in comparison with nonexposed population suggests the need for extended follow-up.


16. Osa LE, Horjen J, Aanderud S, Lund-Johansen M: [Surgical treatment of hormone-producing pituitary adenomas]. Tidsskr Nor Laegeforen; 2006 May 11;126(10):1330-2
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Surgical treatment of hormone-producing pituitary adenomas].
  • BACKGROUND: Transsphenoidal surgical treatment is established as a treatment of hormonally active pituitary tumours, except prolactinomas.
  • METHODS: We did a retrospective survey evaluating the operative results of one surgeon operating hormonally active pituitary tumours from 1993 through 2002 at Haukeland University Hospital.
  • [MeSH-major] Adenoma / surgery. Pituitary Neoplasms / surgery
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Clinical Competence. Female. Humans. Male. Middle Aged. Neurosurgical Procedures / adverse effects. Neurosurgical Procedures / methods. Postoperative Complications / diagnosis. Postoperative Complications / etiology. Retrospective Studies. Sphenoid Bone / surgery. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16691270.001).
  • [ISSN] 0807-7096
  • [Journal-full-title] Tidsskrift for den Norske lægeforening : tidsskrift for praktisk medicin, ny række
  • [ISO-abbreviation] Tidsskr. Nor. Laegeforen.
  • [Language] nor
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Norway
  •  go-up   go-down


17. Cho EH, Lee SA, Chung JY, Koh EH, Cho YH, Kim JH, Kim CJ, Kim MS: Efficacy and safety of cabergoline as first line treatment for invasive giant prolactinoma. J Korean Med Sci; 2009 Oct;24(5):874-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Efficacy and safety of cabergoline as first line treatment for invasive giant prolactinoma.
  • Although cabergoline is effective in the treatment of micro- and macro-prolactinoma, little is known about its efficacy in the treatment of invasive giant prolactinoma.
  • We investigated the efficacy and safety of cabergoline in 10 male patients with invasive giant prolactinoma.
  • Before treatment, mean serum prolactin level was 11,426 ng/mL (range, 1,450-33,200 ng/mL) and mean maximum tumor diameter was 51 mm (range, 40-77 mm).
  • Three months after initiation of cabergoline treatment, serum prolactin concentrations decreased more than 97% in 9 patients; at last follow-up (mean treatment duration, 19 months), the mean decrease in serum prolactin concentrations was 98%, with 5 patients having normal serum prolactin levels.
  • These findings indicate that cabergoline treatment led to a significant and rapid reduction in serum prolactin concentrations and tumor size in patients with giant prolactinoma.
  • Therefore, cabergoline represents an effective and well-tolerated treatment for invasive giant prolactinoma.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Ergolines / therapeutic use. Pituitary Neoplasms / drug therapy. Prolactinoma / drug therapy
  • [MeSH-minor] Adult. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Prolactin / blood. Retrospective Studies

  • 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] Clin Endocrinol (Oxf). 2000 Jan;52(1):43-9 [10651752.001]
  • [Cites] J Clin Endocrinol Metab. 2007 Oct;92(10):3829-35 [17623759.001]
  • [Cites] Clin Endocrinol (Oxf). 2003 May;58(5):662-70 [12699451.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Apr;89(4):1704-11 [15070934.001]
  • [Cites] N Engl J Med. 1982 Jan 21;306(3):178 [7054671.001]
  • [Cites] N Engl J Med. 1983 Aug 4;309(5):280-3 [6866052.001]
  • [Cites] Neurosurgery. 1983 Dec;13(6):634-41 [6361599.001]
  • [Cites] Acta Med Scand. 1985;217(1):101-9 [3919529.001]
  • [Cites] J Clin Endocrinol Metab. 1996 Jun;81(6):2338-43 [8964874.001]
  • [Cites] Drugs. 1996 Jun;51(6):954-65 [8736617.001]
  • [Cites] Clin Endocrinol (Oxf). 1997 Apr;46(4):409-13 [9196602.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Jul;82(7):2102-7 [9215279.001]
  • [Cites] Neuro Endocrinol Lett. 2005 Apr;26(2):152-9 [15855888.001]
  • [Cites] Eur J Endocrinol. 2007 Feb;156(2):225-31 [17287412.001]
  • [Cites] J Neurosurg. 2002 Aug;97(2):299-306 [12186457.001]
  • (PMID = 19794986.001).
  • [ISSN] 1598-6357
  • [Journal-full-title] Journal of Korean medical science
  • [ISO-abbreviation] J. Korean Med. Sci.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Ergolines; 9002-62-4 / Prolactin; LL60K9J05T / cabergoline
  • [Other-IDs] NLM/ PMC2752771
  • [Keywords] NOTNLM ; Cabergoline / Invasive Giant Prolactinoma / Male / Prolactin / Tumor Size
  •  go-up   go-down


18. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • Evidence for direct growth-promoting effect of P(4) was obtained from cultures of primary mouse pituitary cells and rat somatomammotroph GH3 cells.
  • 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.

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. PROGESTERONE .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • 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
  • [Cites] J Clin Endocrinol Metab. 2000 Jan;85(1):168-74 [10634382.001]
  • [Cites] Endocr Relat Cancer. 2009 Mar;16(1):113-22 [18852162.001]
  • [Cites] J Mammary Gland Biol Neoplasia. 1998 Jan;3(1):63-72 [10819505.001]
  • [Cites] J Neuroendocrinol. 2001 Mar;13(3):302-9 [11207946.001]
  • [Cites] Endocrinology. 2001 Oct;142(10):4479-85 [11564713.001]
  • [Cites] J Clin Invest. 2002 Jan;109(2):277-83 [11805140.001]
  • [Cites] Endocrinology. 2002 Oct;143(10):4084-95 [12239120.001]
  • [Cites] J Biol Chem. 2002 Sep 27;277(39):35819-25 [12121979.001]
  • [Cites] Endocrinology. 2002 Dec;143(12):4536-43 [12446580.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Feb 4;100(3):1034-9 [12552124.001]
  • [Cites] Front Horm Res. 2004;32:34-62 [15281339.001]
  • [Cites] Mol Cell Biol. 2004 Aug;24(16):7260-74 [15282324.001]
  • [Cites] Science. 1966 Oct 21;154(3747):402-3 [4288164.001]
  • [Cites] Endocrinology. 1970 Mar;86(3):503-5 [5410438.001]
  • [Cites] J Endocrinol. 1973 Feb;56(2):309-14 [4703244.001]
  • [Cites] Endocrinology. 1976 Dec;99(6):1482-9 [826392.001]
  • [Cites] J Biol Chem. 1982 Mar 10;257(5):2133-6 [7061411.001]
  • [Cites] Adv Exp Med Biol. 1981;138:151-63 [7342713.001]
  • [Cites] Arch Pathol Lab Med. 1983 Sep;107(9):488-91 [6309114.001]
  • [Cites] Cancer Res. 1985 Mar;45(3):1015-9 [2982481.001]
  • [Cites] J Endocrinol. 1989 Jun;121(3):409-17 [2547009.001]
  • [Cites] Endocrinology. 1991 Jul;129(1):270-6 [1711463.001]
  • [Cites] Nature. 1992 Sep 24;359(6393):295-300 [1406933.001]
  • [Cites] Cancer Res. 1993 Apr 1;53(7):1546-9 [8453621.001]
  • [Cites] Acta Endocrinol (Copenh). 1993 Jul;129 Suppl 1:1-5 [8396832.001]
  • [Cites] Hum Reprod. 1994 Jun;9 Suppl 1:63-8 [7962471.001]
  • [Cites] J Cell Sci Suppl. 1994;18:89-96 [7883799.001]
  • [Cites] Cancer Res. 1995 Nov 1;55(21):4892-8 [7585526.001]
  • [Cites] J Biol Chem. 1996 Aug 23;271(34):20608-16 [8702807.001]
  • [Cites] J Endocrinol. 1996 Nov;151(2):175-84 [8958777.001]
  • [Cites] Endocrinology. 1998 Apr;139(4):1602-9 [9528940.001]
  • [Cites] EMBO J. 1998 Apr 1;17(7):2008-18 [9524123.001]
  • [Cites] Nat Genet. 1998 Apr;18(4):360-4 [9537419.001]
  • [Cites] Genes Dev. 1998 Sep 15;12(18):2899-911 [9744866.001]
  • [Cites] Endocrinology. 2005 Nov;146(11):4917-25 [16123159.001]
  • [Cites] Oncogene. 2005 Nov 10;24(49):7301-9 [16007123.001]
  • [Cites] Cancer Cell. 2006 Jun;9(6):459-71 [16766265.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Dec;91(12):4769-75 [16968795.001]
  • [Cites] Cell Cycle. 2008 Jan 1;7(1):71-80 [18196959.001]
  • [Cites] Horm Metab Res. 2008 Apr;40(4):245-50 [18548383.001]
  • [Cites] Eur J Endocrinol. 2008 Sep;159(3):197-202 [18567667.001]
  • [Cites] J Reprod Med. 1999 Dec;44(12 Suppl):1121-6 [10649822.001]
  • (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
  •  go-up   go-down


19. Bonneville JF, Bonneville F, Cattin F: [MRI of the pituitary gland: indications and results in gynaecology and in obstetrics]. Gynecol Obstet Fertil; 2005 Mar;33(3):147-53
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [MRI of the pituitary gland: indications and results in gynaecology and in obstetrics].
  • [Transliterated title] L'IRM hypophysaire: indications et résultats en gynécologie et en obstétrique.
  • MRI is the sole radiological examination to be obtained if abnormal menses, galactorrhea or anovulation evokes the diagnosis of prolactinoma.
  • Nevertheless, iatrogenic hyperprolactinemia or presence of big prolactin has to be ruled out before MRI is asked for.
  • MRI of the pituitary gland must be technically optimal; analysis of the images has to be directed by clinical and biological data.
  • [MeSH-major] Magnetic Resonance Imaging / methods. Pituitary Gland / pathology. Pituitary Neoplasms / diagnosis. Prolactinoma / diagnosis
  • [MeSH-minor] Amenorrhea / diagnosis. Amenorrhea / etiology. Female. Galactorrhea / diagnosis. Galactorrhea / etiology. Humans

  • MedlinePlus Health Information. consumer health - MRI Scans.
  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15848087.001).
  • [ISSN] 1297-9589
  • [Journal-full-title] Gynécologie, obstétrique & fertilité
  • [ISO-abbreviation] Gynecol Obstet Fertil
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Number-of-references] 6
  •  go-up   go-down


20. Uccella S, Tibiletti MG, Bernasconi B, Finzi G, Oldrini R, Capella C: Aneuploidy, centrosome alteration and securin overexpression as features of pituitary somatotroph and lactotroph adenomas. Anal Quant Cytol Histol; 2005 Oct;27(5):241-52
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aneuploidy, centrosome alteration and securin overexpression as features of pituitary somatotroph and lactotroph adenomas.
  • OBJECTIVE: To verify the presence of numerical chromosomal aberrations (NCAs) in different types of pituitary adenomas (PAs) and to investigate 2 of the mechanisms that are possibly related to aneuploidies in PAs: securin overexpression and centrosome alterations.
  • RESULTS: At interphase FISH analysis, growth hormone (GH)-cell and prolactin (PRL)-cell PAs showed multiple chromosome gains and a low frequency of chromosome losses, suggesting a hyperdiploid chromosome assessment.
  • In addition, when compared to other types of PAs, GH-cell and PRL-cell adenomas showed overexpression of securin and a higher number of both cells with abnormal nuclear shape and cells with centrosomes.
  • CONCLUSION: Somatotroph and lactotroph adenomas are characterized by aneuploidy, abnormal nuclear shape and centrosome amplification, which are possibly related to securin overexpression.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16447816.001).
  • [ISSN] 0884-6812
  • [Journal-full-title] Analytical and quantitative cytology and histology
  • [ISO-abbreviation] Anal. Quant. Cytol. Histol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Securin; 0 / pituitary tumor-transforming protein 1, human
  •  go-up   go-down


21. Hereñú CB, Morel GR, Bellini MJ, Reggiani PC, Sosa YE, Brown OA, Goya RG: Gene therapy in the neuroendocrine system. Front Horm Res; 2006;35:135-42
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In rats, aging brings about a progressive degeneration and loss of hypothalamic tuberoinfundibular dopaminergic (TIDA) neurons, which are involved in the tonic inhibitory control of prolactin secretion and lactotropic cell proliferation.
  • Spontaneous intermediate lobe pituitary tumors in a retinoblastoma (Rb) gene mutant mouse were corrected by injection of an adenoviral vector expressing the human Rb cDNA and experimental prolactinomas in rats were partially reduced by intrapituitary injection of an adenoviral vector expressing the HSV1-thymidine kinase suicide gene.
  • [MeSH-minor] Aging / genetics. Animals. Animals, Genetically Modified. Genes, Transgenic, Suicide. Hypothalamus / metabolism. Mice. Mutant Proteins / genetics. Pituitary Gland / metabolism. Pituitary Neoplasms / genetics. Pituitary Neoplasms / therapy. Rats. Rats, Brattleboro. Receptors, Cell Surface / genetics. Receptors, Leptin. Retinoblastoma / genetics

  • MedlinePlus Health Information. consumer health - Endocrine Diseases.
  • MedlinePlus Health Information. consumer health - Genes and Gene Therapy.
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • 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
  • (PMID = 16809929.001).
  • [ISSN] 0301-3073
  • [Journal-full-title] Frontiers of hormone research
  • [ISO-abbreviation] Front Horm Res
  • [Language] eng
  • [Grant] United States / FIC NIH HHS / TW / 1R21 TW 006665
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Mutant Proteins; 0 / Receptors, Cell Surface; 0 / Receptors, Leptin
  • [Number-of-references] 27
  •  go-up   go-down


22. Inguenault C, Capon-Degardin N, Martinot-Duquennoy V, Pellerin P: [Galactorrhea after mammary plastic surgery]. Ann Chir Plast Esthet; 2005 Apr;50(2):171-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • However, it may reveal the presence of o prolactin secreting adenoma, as was the case with one of our patients.
  • When faced with postsurgical galactorrhoea, serum prolactin levels should be measured.
  • If serum prolactin levels exceed 150 ng/ml further investigation by way of an MRI of the sella turcica is advisable to rule out pituitary adenoma.

  • MedlinePlus Health Information. consumer health - Breast Reconstruction.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15820605.001).
  • [ISSN] 0294-1260
  • [Journal-full-title] Annales de chirurgie plastique et esthétique
  • [ISO-abbreviation] Ann Chir Plast Esthet
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  •  go-up   go-down


23. Hansen KA, Zhang Y, Colver R, Tho SP, Plouffe L Jr, McDonough PG: The dopamine receptor D2 genotype is associated with hyperprolactinemia. Fertil Steril; 2005 Sep;84(3):711-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Previous studies of lactotrophs from prolactinomas have found normal DRD2 receptors but differing isoform density.
  • Homozygosity of polymorphism 1 may influence the distribution of the DRD2 isoforms on the lactotroph.
  • Other potential mechanisms include an association with a molecular defect in a postreceptor signaling mechanism, such as a somatic inactivating mutation in a G1 protein, which could result in autonomous function of the lactotroph.
  • Mutations could also result in different receptor-G protein interactions, such as a Gs instead of Gi, and result in autonomous lactotroph function.

  • Genetic Alliance. consumer health - Galactorrhoea-Hyperprolactinaemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16169407.001).
  • [ISSN] 1556-5653
  • [Journal-full-title] Fertility and sterility
  • [ISO-abbreviation] Fertil. Steril.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Dopamine D2
  •  go-up   go-down


24. Dekkers OM, Romijn JA, de Boer A, Vandenbroucke JP: The risk for breast cancer is not evidently increased in women with hyperprolactinemia. Pituitary; 2010 Sep;13(3):195-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We aimed to assess the risk of breast cancer in a previously defined large cohort of patients treated for idiopathic hyperprolactinemia or prolactinomas.
  • In conclusion, there is no clear evidence for increased breast cancer risk in female patients treated for either idiopathic hyperprolactinemia or prolactinomas.

  • Genetic Alliance. consumer health - Galactorrhoea-Hyperprolactinaemia.
  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Endocrinol Invest. 2001 Jun;24(6):454-9 [11434671.001]
  • [Cites] Int J Epidemiol. 2010 Feb;39(1):89-94 [19376882.001]
  • [Cites] N Engl J Med. 2003 Nov 20;349(21):2035-41 [14627789.001]
  • [Cites] J Surg Oncol. 1997 Jan;64(1):74-8 [9040805.001]
  • [Cites] Pathology. 1997 Aug;29(3):320-3 [9271027.001]
  • [Cites] Clin Endocrinol (Oxf). 1998 Oct;49(4):441-5 [9876340.001]
  • [Cites] Cancer Res. 2006 Feb 15;66(4):2476-82 [16489055.001]
  • [Cites] Endocr Rev. 2006 Aug;27(5):485-534 [16705142.001]
  • [Cites] Breast Dis. 2005-2006;24:3-15 [16917136.001]
  • [Cites] J Clin Oncol. 2007 Apr 20;25(12):1482-8 [17372279.001]
  • [Cites] Eur J Endocrinol. 2007 Aug;157(2):133-9 [17656590.001]
  • [Cites] Clin Endocrinol (Oxf). 2007 Sep;67(3):426-33 [17573902.001]
  • [Cites] Med Hypotheses. 2008;70(2):244-51 [17658223.001]
  • [Cites] Endocrinol Metab Clin North Am. 2008 Mar;37(1):67-99, viii [18226731.001]
  • [Cites] J Psychopharmacol. 2008 Mar;22(2 Suppl):20-7 [18709700.001]
  • [Cites] J Clin Endocrinol Metab. 2009 Aug;94(8):2729-34 [19491225.001]
  • [Cites] Eur J Endocrinol. 2003 Mar;148(3):325-31 [12611613.001]
  • (PMID = 20012697.001).
  • [ISSN] 1573-7403
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dopamine Agonists
  • [Other-IDs] NLM/ PMC2913002
  •  go-up   go-down


25. Raverot G, Arnous W, Calender A, Trouillas J, Sassolas G, Bournaud C, Pugeat M, Borson-Chazot F: Familial pituitary adenomas with a heterogeneous functional pattern: clinical and genetic features. J Endocrinol Invest; 2007 Oct;30(9):787-90
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Familial pituitary adenomas with a heterogeneous functional pattern: clinical and genetic features.
  • Familial pituitary adenoma is a rare syndrome which may present either as isolated lesions, or in association with other endocrine tumors, for example in the frame of multiple endocrine neoplasia (MEN-1) or Carney complex (CNC).
  • The most frequently described forms of familial isolated pituitary adenoma (FIPA) are familial somatotropinomas or prolactinomas.
  • Recently, some cases of familial isolated somatotropinoma have been associated with germline mutations in the aryl hydrocarbon receptor interacting protein (AIP) gene.
  • The present report shows heterogeneous FIPA with 3 subtypes of tumor in 3 individuals of the same family: somatotropinoma in the proband, giant prolactinoma in a brother, and gonadotroph cell macroadenoma in the father.
  • A prospective survey also suggested the occurrence of a silent microadenoma in the proband's sister.
  • In conclusion, these data suggest that familial pituitary adenomas can occur with a heterogeneous functional pattern that is distinguished from MEN-1 or CNC.
  • [MeSH-major] Adenoma / genetics. Adenoma / physiopathology. Pituitary Neoplasms / genetics. Pituitary Neoplasms / physiopathology
  • [MeSH-minor] Female. Genetic Predisposition to Disease / genetics. Genetic Testing. Humans. Male. Middle Aged. Pedigree. Polymorphism, Single Nucleotide / genetics. Proto-Oncogene Proteins / genetics. Receptors, Aryl Hydrocarbon / genetics

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • 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
  • [Cites] Mayo Clin Proc. 1986 Mar;61(3):165-72 [3945116.001]
  • [Cites] Nat Genet. 2000 Sep;26(1):89-92 [10973256.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Sep;91(9):3316-23 [16787992.001]
  • [Cites] Pituitary. 2004;7(2):73-82 [15761655.001]
  • [Cites] J Clin Invest. 2000 Sep;106(5):R31-8 [10974026.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Feb;87(2):457-65 [11836268.001]
  • [Cites] Ann Intern Med. 1994 May 15;120(10):817-20 [8154641.001]
  • [Cites] Am J Hum Genet. 1998 Aug;63(2):455-67 [9683585.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Dec;91(12):4769-75 [16968795.001]
  • [Cites] Hum Mol Genet. 2000 Dec 12;9(20):3037-46 [11115848.001]
  • [Cites] Science. 2006 May 26;312(5777):1228-30 [16728643.001]
  • [Cites] Horm Metab Res. 2005 Jun;37(6):347-54 [16001326.001]
  • [Cites] Endocrinology. 2004 Dec;145(12):5452-8 [15331577.001]
  • [Cites] Growth Horm IGF Res. 2004 Jun;14 Suppl A:S90-6 [15135786.001]
  • (PMID = 17993773.001).
  • [ISSN] 1720-8386
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / MEN1 protein, human; 0 / Proto-Oncogene Proteins; 0 / Receptors, Aryl Hydrocarbon
  •  go-up   go-down


26. Scarone P, Losa M, Mortini P, Giovanelli M: Obstructive hydrocephalus and intracranial hypertension caused by a giant macroprolactinoma. Prompt response to medical treatment. J Neurooncol; 2006 Jan;76(1):51-4
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Patients with large prolactin (PRL)-secreting pituitary adenoma often have symptoms due to varying degree of hypopituitarism and/or mass effect on visual structures, while presentation with hydrocephalus is extremely uncommon.
  • Clinical and radiological assessment led to the diagnosis of obstructive hydrocephalus caused by a giant macroprolactinoma.
  • The same day, after we received the result of the basal PRL level, medical treatment with cabergoline was initiated.
  • [MeSH-major] Dopamine Agonists / therapeutic use. Ergolines / therapeutic use. Hydrocephalus / etiology. Intracranial Hypertension / etiology. Pituitary Neoplasms / complications. Pituitary Neoplasms / drug therapy. Prolactinoma / complications. Prolactinoma / drug therapy

  • Genetic Alliance. consumer health - Hydrocephalus.
  • Genetic Alliance. consumer health - Intracranial Hypertension.
  • MedlinePlus Health Information. consumer health - Hydrocephalus.
  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Endocr Rev. 1992 May;13(2):220-40 [1352243.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Nov;84(11):3859-66 [10566620.001]
  • [Cites] Mayo Clin Proc. 1999 May;74(5):475-7 [10319078.001]
  • [Cites] Endocrinol Metab Clin North Am. 1999 Mar;28(1):143-69, vii [10207689.001]
  • [Cites] Age Ageing. 2001 Sep;30(5):426-8 [11709386.001]
  • [Cites] N Engl J Med. 2003 Nov 20;349(21):2035-41 [14627789.001]
  • [Cites] Acta Clin Belg. 1998 Feb;53(1):47-52 [9562706.001]
  • [Cites] J Neurol Neurosurg Psychiatry. 1973 Dec;36(6):1063-8 [4772720.001]
  • [Cites] J Clin Endocrinol Metab. 1985 Apr;60(4):698-705 [3882737.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Jun;85(6):2247-52 [10852458.001]
  • [Cites] Age Ageing. 2004 Jul;33(4):410-2 [15136289.001]
  • [Cites] J Neurol Sci. 1973 Jul;19(3):341-9 [4541480.001]
  • [Cites] J Comput Assist Tomogr. 1984 Feb;8(1):131-3 [6690496.001]
  • (PMID = 16205966.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dopamine Agonists; 0 / Ergolines; LL60K9J05T / cabergoline
  •  go-up   go-down


27. Grotas AB, Nagler HM: Presentation of a functional pituitary adenoma as a significant decrease in prostate-specific antigen level in a patient followed for prostate cancer. Can J Urol; 2006 Dec;13(6):3346-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Presentation of a functional pituitary adenoma as a significant decrease in prostate-specific antigen level in a patient followed for prostate cancer.
  • Testosterone production by the testes is dependent on a functional hypothalamic-pituitary-gonadal axis.
  • High prolactin levels have been shown to disrupt this axis, resulting in decreases in gonadotropins and testosterone levels.
  • The patient was found to have an asymptomatic prolactin-secreting pituitary macroadenoma.
  • [MeSH-major] Neoplasms, Second Primary / diagnosis. Pituitary Neoplasms / diagnosis. Prolactinoma / diagnosis. Prostate-Specific Antigen / metabolism. Prostatic Neoplasms / metabolism


28. Wan H, Chihiro O, Yuan S: MASEP gamma knife radiosurgery for secretory pituitary adenomas: experience in 347 consecutive cases. J Exp Clin Cancer Res; 2009;28:36
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MASEP gamma knife radiosurgery for secretory pituitary adenomas: experience in 347 consecutive cases.
  • BACKGROUND: Secretory pituitary adenomas are very common brain tumors.
  • Historically, the treatment armamentarium for secretory pituitary adenomas included neurosurgery, medical management, and fractionated radiotherapy.
  • In recent years, MASEP gamma knife radiosurgery (MASEP GKRS) has emerged as an important treatment modality in the management of secretory pituitary adenomas.
  • The goal of this research is to define accurately the efficacy, safety, complications, and role of MASEP GKRS for treatment of secretory pituitary adenomas.
  • METHODS: Between 1997 and 2007 a total of 347 patients with secretory pituitary adenomas treated with MASEP GKRS and with at least 60 months of follow-up data were identified.
  • Of the 68 patients with adrenocorticotropic hormone-secreting(ACTH) adenomas, 89.7% showed tumor volume decrease or remain unchanged and 27.9% experienced normalization of hormone level.
  • Of the 176 patients with prolactinomas, 23.3% had normalization of hormone level and 90.3% showed tumor volume decrease or remain unchanged.
  • Of the 103 patients with growth hormone-secreting(GH) adenomas, 95.1% experienced tumor volume decrease or remain unchanged and 36.9% showed normalization of hormone level.
  • CONCLUSION: MASEP GKRS is safe and effective in treating secretory pituitary adenomas.
  • [MeSH-major] Adenoma / surgery. Pituitary Neoplasms / surgery. Radiosurgery / methods

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Stereotact Funct Neurosurg. 1999;72 Suppl 1:111-8 [10681698.001]
  • [Cites] J Neurosurg. 2007 May;106(5):833-8 [17542527.001]
  • [Cites] Neurosurgery. 2000 Jul;47(1):33-6; discussion 37-9 [10917344.001]
  • [Cites] J Neurooncol. 2000 Mar;47(1):79-84 [10930104.001]
  • [Cites] J Neurosurg. 2000 Nov;93(5):738-42 [11059652.001]
  • [Cites] J Neurosurg. 2000 Dec;93 Suppl 3:14-8 [11143231.001]
  • [Cites] Neurosurgery. 2001 Aug;49(2):284-91; discussion 291-2 [11504104.001]
  • [Cites] J Neurooncol. 2001 Sep;54(2):197-203 [11761436.001]
  • [Cites] Neuropathology. 2002 Mar;22(1):19-25 [12030411.001]
  • [Cites] Strahlenther Onkol. 2002 Apr;178(4):173-86 [12040754.001]
  • [Cites] Neurosurgery. 2002 Jul;51(1):57-61; discussion 61-2 [12182435.001]
  • [Cites] Neurosurg Clin N Am. 2003 Jan;14(1):25-39, vi [12690977.001]
  • [Cites] Neurosurg Clin N Am. 2003 Jan;14(1):147-66 [12690986.001]
  • [Cites] Neurosurgery. 2003 Jul;53(1):51-9; discussion 59-61 [12823873.001]
  • [Cites] Yonsei Med J. 2003 Aug 30;44(4):602-7 [12950114.001]
  • [Cites] Arch Neurol. 1981 Apr;38(4):217-9 [7213145.001]
  • [Cites] Acta Paediatr Scand. 1986 May;75(3):388-95 [3014807.001]
  • [Cites] Can J Neurol Sci. 1990 Feb;17(1):74-7 [2155694.001]
  • [Cites] Am J Clin Oncol. 1992 Dec;15(6):467-73 [1449108.001]
  • [Cites] Ann Neurol. 1995 Jan;37(1):67-73 [7818260.001]
  • [Cites] Radiother Oncol. 1996 Oct;41(1):45-53 [8961367.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1997 Sep 1;39(2):437-44 [9308948.001]
  • [Cites] J Neurosurg. 1998 Jun;88(6):1002-8 [9609294.001]
  • [Cites] Stereotact Funct Neurosurg. 1998 Oct;70 Suppl 1:119-26 [9782243.001]
  • [Cites] Neurosurg Clin N Am. 1999 Apr;10(2):327-36 [10099097.001]
  • [Cites] Endocrinol Metab Clin North Am. 1999 Mar;28(1):119-31 [10207687.001]
  • [Cites] Endocrinol Metab Clin North Am. 1999 Mar;28(1):133-42 [10207688.001]
  • [Cites] Stereotact Funct Neurosurg. 1999;72 Suppl 1:119-24 [10681699.001]
  • (PMID = 19284583.001).
  • [ISSN] 1756-9966
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Other-IDs] NLM/ PMC2660297
  •  go-up   go-down


29. Camihort GA, Hereñú CB, Luna GC, Rodríguez SS, Bracamonte MI, Goya RG, Cónsole GM: Morphological changes induced by insulin-like growth factor-I gene therapy in pituitary cell populations in experimental prolactinomas. Cells Tissues Organs; 2010;191(4):316-25
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Morphological changes induced by insulin-like growth factor-I gene therapy in pituitary cell populations in experimental prolactinomas.
  • In previous studies, we assessed the effects of intrapituitary injection of a recombinant adenoviral vector (RAd) harboring the cDNA for rat insulin-like growth factor type I (RAd-IGF-I) on the lactotrope and somatotrope populations in estrogen-induced prolactinomas.
  • In the present study, we aimed to confirm these findings and further analyze the effect of transgenic RAd-IGF-I on the other pituitary cell populations in female rats.
  • The RAd-IGF-I group showed a significant decrease in serum growth hormone and prolactin levels and lactotrope and somatotrope cell size induced by estrogen treatment.
  • Cell density was not affected by 7 days of IGF-I gene therapy.
  • Estrogen had an inhibitory effect on thyrotrope cell density, whereas with RAd-IGF-I there was a nonsignificant trend towards restoration of cell density, without changes in cell size.
  • RAd-IGF-I treatment decreased corticotrope cell size without changing cell density.
  • Estrogen decreased gonadotrope cell size and density, which was reversed by RAd-IGF-I.
  • We conclude that in estrogen-induced pituitary tumors, IGF-I gene therapy has inhibitory effects on the lactotrope, somatotrope and corticotrope populations, while reversing the effect of estrogen on gonadotropic cells.
  • [MeSH-major] Insulin-Like Growth Factor I / genetics. Pituitary Gland / pathology. Prolactinoma / pathology. Prolactinoma / therapy

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Lab Invest. 1992 May;66(5):639-45 [1573857.001]
  • [Cites] Endocrinology. 1992 Feb;130(2):882-94 [1310281.001]
  • [Cites] Endocrinology. 1993 Jan;132(1):23-9 [7678216.001]
  • [Cites] J Clin Endocrinol Metab. 1993 Oct;77(4):1059-66 [7691862.001]
  • [Cites] Oncogene. 1994 Apr;9(4):1021-7 [8134105.001]
  • [Cites] Peptides. 1994;15(3):547-82 [7937331.001]
  • [Cites] Endocr Rev. 1997 Apr;18(2):206-28 [9101137.001]
  • [Cites] Eur J Endocrinol. 1998 Mar;138(3):309-15 [9539306.001]
  • [Cites] Physiol Res. 1998;47(2):125-31 [9706996.001]
  • [Cites] Ann Intern Med. 1998 Sep 15;129(6):472-83 [9735086.001]
  • [Cites] Endocrinology. 1999 Mar;140(3):1183-91 [10067842.001]
  • [Cites] Endocrinology. 1999 Sep;140(9):3881-9 [10465256.001]
  • [Cites] Exp Biol Med (Maywood). 2005 Dec;230(11):800-7 [16339744.001]
  • [Cites] Gene Ther. 2007 Feb;14(3):237-45 [16988717.001]
  • [Cites] Eur J Neurosci. 2007 Jan;25(1):191-200 [17241280.001]
  • [Cites] Endocrinology. 2007 Jul;148(7):3131-9 [17412817.001]
  • [Cites] Mol Cancer. 2008;7:13 [18218140.001]
  • [Cites] Curr Med Chem. 2008;15(29):3095-112 [19075656.001]
  • [Cites] Cells Tissues Organs. 2009;190(1):20-6 [18957836.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Mar;85(3):1296-305 [10720079.001]
  • [Cites] Biol Reprod. 2000 Sep;63(3):865-71 [10952933.001]
  • [Cites] Cells Tissues Organs. 2001;169(1):64-72 [11340263.001]
  • [Cites] Eur J Endocrinol. 2001 Oct;145(4):497-503 [11581010.001]
  • [Cites] Endocr Rev. 2001 Oct;22(5):631-56 [11588145.001]
  • [Cites] Neuropsychopharmacology. 2001 Dec;25(6):881-91 [11750181.001]
  • [Cites] Steroids. 2002 Jun;67(7):573-9 [11996929.001]
  • [Cites] Neuroendocrinology. 2002 May;75(5):316-25 [12006785.001]
  • [Cites] Endocrinology. 2002 Jul;143(7):2750-8 [12072410.001]
  • [Cites] Reprod Biol. 2003 Mar;3(1):7-28 [14666141.001]
  • [Cites] Am J Physiol. 1977 Sep;233(3):E235-9 [410310.001]
  • [Cites] Science. 1982 Nov 12;218(4573):684-6 [7134966.001]
  • [Cites] JAMA. 1983 Apr 22-29;249(16):2204-7 [6834618.001]
  • [Cites] Am J Pathol. 1983 Nov;113(2):198-206 [6638150.001]
  • [Cites] Proc Natl Acad Sci U S A. 1984 Feb;81(3):935-9 [6583688.001]
  • [Cites] Endocr Rev. 1989 Feb;10(1):68-91 [2666112.001]
  • [Cites] Endocrinology. 1992 Dec;131(6):2588-94 [1280202.001]
  • (PMID = 19923782.001).
  • [ISSN] 1422-6421
  • [Journal-full-title] Cells, tissues, organs
  • [ISO-abbreviation] Cells Tissues Organs (Print)
  • [Language] eng
  • [Grant] United States / NIA NIH HHS / AG / R01 AG029798
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 67763-96-6 / Insulin-Like Growth Factor I
  • [Other-IDs] NLM/ PMC3696382
  •  go-up   go-down


30. Brown RL, Muzzafar T, Wollman R, Weiss RE: A pituitary carcinoma secreting TSH and prolactin: a non-secreting adenoma gone awry. Eur J Endocrinol; 2006 May;154(5):639-43
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A pituitary carcinoma secreting TSH and prolactin: a non-secreting adenoma gone awry.
  • To our knowledge, only one case of a TSH-secreting carcinoma has previously been reported.
  • We describe here a second patient with a pituitary carcinoma producing TSH and prolactin (PRL).
  • Except for mildly increased PRL and elevated alpha-subunit, hormone evaluation was normal.
  • Pathologic examination revealed a chromophobe adenoma with increased mitotic forms.
  • The patient completed a course of external beam radiation to the pituitary and was prescribed l-thyroxine, bromocriptine, and hydrocortisone.
  • Emergent resection of the larger mass revealed a pituitary cancer with positive staining for PRL, but not for TSH.
  • Nine months later, the patient underwent further debulking of metastatic disease.
  • Although development of a carcinoma from a pituitary adenoma is very rare (<0.5%), macroadenomas that become hormonally active should be suspect for transformation into pituitary cancer.

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16645009.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK07011; United States / NCRR NIH HHS / RR / RR00055; United States / NCRR NIH HHS / RR / RR18372
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 9002-62-4 / Prolactin; 9002-71-5 / Thyrotropin
  •  go-up   go-down


31. Colao A: Pituitary tumours: the prolactinoma. Best Pract Res Clin Endocrinol Metab; 2009 Oct;23(5):575-96
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pituitary tumours: the prolactinoma.
  • This review focus on the epidemiology, diagnosis and treatment of prolactinomas.
  • The diagnosis of hyperprolactinaemia has been simplified in recent years, and only prolactin (PRL) assay and magnetic resonance imaging of the sella are required.
  • Nonetheless, macroprolactinaemia should be assessed in patients with hyperprolactinaemia in the absence of clinical symptoms of elevated PRL levels.
  • The patients achieving disappearance of the tumours and suppression of PRL levels during treatment are those showing the highest likelihood to have persistent remission of hyperprolactinaemia after treatment withdrawal.
  • [MeSH-major] Pituitary Neoplasms / etiology. Prolactinoma / etiology
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Dopamine Agonists / therapeutic use. Drug Resistance, Neoplasm / physiology. Female. Humans. Pregnancy. Pregnancy Complications, Neoplastic / therapy. Treatment Outcome. Withholding Treatment

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19945024.001).
  • [ISSN] 1878-1594
  • [Journal-full-title] Best practice & research. Clinical endocrinology & metabolism
  • [ISO-abbreviation] Best Pract. Res. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Dopamine Agonists
  • [Number-of-references] 157
  •  go-up   go-down


32. Colao A, Galderisi M, Di Sarno A, Pardo M, Gaccione M, D'Andrea M, Guerra E, Pivonello R, Lerro G, Lombardi G: Increased prevalence of tricuspid regurgitation in patients with prolactinomas chronically treated with cabergoline. J Clin Endocrinol Metab; 2008 Oct;93(10):3777-84
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Increased prevalence of tricuspid regurgitation in patients with prolactinomas chronically treated with cabergoline.
  • BACKGROUND: Cabergoline, a dopamine receptor-2 agonist used to treat prolactinomas, was associated with increased risk of cardiac valve disease in Parkinson's disease.
  • OBJECTIVE: Our objective was to evaluate prevalence of cardiac valve regurgitation in cabergoline-treated patients with prolactinomas.
  • PATIENTS: Fifty treated patients (44 women and six men) and 50 sex- and age-matched control subjects participated; 20 de novo patients were also studied.
  • RESULTS: In de novo patients, treated patients, and controls, the prevalence of mild regurgitation of mitral (35, 22, and 12%, P = 0.085), aortic (0, 4, and 2%, P = 0.59), tricuspid (55, 30, and 42%, P = 0.13) or pulmonic (20, 12, and 6%, P = 0.22) valves was similar.
  • Conversely, the prevalence of moderate tricuspid regurgitation was higher in the treated patients (54%) than in de novo patients (0%) and controls (18%, P < 0.0001).
  • CONCLUSION: Moderate tricuspid regurgitation is more frequent in patients taking cabergoline (at higher cumulative doses) than in de novo patients and control subjects, but the clinical significance of this finding has not been established.
  • [MeSH-major] Ergolines / administration & dosage. Ergolines / adverse effects. Pituitary Neoplasms / drug therapy. Prolactinoma / drug therapy. Tricuspid Valve Insufficiency / chemically induced. Tricuspid Valve Insufficiency / epidemiology
  • [MeSH-minor] Adult. Antineoplastic Agents / administration & dosage. Antineoplastic Agents / adverse effects. Case-Control Studies. Chronic Disease. Dose-Response Relationship, Drug. Female. Humans. Male. Middle Aged. Prevalence. Time Factors

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18682513.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00460616
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Ergolines; LL60K9J05T / cabergoline
  •  go-up   go-down


33. Chatfield J, Zhang L, Ramey J, Bowsher T, Loskutoff N, O'Neill K: Resolution of a hyperprolactinemia in a western lowland gorilla (Gorilla gorilla gorilla). J Zoo Wildl Med; 2006 Dec;37(4):565-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Resolution of a hyperprolactinemia in a western lowland gorilla (Gorilla gorilla gorilla).
  • Prolactin-secreting pituitary adenomas are one of the most common causes of infertility in women.
  • Prolactin plays an important role in lactation and is involved in producing some of the normal mammalian breeding and maternal behaviors.
  • Elevated serum prolactin concentrations can adversely affect the reproductive cycle in females by inhibiting the normal lutenizing hormone surge that stimulates ovulation.
  • An MRI confirmed a pituitary mass and treatment was initiated with cabergoline.
  • Following 8 mo of treatment, mass size decreased and serum prolactin was within normal limits.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Ape Diseases / drug therapy. Ergolines / therapeutic use. Gorilla gorilla. Pituitary Neoplasms / veterinary. Prolactinoma / veterinary

  • 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
  • (PMID = 17315448.001).
  • [ISSN] 1042-7260
  • [Journal-full-title] Journal of zoo and wildlife medicine : official publication of the American Association of Zoo Veterinarians
  • [ISO-abbreviation] J. Zoo Wildl. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Ergolines; LL60K9J05T / cabergoline
  •  go-up   go-down


34. Maïza JC, Caron P: [Pituitary carcinomas and aggressive adenomas: an overview and new therapeutic options]. Ann Endocrinol (Paris); 2009 Sep;70 Suppl 1:S12-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Pituitary carcinomas and aggressive adenomas: an overview and new therapeutic options].
  • Pituitary carcinomas are a rare disease with an estimated prevalence around 0.2 % of the pituitary tumours.
  • They are defined by the presence of intra or extra-cranial metastases but initially they can share the same features as aggressive pituitary adenomas.
  • Indeed there are some indicators that help to differentiate adenomas and carcinomas such as histological findings and immunohistochemical characteristics.
  • The majority of carcinomas are prolactin or ACTH-secreting tumors.
  • Dopamine and somatostatin-receptor agonists are not as effective as for the treatment of adenomas.
  • [MeSH-major] Adenoma / therapy. Pituitary Neoplasms / therapy

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19878763.001).
  • [ISSN] 0003-4266
  • [Journal-full-title] Annales d'endocrinologie
  • [ISO-abbreviation] Ann. Endocrinol. (Paris)
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents
  • [Number-of-references] 36
  •  go-up   go-down


35. Peker S, Sun I, Kurtkaya-Yapicier O, Elmaci I, Pamir MN: Ectopic pituitary adenoma located at the pituitary stalk. Case report. J Neurosurg Sci; 2005 Mar;49(1):25-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ectopic pituitary adenoma located at the pituitary stalk. Case report.
  • Suprasellar located ectopic pituitary adenomas are unusual tumors.
  • We report a rare case of suprasellar prolactinoma arising from the pars tuberalis in a 37-year-old woman.
  • The pituitary stalk was preserved.
  • Histopathologic diagnosis was a pituitary adenoma immunoreactive for prolactin.
  • Pituitary hormonal functions returned to normal at 6 months postoperatively.
  • An ectopic adenoma should be suspected in a patient with suprasellar tumor and hyperprolactinemia.
  • Surgical excision of this tumor may result with normal pituitary functions and normal visual acuity.
  • [MeSH-major] Pituitary Gland / pathology. Pituitary Neoplasms / pathology. Prolactinoma / pathology
  • [MeSH-minor] Adult. Craniopharyngioma / pathology. Diagnosis, Differential. Female. Humans. Magnetic Resonance Imaging

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15990716.001).
  • [ISSN] 0390-5616
  • [Journal-full-title] Journal of neurosurgical sciences
  • [ISO-abbreviation] J Neurosurg Sci
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  •  go-up   go-down


36. Kubo T, Furujo M, Mori S, Imai K, Ueda Y, Tsukahara K, Morita H, Ogura K, Fukuhara S, Shimizu J, Koyama T, Kanadani T, Shiraga H, Shinozuka M, Terasaki T, Hattori N: An infant case of macroprolactinemia with transient idiopathic central precocious puberty. Endocr J; 2007 Dec;54(5):825-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • At that time, the unexpected finding of high PRL level was also observed.
  • Four months later, she was referred to our clinic for persistently high PRL level.
  • At this time, other endocrinological data showed prepubertal stage and we demonstrated macroprolactinemia and the presence of anti-PRL autoantibody.
  • After other causes of hyperprolactinemia such as prolactinoma and stress were ruled out, we finally diagnosed her with hyperprolactinemia due to macroprolactinemia.
  • [MeSH-major] Hyperprolactinemia / complications. Puberty, Precocious / diagnosis. Puberty, Precocious / etiology
  • [MeSH-minor] Child. Child Development Disorders, Pervasive / complications. Female. Humans. Infant. Prolactin / blood

  • Genetic Alliance. consumer health - Precocious puberty.
  • Genetic Alliance. consumer health - Central precocious puberty.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17785914.001).
  • [ISSN] 1348-4540
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 9002-62-4 / Prolactin
  •  go-up   go-down


37. Kubo S, Hasegawa H, Inui T, Tominaga S, Yoshimine T: Endonasal endoscopic transsphenoidal chiasmapexy with silicone plates for empty sella syndrome: technical note. Neurol Med Chir (Tokyo); 2005 Aug;45(8):428-32; discussion 432
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A 36-year-old woman had been treated for prolactinoma for about 19 years with bromocriptine and then presented with left visual disturbance.
  • [MeSH-minor] Adult. Aged. Atrophy / chemically induced. Atrophy / pathology. Atrophy / surgery. Bromocriptine / adverse effects. Female. Hormone Antagonists / adverse effects. Humans. Male. Nasal Cavity / anatomy & histology. Nasal Cavity / surgery. Prolactinoma / drug therapy. Prolactinoma / pathology. Silicones / therapeutic use. Treatment Outcome. Vision Disorders / etiology. Vision Disorders / physiopathology. Vision Disorders / surgery

  • Genetic Alliance. consumer health - Empty Sella Syndrome.
  • MedlinePlus Health Information. consumer health - Endoscopy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Neurol Med Chir (Tokyo). 2005 Sep;45(9):491 [16195653.001]
  • (PMID = 16127264.001).
  • [ISSN] 0470-8105
  • [Journal-full-title] Neurologia medico-chirurgica
  • [ISO-abbreviation] Neurol. Med. Chir. (Tokyo)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Hormone Antagonists; 0 / Silicones; 3A64E3G5ZO / Bromocriptine
  •  go-up   go-down


38. Molitch ME: Medication-induced hyperprolactinemia. Mayo Clin Proc; 2005 Aug;80(8):1050-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Medication use is a common cause of hyperprolactinemia, and it is important to differentiate this cause from pathologic causes, such as prolactinomas.
  • It is Important to ensure that hyperprolactinemia in an Individual patient is due to medication and not to a structural lesion in the hypothalamic/pituitary area; this can be accomplished by (1) stopping the medication temporarily to determine whether prolactin levels return to normal, (2) switching to a medication that does not cause hyperprolactinemia (in consultation with the patient's psychiatrist for psychoactive medications), or (3) performing magnetic resonance imaging or computed tomography of the hypothalamic/pituitary area.
  • [MeSH-major] Antidepressive Agents / adverse effects. Antipsychotic Agents / adverse effects. Gastrointestinal Agents / adverse effects. Hyperprolactinemia / chemically induced. Prolactin / secretion
  • [MeSH-minor] Female. Humans. Male. Pituitary Neoplasms / complications

  • Genetic Alliance. consumer health - Galactorrhoea-Hyperprolactinaemia.
  • MedlinePlus Health Information. consumer health - Antidepressants.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16092584.001).
  • [ISSN] 0025-6196
  • [Journal-full-title] Mayo Clinic proceedings
  • [ISO-abbreviation] Mayo Clin. Proc.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antidepressive Agents; 0 / Antipsychotic Agents; 0 / Gastrointestinal Agents; 9002-62-4 / Prolactin
  • [Number-of-references] 119
  •  go-up   go-down


39. Rivera J, Alves S, Bianchi CC, Al-Mutawa N, Guiot MC, Zeitouni A: An unusual collision tumor comprising a prolactinoma and a plasmocytoma originating from the sellar region. Pituitary; 2010 Jun;13(2):189-93
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] An unusual collision tumor comprising a prolactinoma and a plasmocytoma originating from the sellar region.
  • MR imaging showed a large sellar mass with significant destruction of the pituitary fossa.
  • Laboratory tests revealed very high serum prolactin (2,483 ng/dl, reference range 3-13 ng/dl).
  • Dopamine agonist therapy was initiated with significant decline in PRL levels; however, nausea, fatigue, and anorexia developed.
  • A transsphenoidal excisional biopsy was performed which demonstrated two distinct populations of cells, corresponding to a plasma cell tumor and a lactotroph adenoma.
  • Only a few cases of solitary plasmocytomas of the pituitary region have been reported.
  • Few cases of prolactinomas coexisting with other sellar tumors has been described.
  • We suggest that in the presence of extensive cranial nerve involvement, atypical imaging findings for a pituitary adenoma and severe hyperprolactinemia, the possibility of a collision tumor should lead the physician to consider excisional tumor biopsy or surgery in addition to dopamine agonist therapy.
  • [MeSH-major] Neoplasms, Multiple Primary / diagnosis. Pituitary Neoplasms / diagnosis. Plasmacytoma / diagnosis. Prolactinoma / diagnosis. Sella Turcica / pathology

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Pituitary. 2006;9(1):65-72 [16703411.001]
  • [Cites] Neurology. 1988 Apr;38(4):614-6 [2832785.001]
  • [Cites] Surg Neurol. 1992 May;37(5):388-93 [1631767.001]
  • [Cites] Mayo Clin Proc. 2007 Jul;82(7):836-42 [17605964.001]
  • [Cites] Breast Dis. 2003;18:75-86 [15687690.001]
  • [Cites] Blood Rev. 2007 Nov;21(6):285-99 [17850941.001]
  • [Cites] Pituitary. 2008;11(3):317-23 [17917812.001]
  • [Cites] Immunol Lett. 2002 Jul 3;82(3):191-6 [12036601.001]
  • [Cites] Biomed Pharmacother. 2004 Jun;58(5):310-9 [15194167.001]
  • [Cites] Arch Pathol Lab Med. 1977 Jan;101(1):55-6 [576202.001]
  • [Cites] J Endocrinol Invest. 2000 Jan;23(1):37-41 [10698050.001]
  • [Cites] Trends Endocrinol Metab. 2006 Apr;17(3):110-6 [16517173.001]
  • [Cites] Neuroimmunomodulation. 2001;9(4):231-6 [11847486.001]
  • [Cites] Neuroimmunomodulation. 2001;9(2):95-102 [11549891.001]
  • [Cites] Semin Arthritis Rheum. 2001 Aug;31(1):21-32 [11503136.001]
  • [Cites] Blood. 1995 Feb 15;85(4):863-72 [7849308.001]
  • [Cites] Ann Med. 2004;36(6):414-25 [15513293.001]
  • [Cites] Pituitary. 2004;7(3):179-181 [16328566.001]
  • [Cites] Acta Neurochir (Wien). 1999;141(2):219-20 [10189508.001]
  • [Cites] Neurosurgery. 1998 May;42(5):1197-9 [9588573.001]
  • [Cites] Autoimmun Rev. 2007 Sep;6(8):537-42 [17854745.001]
  • (PMID = 18846427.001).
  • [ISSN] 1573-7403
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


40. Vlotides G, Siegel E, Donangelo I, Gutman S, Ren SG, Melmed S: Rat prolactinoma cell growth regulation by epidermal growth factor receptor ligands. Cancer Res; 2008 Aug 1;68(15):6377-86
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rat prolactinoma cell growth regulation by epidermal growth factor receptor ligands.
  • Epidermal growth factor (EGF) regulates pituitary development, hormone synthesis, and cell proliferation.
  • Although ErbB receptor family members are expressed in pituitary tumors, the effects of EGF signaling on pituitary tumors are not known.
  • Immunoprecipitation and Western blot confirmed EGF receptor (EGFR) and p185(c-neu) protein expression in GH3 lacto-somatotroph but not in adrenocorticotropic hormone-secreting AtT20 pituitary tumor cells.
  • EGF (5 nmol/L) selectively enhanced baseline ( approximately 4-fold) and serum-induced (>6-fold) prolactin (PRL) mRNA levels, whereas gefitinib, an EGFR antagonist, suppressed serum-induced cell proliferation and Pttg1 expression, blocked PRL gene expression, and reversed EGF-mediated somatotroph-lactotroph phenotype switching.
  • Tumors in athymic mice implanted s.c. with GH3 cells resulted in weight gain accompanied by increased serum PRL, growth hormone, and insulin growth factor 1.
  • Mice treated with gefitinib exhibited decreased tumor tissue ERK1/2 phosphorylation and down-regulated tumor PRL and Pttg1 mRNA abundance.
  • These results show that EGFR inhibition controls tumor growth and PRL secretion in experimental lacto-somatotroph tumors.
  • EGFR inhibitors could therefore be useful for the control of PRL secretion and tumor load in prolactinomas resistant to dopaminergic treatment, or for those prolactinomas undergoing rare malignant transformation.

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Endocrinology. 1992 Jun;130(6):3453-8 [1534540.001]
  • [Cites] J Neurosurg. 2003 Aug;99(2):402-8 [12924717.001]
  • [Cites] Cell. 1995 Jan 27;80(2):179-85 [7834738.001]
  • [Cites] Endocrinology. 1995 Mar;136(3):939-46 [7867603.001]
  • [Cites] Endocrinology. 1995 Apr;136(4):1595-602 [7895669.001]
  • [Cites] Endocrinology. 1995 May;136(5):2284-93 [7720677.001]
  • [Cites] Endocrinology. 1995 Oct;136(10):4479-88 [7664668.001]
  • [Cites] Endocrinology. 1998 May;139(5):2209-16 [9564824.001]
  • [Cites] J Endocrinol. 1998 Sep;158(3):425-33 [9846172.001]
  • [Cites] Mol Endocrinol. 1999 Jan;13(1):156-66 [9892021.001]
  • [Cites] J Cell Biol. 1999 Aug 23;146(4):697-702 [10459005.001]
  • [Cites] J Endocrinol. 2004 Nov;183(2):385-94 [15531726.001]
  • [Cites] Neurosurgery. 2005 May;56(5):1066-74; discussion 1066-74 [15854256.001]
  • [Cites] J Clin Endocrinol Metab. 2005 May;90(5):3089-99 [15741248.001]
  • [Cites] Arq Neuropsiquiatr. 2006 Mar;64(1):60-6 [16622555.001]
  • [Cites] Lancet. 2006 May 13;367(9522):1605-17 [16698415.001]
  • [Cites] Clin Endocrinol (Oxf). 2006 Aug;65(2):265-73 [16886971.001]
  • [Cites] Semin Oncol. 2006 Aug;33(4):466-78 [16890801.001]
  • [Cites] Endocr Rev. 2006 Aug;27(5):485-534 [16705142.001]
  • [Cites] Nat Clin Pract Endocrinol Metab. 2006 Oct;2(10):571-81 [17024156.001]
  • [Cites] Mol Endocrinol. 2006 Dec;20(12):3321-35 [16959877.001]
  • [Cites] N Engl J Med. 2006 Dec 14;355(24):2558-73 [17167139.001]
  • [Cites] Clin Cancer Res. 2003 Sep 1;9(10 Pt 1):3773-8 [14506170.001]
  • [Cites] J Clin Invest. 2003 Dec;112(11):1603-18 [14660734.001]
  • [Cites] Mod Pathol. 2004 Jul;17(7):772-80 [15098012.001]
  • [Cites] Nature. 1984 Dec 6-12;312(5994):545-8 [6504162.001]
  • [Cites] Cell. 1986 Jun 6;45(5):649-57 [2871941.001]
  • [Cites] DNA. 1989 Dec;8(10):723-32 [2575488.001]
  • [Cites] Pituitary. 2007;10(1):81-6 [17285366.001]
  • [Cites] Cell. 2007 Jun 29;129(7):1261-74 [17604717.001]
  • [Cites] J Clin Invest. 2007 Aug;117(8):2051-8 [17671639.001]
  • [Cites] Endocrinology. 2007 Dec;148(12):6107-14 [17656461.001]
  • [Cites] Hum Pathol. 2007 Jan;38(1):185-9 [17056093.001]
  • [Cites] Endocr Rev. 2007 Apr;28(2):165-86 [17325339.001]
  • [Cites] Cell Tissue Res. 2000 Feb;299(2):237-43 [10741464.001]
  • [Cites] Clin Cancer Res. 2000 May;6(5):2053-63 [10815932.001]
  • [Cites] Mol Endocrinol. 2000 Sep;14(9):1328-37 [10976912.001]
  • [Cites] Clin Cancer Res. 2000 Dec;6(12):4885-92 [11156248.001]
  • [Cites] Endocrinology. 2001 Feb;142(2):847-53 [11159858.001]
  • [Cites] Mol Endocrinol. 2001 Apr;15(4):600-13 [11266511.001]
  • [Cites] Oncogene. 2001 Mar 26;20(13):1594-600 [11313906.001]
  • [Cites] J Biol Chem. 2001 Jun 15;276(24):21146-52 [11287413.001]
  • [Cites] Mol Endocrinol. 2001 Nov;15(11):1870-9 [11682618.001]
  • [Cites] J Biol Chem. 2002 Feb 8;277(6):4010-7 [11726647.001]
  • [Cites] Biochem Pharmacol. 2002 Sep;64(5-6):755-63 [12213567.001]
  • [Cites] Cancer Res. 2002 Oct 15;62(20):5749-54 [12384534.001]
  • [Cites] Mol Endocrinol. 2002 Dec;16(12):2840-52 [12456804.001]
  • [Cites] Pituitary. 2002;5(2):89-98 [12675506.001]
  • [Cites] Endocrinology. 1994 Nov;135(5):2012-21 [7956924.001]
  • (PMID = 18676863.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA075979-10; United States / NCI NIH HHS / CA / R01 CA075979; United States / NCI NIH HHS / CA / CA 075979; United States / NCI NIH HHS / CA / R01 CA075979-10
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA Primers; 0 / Ligands; 0 / Quinazolines; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib
  • [Other-IDs] NLM/ NIHMS56463; NLM/ PMC2497431
  •  go-up   go-down


41. Minniti G, Esposito V, Piccirilli M, Fratticci A, Santoro A, Jaffrain-Rea ML: Diagnosis and management of pituitary tumours in the elderly: a review based on personal experience and evidence of literature. Eur J Endocrinol; 2005 Dec;153(6):723-35
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diagnosis and management of pituitary tumours in the elderly: a review based on personal experience and evidence of literature.
  • An increasing proportion of pituitary adenomas are recognized in the elderly, raising the question of their optimal diagnosis and management.
  • About 80% of pituitary adenomas in this age group are non-secreting, requiring careful differential diagnosis with non-adenomatous sellar lesions.
  • Recognized secreting tumours are mainly GH-secreting, most of them intrasellar, followed by prolactinomas, which present as clinically non-secreting and are usually invasive.
  • Cushing's disease appears as a very rare eventuality in the elderly.
  • Optimal therapeutic management should aim to control the disease while preserving or improving patient's quality of life.
  • Transsphenoidal surgery has proved to be an efficient and well-tolerated option for non-secreting adenomas with visual defects and intrasellar GH-secreting adenomas, being able to improve metabolic and cardiovascular complications of acromegaly even in this age group.
  • In contrast, dopamine-agonist drugs can be proposed as a primary therapy for prolactinomas even in the presence of severe neurological complications.

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16322376.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hormones
  • [Number-of-references] 88
  •  go-up   go-down


42. Kajiwara K, Saito K, Yoshikawa K, Kato S, Akimura T, Nomura S, Ishihara H, Suzuki M: Image-guided stereotactic radiosurgery with the CyberKnife for pituitary adenomas. Minim Invasive Neurosurg; 2005 Apr;48(2):91-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Image-guided stereotactic radiosurgery with the CyberKnife for pituitary adenomas.
  • Twenty-one patients with pituitary adenomas received image-guided stereotactic radiosurgery with the CyberKnife, and were followed up for more than 18 months.
  • The patients consisted of 14 with non-functioning adenomas, 3 with prolactinomas, 2 with acromegaly, and 2 with ACTH-producing tumors.
  • The mean volumes of the non-functioning and functioning adenomas were 13.3 cm (3) and 7.5 cm (3), respectively.
  • The marginal irradiation dose ranged from 6.4 Gy to 27.7 Gy (mean: non-functioning adenomas 12.6 Gy, functioning adenomas 17.5 Gy), as a dose of a single fraction.
  • Hormonal function improved in all of the 7 functioning adenomas.
  • The hormone level normalized in 1 prolactinoma, and decreased to less than normal in 1 ACTH-producing adenoma.
  • Image-guided stereotactic radiosurgery with the CyberKnife is effective and safe against relatively large pituitary adenomas.
  • [MeSH-major] Adenoma / surgery. Pituitary Neoplasms / surgery. Radiosurgery / instrumentation. Surgery, Computer-Assisted / instrumentation

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15906203.001).
  • [ISSN] 0946-7211
  • [Journal-full-title] Minimally invasive neurosurgery : MIN
  • [ISO-abbreviation] Minim Invasive Neurosurg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  •  go-up   go-down


43. Mukdsi JH, De Paul AL, Petiti JP, Gutiérrez S, Aoki A, Torres AI: Pattern of FGF-2 isoform expression correlated with its biological action in experimental prolactinomas. Acta Neuropathol; 2006 Oct;112(4):491-501
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pattern of FGF-2 isoform expression correlated with its biological action in experimental prolactinomas.
  • Fibroblast growth factor-2 (FGF-2) synthesized in the pituitary is involved in the formation and progression of pituitary tumors.
  • The aim of this study was to analyze the pattern expression of two FGF-2 isoforms at different subcellular levels and to determine its correlation with prolactinoma development.
  • Estrogen administration to male rats for 7, 20, and 60 days generated pituitary tumors, with lactotrophs being the prevalent cell type.
  • The 18 kDa isoform observed in cytosol extracts reached the highest levels after 60 days of hormonal stimulation and this was related to lactotroph proliferation.
  • However, the 22 kDa FGF-2 isoform was only detected in the nuclear compartment and achieved the maximum expression at 7 days of estrogen treatment, without any correlation with lactotroph proliferation.
  • These results suggest that the 18 kDa FGF-2 may play a role in the modulation of lactotroph proliferation in prolactinomas induced by estrogen.
  • The overproduction of both FGF-2 isoforms appears to be implicated in autocrine-paracrine-intracrine mitogenic loops; this FGF-2 activity could lead to uncontrolled cell growth, angiogenesis, and tumor formation.
  • [MeSH-major] Fibroblast Growth Factor 2 / metabolism. Gene Expression Regulation, Neoplastic / physiology. Pituitary Neoplasms / metabolism. Prolactinoma / metabolism
  • [MeSH-minor] Animals. Blotting, Western / methods. Disease Models, Animal. Estradiol / analogs & derivatives. Immunohistochemistry / methods. Male. Microscopy, Electron, Transmission / methods. Molecular Weight. Prolactin / metabolism. Protein Isoforms / genetics. Protein Isoforms / metabolism. Radioimmunoassay / methods. Rats. Rats, Wistar. Reticulin / metabolism. Time Factors

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. ESTRADIOL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16823503.001).
  • [ISSN] 0001-6322
  • [Journal-full-title] Acta neuropathologica
  • [ISO-abbreviation] Acta Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Protein Isoforms; 0 / Reticulin; 103107-01-3 / Fibroblast Growth Factor 2; 1S4CJB5ZGN / estradiol 3-benzoate; 4TI98Z838E / Estradiol; 9002-62-4 / Prolactin
  •  go-up   go-down


44. Winczyk K, Pawlikowski M: Immunohistochemical detection of PPARgamma receptors in the human pituitary adenomas: correlation with PCNA. Folia Histochem Cytobiol; 2005;43(3):137-41
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunohistochemical detection of PPARgamma receptors in the human pituitary adenomas: correlation with PCNA.
  • The occurrence of peroxisome proliferator-activated receptors gamma (PPARgamma) was investigated in 51 human pituitary adenomas and in 6 non-tumoral human pituitary tissue samples.
  • The mean percentage of cells with positive nuclear reaction was 3-fold higher in pituitary adenomas in comparison with non-tumoral pituitary tissues.
  • It was clearly stronger in pituitary adenomas than in non-tumoral pituitary tissues.
  • A slight, statistically insignificant tendency towards negative correlation between PPARgamma and PCNA was found in somatotropinomas, prolactinomas, corticotropinomas and gonadotropinomas.
  • On the other hand, in null cell adenomas and "silent" corticotropinomas, a strong positve correlation between the expression of PPARgamma and PCNA was observed.
  • The strong expression of PPARgamma in human pituitary adenomas and its possible involvement in control of cell proliferation in these tumors give a good reason for the attempts of their treatment with PPARgamma ligands.

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • 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
  • (PMID = 16201313.001).
  • [ISSN] 0239-8508
  • [Journal-full-title] Folia histochemica et cytobiologica
  • [ISO-abbreviation] Folia Histochem. Cytobiol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / PPAR gamma; 0 / Proliferating Cell Nuclear Antigen
  •  go-up   go-down


45. Kawabata Y, Ueno Y, Horikawa F, Miyake H, Miki N, Ono M: Remarkable effects of cabergoline in a patient with huge prolactinoma resistant to high-dose bromocriptine: case report. Surg Neurol; 2008 Jan;69(1):85-8; discussion 88
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Remarkable effects of cabergoline in a patient with huge prolactinoma resistant to high-dose bromocriptine: case report.
  • BACKGROUND: Cabergoline (CAB) has been proposed as the first-line treatment in the management of prolactin (PRL)-secreting tumors (prolactinoma [PRLoma]), including those resistant to standard dopamine agonist (DAA) therapy.
  • Nonetheless, the tumor grew up to more than 8 cm in diameter, serum PRL increased over 60000 ng/mL, and his visual acuity deteriorated.
  • Cabergoline normalized serum PRL level, shrank the tumor mass remarkably, and caused marked improvement of visual acuity.
  • CONCLUSION: Prolactin normalization and significant tumor shrinkage could be achieved with CAB even in extremely BRC-resistant PRLomas.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Ergolines / therapeutic use. Pituitary Neoplasms / drug therapy. Prolactinoma / drug therapy
  • [MeSH-minor] Adult. Bromocriptine / therapeutic use. Dopamine Agonists / therapeutic use. Drug Resistance, Neoplasm. Humans. Male. Treatment Outcome

  • 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
  • (PMID = 17967478.001).
  • [ISSN] 0090-3019
  • [Journal-full-title] Surgical neurology
  • [ISO-abbreviation] Surg Neurol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Dopamine Agonists; 0 / Ergolines; 3A64E3G5ZO / Bromocriptine; LL60K9J05T / cabergoline
  •  go-up   go-down


46. Wass JA, Karavitaki N: Nonfunctioning pituitary adenomas: the Oxford experience. Nat Rev Endocrinol; 2009 09;5(9):519-22
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nonfunctioning pituitary adenomas: the Oxford experience.
  • Nonfunctioning adenomas are the second most common type of pituitary tumor.
  • Over the past few years, our knowledge of the epidemiology, natural history, diagnosis, treatment, and recurrence rates of these tumors has improved.
  • In addition, we describe our own experience in the clinical management of patients with nonfunctioning adenomas.
  • Serum prolactin levels are generally <2,000 mU/l in patients with these tumors; we propose that this level be used as the cut-off to differentiate nonfunctioning from prolactin-secreting adenomas.
  • [MeSH-major] Adenoma / diagnosis. Adenoma / pathology. Pituitary Neoplasms / diagnosis. Pituitary Neoplasms / pathology
  • [MeSH-minor] Humans. Prolactin / blood

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • 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
  • [Cites] J Clin Endocrinol Metab. 2000 Apr;85(4):1420-5 [10770176.001]
  • [Cites] BMJ. 1992 May 23;304(6838):1343-6 [1611331.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Apr;89(4):1674-83 [15070930.001]
  • [Cites] Rev Endocr Metab Disord. 2009 Jun;10(2):83-90 [18651224.001]
  • [Cites] Rev Endocr Metab Disord. 2009 Jun;10(2):111-23 [18791829.001]
  • [Cites] Reproduction. 2001 Mar;121(3):363-71 [11226062.001]
  • [Cites] Clin Endocrinol (Oxf). 2006 Oct;65(4):524-9 [16984247.001]
  • [Cites] Cancer. 2004 Aug 1;101(3):613-9 [15274075.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Apr;83(4):1368-75 [9543168.001]
  • [Cites] Endocr Relat Cancer. 2008 Dec;15(4):905-15 [18780796.001]
  • [Cites] Clin Endocrinol (Oxf). 2003 Jan;58(1):59-64 [12519413.001]
  • [Cites] Clin Endocrinol (Oxf). 1999 Sep;51(3):281-4 [10469006.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Dec;91(12):4769-75 [16968795.001]
  • [Cites] Clin Endocrinol (Oxf). 2007 Dec;67(6):938-43 [17692109.001]
  • [Cites] J Clin Endocrinol Metab. 2006 May;91(5):1796-801 [16507632.001]
  • [Cites] Clin Endocrinol (Oxf). 2005 Jul;63(1):39-44 [15963059.001]
  • [Cites] JAMA. 1990 May 23-30;263(20):2772-6 [2332920.001]
  • [Cites] Clin Endocrinol (Oxf). 1998 Mar;48(3):331-7 [9578824.001]
  • (PMID = 19690562.001).
  • [ISSN] 1759-5037
  • [Journal-full-title] Nature reviews. Endocrinology
  • [ISO-abbreviation] Nat Rev Endocrinol
  • [Language] eng
  • [Publication-type] Review
  • [Publication-country] England
  • [Chemical-registry-number] 9002-62-4 / Prolactin
  •  go-up   go-down


47. Deepak D, Daousi C, Javadpour M, MacFarlane IA: Macroprolactinomas and epilepsy. Clin Endocrinol (Oxf); 2007 Apr;66(4):503-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • PATIENTS: A case note analysis of all patients with a diagnosis of macroprolactinoma attending a neuroendocrine clinic between 1996 and 2006.
  • Those with epilepsy at diagnosis of macroprolactinoma were examined in detail.
  • Six of these 29 patients (four men), had a history of seizures at the time of diagnosis, five of whom had features suggestive of temporal lobe epilepsy.
  • All six patients with epilepsy had invasive prolactinomas on cranial imaging and marked hyperprolactinaemia (median prolactin 369 000 mU/l, range 28 000 to > 750 000).
  • Seizures had been present for a median of 2 years (range 1-23 years) before the diagnosis of macroprolactinoma.
  • It is essential to enquire about epileptic symptoms, as the seizure disorder may have been undiagnosed/untreated for years.
  • [MeSH-major] Epilepsy / etiology. Pituitary Neoplasms / complications. Prolactinoma / complications

  • Genetic Alliance. consumer health - Epilepsy.
  • MedlinePlus Health Information. consumer health - Epilepsy.
  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • Hazardous Substances Data Bank. PHENYTOIN .
  • Hazardous Substances Data Bank. GADOLINIUM, ELEMENTAL .
  • 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
  • (PMID = 17371466.001).
  • [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 / Anticonvulsants; 0 / Dopamine Agonists; 6158TKW0C5 / Phenytoin; AU0V1LM3JT / Gadolinium
  •  go-up   go-down


48. Kunishio K, Okada M, Matsumoto Y, Nagao S, Nishiyama Y: Technetium-99m sestamibi single photon emission computed tomography findings correlated with P-glycoprotein expression in pituitary adenoma. J Med Invest; 2006 Aug;53(3-4):285-91
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Technetium-99m sestamibi single photon emission computed tomography findings correlated with P-glycoprotein expression in pituitary adenoma.
  • The aim of this study is to evaluate whether the technetium-99m sestamibi ((99m)Tc-MIBI) single photon emission computed tomography (SPECT) characteristics of pituitary adenomas might be correlated with cavernous sinus invasion, proliferative potential or the multidrug-resistance (MDR-1) gene product P-glycoprotein (Pgp) expression in pituitary adenomas.
  • Fifteen patients with pituitary adenomas, including 10 nonfunctioning adenomas, two prolactinomas, two GH producing adenomas, and one ACTH producing adenomas was investigated for this study.
  • The pituitary adenomas specimens were examined by immunohistochemistry using anti-Pgp and MIB-1 monoclonal antibodies.(99m)Tc-MIBI SPECT findings were not related to MIB-1 labeling index or cavernous sinus invasion. (99m)Tc-MIBI SPECT RI (-38.55+/-20.77) of the Pgp-positive group was significantly lower than that (-15.78+/-19.40) of Pgp-negative group (p=0.0494).
  • Our study suggests that although (99m)Tc-MIBI SPECT is not useful to evaluate the proliferative potential or cavernous sinus invasion of pituitary adenomas. (99m)Tc-MIBI SPECT could predict anti-cancer drug resistance related to the expression of Pgp in pituitary adenomas.
  • [MeSH-major] P-Glycoprotein / metabolism. Pituitary Neoplasms / metabolism. Pituitary Neoplasms / radionuclide imaging
  • [MeSH-minor] Adult. Aged. Cavernous Sinus / pathology. Cell Proliferation. Female. Gene Expression Regulation, Neoplastic. Genes, MDR. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Invasiveness. RNA, Messenger / genetics. RNA, Messenger / metabolism. Technetium Tc 99m Sestamibi. Tomography, Emission-Computed, Single-Photon

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16953066.001).
  • [ISSN] 1343-1420
  • [Journal-full-title] The journal of medical investigation : JMI
  • [ISO-abbreviation] J. Med. Invest.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / P-Glycoprotein; 0 / RNA, Messenger; 971Z4W1S09 / Technetium Tc 99m Sestamibi
  •  go-up   go-down


49. Molitch ME: The cabergoline-resistant prolactinoma patient: new challenges. J Clin Endocrinol Metab; 2008 Dec;93(12):4643-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The cabergoline-resistant prolactinoma patient: new challenges.
  • [MeSH-major] Dopamine Agonists / therapeutic use. Ergolines / therapeutic use. Pituitary Neoplasms / drug therapy. Prolactinoma / drug therapy
  • [MeSH-minor] Adult. Drug Resistance. Echocardiography. Female. Heart Valve Diseases / chemically induced. Heart Valve Diseases / ultrasonography. Humans. Male. Prolactin / blood. Receptors, Dopamine / drug effects. Young Adult

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentOn] J Clin Endocrinol Metab. 2008 Dec;93(12):4721-7 [18812485.001]
  • (PMID = 19056842.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Comment; Editorial
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dopamine Agonists; 0 / Ergolines; 0 / Receptors, Dopamine; 9002-62-4 / Prolactin; LL60K9J05T / cabergoline
  •  go-up   go-down


50. Biller BM, Colao A, Petersenn S, Bonert VS, Boscaro M: Prolactinomas, Cushing's disease and acromegaly: debating the role of medical therapy for secretory pituitary adenomas. BMC Endocr Disord; 2010;10:10
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prolactinomas, Cushing's disease and acromegaly: debating the role of medical therapy for secretory pituitary adenomas.
  • Pituitary adenomas are associated with a variety of clinical manifestations resulting from excessive hormone secretion and tumor mass effects, and require a multidisciplinary management approach.
  • This article discusses the treatment modalities for the management of patients with a prolactinoma, Cushing's disease and acromegaly, and summarizes the options for medical therapy in these patients.First-line treatment of prolactinomas is pharmacotherapy with dopamine agonists; recent reports of cardiac valve abnormalities associated with this class of medication in Parkinson's disease has prompted study in hyperprolactinemic populations.
  • Patients with resistance to dopamine agonists may require other treatment.First-line treatment of Cushing's disease is pituitary surgery by a surgeon with experience in this condition.
  • Current medical options for Cushing's disease block adrenal cortisol production, but do not treat the underlying disease.
  • Pituitary-directed medical therapies are now being explored.
  • The multi-receptor targeted somatostatin analogue pasireotide (SOM230) shows promise as a pituitary-directed medical therapy in Cushing's disease; further studies will determine its efficacy and safety.
  • Radiation therapy, with medical adrenal blockade while awaiting the effects of radiation, and bilateral adrenalectomy remain standard treatment options for patients not cured with pituitary surgery.In patients with acromegaly, surgery remains the first-line treatment option when the tumor is likely to be completely resected, or for debulking, especially when the tumor is compressing neurovisual structures.
  • Pegvisomant is indicated in patients who have not responded to surgery and other medical therapy, although there are regional differences in when it is prescribed.In conclusion, the treatment of patients with pituitary adenomas requires a multidisciplinary approach.
  • Dopamine agonists are an effective first-line medical therapy in most patients with a prolactinoma, and somatostatin analogues can be used as first-line therapy in selected patients with acromegaly.
  • Current medical therapies for Cushing's disease primarily focus on adrenal blockade of cortisol production, although pasireotide and cabergoline show promise as pituitary-directed medical therapy for Cushing's disease; further long-term evaluation of efficacy and safety is important.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Endocrinol Metab. 2005 Jul;90(7):4081-6 [15886256.001]
  • [Cites] Eur J Endocrinol. 2005 Jul;153(1):135-41 [15994755.001]
  • [Cites] Clin Endocrinol (Oxf). 2005 Aug;63(2):168-75 [16060910.001]
  • [Cites] Clin Endocrinol (Oxf). 2005 Aug;63(2):176-84 [16060911.001]
  • [Cites] Eur J Endocrinol. 2005 Sep;153(3):R7-R10 [16131595.001]
  • [Cites] Horm Res. 2005;64(3):140-3 [16192738.001]
  • [Cites] Clin Endocrinol (Oxf). 2005 Nov;63(5):549-59 [16268808.001]
  • [Cites] Eur J Endocrinol. 2005 Dec;153(6):737-40 [16322377.001]
  • [Cites] Horm Metab Res. 2005 Dec;37(12):722-8 [16372224.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Apr;91(4):1239-45 [16403824.001]
  • [Cites] Endocr J. 2005 Dec;52(6):775-9 [16410672.001]
  • [Cites] Clin Endocrinol (Oxf). 2006 Feb;64(2):219-24 [16430724.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Apr;91(4):1397-403 [16449332.001]
  • [Cites] Clin Endocrinol (Oxf). 2006 Mar;64(3):342-51 [16487447.001]
  • [Cites] J Endocrinol Invest. 2005;28(11 Suppl International):21-7 [16625841.001]
  • [Cites] Endocr Rev. 2006 Aug;27(5):485-534 [16705142.001]
  • [Cites] Endocrinology. 2006 Sep;147(9):4438-44 [16740975.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Oct;91(10):3746-53 [16868050.001]
  • [Cites] Clin Endocrinol (Oxf). 2006 Sep;65(3):389-95 [16918962.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Nov;91(11):4482-8 [16940446.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Dec;91(12):4769-75 [16968795.001]
  • [Cites] Nat Clin Pract Endocrinol Metab. 2006 Oct;2(10):552-61 [17024154.001]
  • [Cites] J Clin Endocrinol Metab. 2007 Jan;92(1):172-9 [17062771.001]
  • [Cites] N Engl J Med. 2006 Dec 14;355(24):2558-73 [17167139.001]
  • [Cites] N Engl J Med. 2007 Jan 4;356(1):29-38 [17202453.001]
  • [Cites] N Engl J Med. 2007 Jan 4;356(1):39-46 [17202454.001]
  • [Cites] Eur J Endocrinol. 2007 Jan;156(1):91-8 [17218730.001]
  • [Cites] Clin Endocrinol (Oxf). 2007 Jun;66(6):859-68 [17465997.001]
  • [Cites] N Engl J Med. 2007 Jun 14;356(24):2457-71 [17517853.001]
  • [Cites] Endocrinology. 2007 Dec;148(12):6107-14 [17656461.001]
  • [Cites] J Clin Endocrinol Metab. 2007 Aug;92(8):2861-5 [17682084.001]
  • [Cites] J Clin Endocrinol Metab. 2007 Dec;92(12):4598-601 [17895318.001]
  • [Cites] Mol Cell Endocrinol. 2008 May 14;286(1-2):69-74 [17977644.001]
  • [Cites] Eur J Endocrinol. 2007 Nov;157(5):579-87 [17984237.001]
  • [Cites] Neurosurg Focus. 2007;23(6):E14 [18081479.001]
  • [Cites] Eur J Endocrinol. 2008 Jan;158(1):91-9 [18166822.001]
  • [Cites] Endocr Pract. 2007 Nov-Dec;13(7):726-34 [18194929.001]
  • [Cites] Eur J Endocrinol. 2008 Jul;159(1):1-5 [18456868.001]
  • [Cites] Int J Clin Pract. 2008 Dec;62(12):1864-9 [18462372.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Sep;93(9):3348-56 [18559921.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Sep;93(9):3436-42 [18593770.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Sep;93(9):3515-8 [18611977.001]
  • [Cites] Eur J Endocrinol. 2008 Oct;159(4):R11-4 [18625690.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Oct;93(10):3853-9 [18647806.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Oct;93(10):3777-84 [18682513.001]
  • [Cites] Neurosurgery. 2008 Jun;62(6):1262-9; discussion 1269-70 [18824992.001]
  • [Cites] J Clin Endocrinol Metab. 2009 Jan;94(1):223-30 [18957500.001]
  • [Cites] J Clin Endocrinol Metab. 2009 Jan;94(1):115-22 [18957506.001]
  • [Cites] Endocr Pract. 2008 Sep;14(6):672-7 [18996784.001]
  • [Cites] Clin Endocrinol (Oxf). 2009 Jan;70(1):104-8 [19128367.001]
  • [Cites] J Clin Endocrinol Metab. 2009 Apr;94(4):1118-24 [19141584.001]
  • [Cites] Clin Endocrinol (Oxf). 2009 May;70(5):757-68 [19178516.001]
  • [Cites] J Endocrinol Invest. 2008 Dec;31(12):1119-23 [19246980.001]
  • [Cites] Eur J Endocrinol. 2009 Jun;160(6):1003-10 [19289534.001]
  • [Cites] Clin Endocrinol (Oxf). 2010 Jan;72(1):53-8 [19508591.001]
  • [Cites] Nat Med. 2002 Nov;8(11):1281-7 [12379847.001]
  • [Cites] Endocr Rev. 2003 Feb;24(1):28-47 [12588807.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Jul;93(7):2454-62 [18413427.001]
  • [Cites] Eur J Endocrinol. 2008 May;158(5):595-603 [18426817.001]
  • [Cites] N Engl J Med. 1979 Mar 1;300(9):459-64 [215912.001]
  • [Cites] Clin Endocrinol (Oxf). 1991 Aug;35(2):169-78 [1657460.001]
  • [Cites] J Endocrinol Invest. 1990 Mar;13(3):257-61 [1973178.001]
  • [Cites] Clin Endocrinol (Oxf). 1990 Mar;32(3):275-81 [2160871.001]
  • [Cites] J Clin Endocrinol Metab. 1985 Apr;60(4):698-705 [3882737.001]
  • [Cites] JAMA. 1982 Mar 5;247(9):1320 [6121067.001]
  • [Cites] Ann Intern Med. 1980 May;92(5):613-9 [6247946.001]
  • [Cites] Clin Endocrinol (Oxf). 1981 Nov;15(5):479-84 [6276051.001]
  • [Cites] Endocr Rev. 1993 Aug;14(4):443-58 [7693447.001]
  • [Cites] Clin Endocrinol (Oxf). 1994 Jul;41(1):95-102 [8050136.001]
  • [Cites] Am J Med. 1993 Sep;95(3):305-8 [8396322.001]
  • [Cites] J Clin Endocrinol Metab. 1996 Jul;81(7):2647-52 [8675592.001]
  • [Cites] Drug Saf. 1996 Apr;14(4):228-38 [8713691.001]
  • [Cites] J Endocrinol. 1997 Oct;155 Suppl 1:S23-9; discussion S31-2 [9389992.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Feb;83(2):374-8 [9467544.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Aug;83(8):2730-4 [9709939.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Sep;83(9):3034-40 [9745397.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Oct;83(10):3542-4 [9768661.001]
  • [Cites] Lancet. 1998 Oct 31;352(9138):1455-61 [9808008.001]
  • [Cites] Ann Med. 1998 Oct;30(5):452-9 [9814831.001]
  • [Cites] Eur J Endocrinol. 1998 Nov;139(5):516-21 [9849816.001]
  • [Cites] J Endocrinol Invest. 1999 Apr;22(4):306-9 [10342366.001]
  • [Cites] Front Neuroendocrinol. 1999 Jul;20(3):157-98 [10433861.001]
  • [Cites] Mol Cell Endocrinol. 1999 Nov 25;157(1-2):75-85 [10619399.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Jan;85(1):8-13 [10634356.001]
  • [Cites] N Engl J Med. 2000 Apr 20;342(16):1171-7 [10770982.001]
  • [Cites] Acta Med Austriaca. 2000;27(1):27-31 [10812460.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Jun;85(6):2247-52 [10852458.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Jun;86(6):2779-86 [11397887.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Jul;86(7):2929-34 [11443145.001]
  • [Cites] Endocrine. 2001 Apr;14(3):329-36 [11444429.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Aug;86(8):3568-73 [11502780.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Sep;86(9):4104-8 [11549633.001]
  • [Cites] Endocr Relat Cancer. 2001 Dec;8(4):287-305 [11733226.001]
  • [Cites] Lancet. 2001 Nov 24;358(9295):1754-9 [11734231.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Jan;87(1):99-104 [11788630.001]
  • [Cites] Clin Endocrinol (Oxf). 2002 Jan;56(1):65-71 [11849248.001]
  • [Cites] Eur J Endocrinol. 2002 May;146(5):707-16 [11980628.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Jul;87(7):3013-8 [12107192.001]
  • [Cites] Eur J Endocrinol. 2003 Mar;148(3):325-31 [12611613.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Jul;88(7):3105-12 [12843150.001]
  • [Cites] Ann Intern Med. 1960 Mar;52:560-9 [14426442.001]
  • [Cites] N Engl J Med. 2003 Nov 20;349(21):2023-33 [14627787.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Dec;88(12):5593-602 [14671138.001]
  • [Cites] Pituitary. 2003;6(1):19-27 [14674720.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Feb;89(2):638-45 [14764775.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Feb;89(2):667-74 [14764779.001]
  • [Cites] Clin Endocrinol (Oxf). 2004 Mar;60(3):375-81 [15009004.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Apr;89(4):1577-85 [15070915.001]
  • [Cites] J Clin Endocrinol Metab. 2004 May;89(5):2452-62 [15126577.001]
  • [Cites] Clin Endocrinol (Oxf). 2004 Aug;61(2):209-15 [15272916.001]
  • [Cites] Cancer. 2004 Aug 1;101(3):613-9 [15274075.001]
  • [Cites] J Clin Invest. 2004 Aug;114(3):349-56 [15286801.001]
  • [Cites] Eur J Endocrinol. 2004 Aug;151(2):173-8 [15296471.001]
  • [Cites] Endocr Pract. 2004 May-Jun;10(3):213-25 [15382339.001]
  • [Cites] Neuroendocrinology. 2004;80 Suppl 1:47-50 [15477717.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Mar;90(3):1588-93 [15585549.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Mar;90(3):1340-6 [15585550.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Mar;90(3):1856-63 [15613435.001]
  • [Cites] Eur J Endocrinol. 2005 Mar;152(3):379-87 [15757854.001]
  • [Cites] Am J Physiol Endocrinol Metab. 2005 Aug;289(2):E278-87 [15769796.001]
  • [Cites] Eur J Endocrinol. 2005 Apr;152(4):645-54 [15817922.001]
  • [Cites] Lancet. 2005 May 7-13;365(9471):1644-6 [15885297.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Aug;90(8):4465-73 [15886238.001]
  • (PMID = 20478050.001).
  • [ISSN] 1472-6823
  • [Journal-full-title] BMC endocrine disorders
  • [ISO-abbreviation] BMC Endocr Disord
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2887860
  •  go-up   go-down


51. de la Torre NG, Turner HE, Wass JA: Angiogenesis in prolactinomas: regulation and relationship with tumour behaviour. Pituitary; 2005;8(1):17-23
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Angiogenesis in prolactinomas: regulation and relationship with tumour behaviour.
  • In the pituitary, unlike other tissues, vascularization is lower in adenomas compared to the normal gland.
  • Despite this finding, a relationship between increased vascularity and several aspects of prolactinoma behaviour such as size, invasiveness, surgical outcome and malignancy, has been demonstrated.
  • The process of angiogenesis is the result of a balance of stimulating and inhibiting factors.
  • It is likely that an interaction between gene expression (such as pituitary tumour transforming gene (PTTG) and a novel gene located within the Edpm5 quantitative trait locus), hormonal stimuli including oestrogens, dopamine, 16 kDa fragments of prolactin and proangiogenic and antiangiogenic growth factors (for example, vascular endothelial growth factor (VEGF) and fibroblast growth factor (FGF-2), determine the final angiogenic phenotype of prolactinomas, and thus subsequent tumour behaviour.
  • The elucidation of all the factors involved in the regulation of angiogenesis and their interactions might open new possibilities in the treatment of prolactinomas, especially in those cases with resistance or intolerance to dopamine agonists.
  • [MeSH-major] Neovascularization, Pathologic. Pituitary Neoplasms / blood supply. Pituitary Neoplasms / physiopathology. Prolactinoma / blood supply. Prolactinoma / physiopathology
  • [MeSH-minor] Dopamine / genetics. Dopamine / physiology. Dopamine Agonists / therapeutic use. Drug Resistance, Neoplasm. Estrogens / genetics. Estrogens / physiology. Fibroblast Growth Factor 2 / genetics. Fibroblast Growth Factor 2 / physiology. Gene Expression Regulation, Neoplastic. Genes, Neoplasm. Humans. Neoplasm Invasiveness. Neoplasm Proteins / genetics. Neoplasm Proteins / physiology. Prolactin / genetics. Prolactin / physiology. Securin. Vascular Endothelial Growth Factor A / genetics. Vascular Endothelial Growth Factor A / physiology

  • 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
  • [Cites] Science. 1982 Oct 15;218(4569):293-5 [6181563.001]
  • [Cites] Anticancer Res. 2000 Jul-Aug;20(4):2641-5 [10953337.001]
  • [Cites] Histopathology. 1996 Jul;29(1):37-43 [8818692.001]
  • [Cites] Carcinogenesis. 2004 Oct;25(10):1829-38 [15166088.001]
  • [Cites] Am J Pathol. 1993 Aug;143(2):401-9 [7688183.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Jun;89(6):2890-6 [15181073.001]
  • [Cites] Nat Med. 2001 May;7(5):569-74 [11329058.001]
  • [Cites] Nature. 1989 May 4;339(6219):58-61 [2469964.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Jul;82(7):2102-7 [9215279.001]
  • [Cites] Biochem Biophys Res Commun. 1989 Jun 15;161(2):851-8 [2735925.001]
  • [Cites] Br J Cancer. 2000 Apr;82(8):1441-5 [10780524.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Aug;85(8):2931-5 [10946906.001]
  • [Cites] Radiology. 1974 Mar;110(3):589-95 [4811679.001]
  • [Cites] J Natl Cancer Inst. 1995 Nov 1;87(21):1603-12 [7563203.001]
  • [Cites] Proc Natl Acad Sci U S A. 1984 Jul;81(14):4549-53 [6589610.001]
  • [Cites] Cell. 1996 Aug 9;86(3):353-64 [8756718.001]
  • [Cites] Br J Cancer. 1997;76(11):1410-5 [9400935.001]
  • [Cites] Metabolism. 1995 Oct;44(10 Suppl 4):72-5 [7476315.001]
  • [Cites] Neurosurgery. 1988 Jan;22(1 Pt 1):1-6 [2449627.001]
  • [Cites] Cell. 1998 May 1;93(3):411-22 [9590175.001]
  • [Cites] J Clin Endocrinol Metab. 1988 Oct;67(4):713-9 [3417848.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Mar;85(3):1159-62 [10720055.001]
  • [Cites] Cell Tissue Res. 2000 Apr;300(1):83-8 [10805077.001]
  • [Cites] Endocrinology. 1988 Jun;122(6):2892-8 [3371265.001]
  • [Cites] Neuroendocrinology. 2001 Aug;74(2):95-105 [11474217.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Nov;87(11):4961-5 [12414859.001]
  • [Cites] Lancet. 2000 Feb 26;355(9205):716-9 [10703804.001]
  • [Cites] Am J Pathol. 1994 Apr;144(4):820-8 [7512793.001]
  • [Cites] Acta Neuropathol. 1998 Nov;96(5):453-62 [9829808.001]
  • [Cites] Am J Pathol. 1972 Apr;67(1):109-26 [5055626.001]
  • [Cites] Endocrinology. 1993 Sep;133(3):1292-9 [7689950.001]
  • [Cites] Endocr Pathol. 1999 Autumn;10(3):229-235 [12114703.001]
  • [Cites] J Natl Cancer Inst. 1990 Jan 3;82(1):4-6 [1688381.001]
  • [Cites] Endocr Pathol. 2003 Fall;14(3):239-47 [14586069.001]
  • [Cites] Am J Anat. 1987 Aug;179(4):315-23 [3661455.001]
  • [Cites] J Cell Sci. 1995 Feb;108 ( Pt 2):797-809 [7539439.001]
  • [Cites] J Clin Oncol. 1995 Feb;13(2):477-81 [7531224.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Feb;84(2):761-7 [10022450.001]
  • [Cites] Virchows Arch. 2001 Jun;438(6):595-602 [11469692.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Feb;86(2):867-74 [11158059.001]
  • [Cites] Clin Endocrinol (Oxf). 2000 Sep;53(3):337-44 [10971451.001]
  • [Cites] Carcinogenesis. 1997 Jun;18(6):1155-61 [9214597.001]
  • [Cites] J Endocrinol. 1996 Jul;150(1):99-106 [8708569.001]
  • [Cites] J Biol Chem. 1992 Jun 5;267(16):10931-4 [1375931.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Sep;87(9):4238-44 [12213878.001]
  • [Cites] J Natl Cancer Inst. 1992 Dec 16;84(24):1875-87 [1281237.001]
  • [Cites] Mol Endocrinol. 1999 May;13(5):692-704 [10319320.001]
  • [Cites] Cytogenet Cell Genet. 1996;72(2-3):159-61 [8978762.001]
  • [Cites] Cytobios. 2000;101(398):151-9 [10755214.001]
  • [Cites] Cancer. 1978 Jan;41(1):239-44 [626933.001]
  • [Cites] J Endocrinol. 2000 May;165(2):475-81 [10810311.001]
  • [Cites] Nat Med. 1995 Oct;1(10):1024-8 [7489357.001]
  • [Cites] Proc Natl Acad Sci U S A. 1987 Aug;84(16):5773-7 [2441393.001]
  • [Cites] J Endocrinol Invest. 2003 Jan;26(1):23-8 [12602530.001]
  • [Cites] Mol Cell Endocrinol. 1997 Nov 15;134(2):91-100 [9426152.001]
  • [Cites] J Anat. 1960 Apr;94:257-73 [13833758.001]
  • [Cites] Endocr Pathol. 1995 Summer;6(2):115-124 [12114647.001]
  • [Cites] Cancer Res. 1994 Feb 1;54(3):800-4 [7508337.001]
  • [Cites] Nat Med. 1999 Nov;5(11):1317-21 [10546001.001]
  • [Cites] Science. 1977 Mar 4;195(4281):880-2 [402692.001]
  • [Cites] Ann Rheum Dis. 1992 Jul;51(7):919-25 [1378718.001]
  • [Cites] J Clin Invest. 2002 Jan;109(2):277-83 [11805140.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1999 Oct;40(11):2498-505 [10509642.001]
  • [Cites] Proc Natl Acad Sci U S A. 1987 Apr;84(8):2292-6 [3470794.001]
  • [Cites] Curr Opin Nephrol Hypertens. 1996 Jan;5(1):35-44 [8834160.001]
  • [Cites] J Clin Oncol. 1995 Mar;13(3):765-82 [7533829.001]
  • [Cites] AJNR Am J Neuroradiol. 1994 Jan;15(1):101-8 [8141039.001]
  • (PMID = 16411064.001).
  • [ISSN] 1386-341X
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dopamine Agonists; 0 / Estrogens; 0 / Neoplasm Proteins; 0 / Securin; 0 / Vascular Endothelial Growth Factor A; 0 / pituitary tumor-transforming protein 1, human; 103107-01-3 / Fibroblast Growth Factor 2; 9002-62-4 / Prolactin; VTD58H1Z2X / Dopamine
  • [Number-of-references] 69
  •  go-up   go-down


52. Tateno T, Kato M, Tani Y, Oyama K, Yamada S, Hirata Y: Differential expression of somatostatin and dopamine receptor subtype genes in adrenocorticotropin (ACTH)-secreting pituitary tumors and silent corticotroph adenomas. Endocr J; 2009;56(4):579-84
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differential expression of somatostatin and dopamine receptor subtype genes in adrenocorticotropin (ACTH)-secreting pituitary tumors and silent corticotroph adenomas.
  • Somatostatin analogs and dopamine agonists are clinically used for medical therapy of functioning pituitary tumors, such as growth hormone- and prolactin-secreting tumors, however, their effects on ACTH-secreting tumors are controversial.
  • This study was aimed to determine whether somatostatin receptor (SSTR) subtype (1-5) and dopamine receptor type 2 (D2R) are differentially expressed in pituitary tumors causing Cushing's disease (CD), silent corticotroph adenoma (SCA), and non-functioning pituitary tumor (NFT).
  • Tissue specimens were obtained from 35 pituitary tumors during transsphenoidal surgery.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / genetics. Adenoma / genetics. Pituitary ACTH Hypersecretion / metabolism. Pituitary Neoplasms / genetics. Receptors, Dopamine D2 / genetics. Receptors, Somatostatin / physiology

  • 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 = 19318729.001).
  • [ISSN] 1348-4540
  • [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 / Receptors, Dopamine D2; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 0 / somatostatin receptor 5; 0 / somatostatin receptor type 1; 9002-60-2 / Adrenocorticotropic Hormone
  •  go-up   go-down


53. Prabhakar VK, Davis JR: Hyperprolactinaemia. Best Pract Res Clin Obstet Gynaecol; 2008 Apr;22(2):341-53
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A variety of pathophysiological conditions can lead to hyperprolactinaemia; therefore, pregnancy, drug effects, hypothyroidism and polycystic ovary syndrome should be excluded before investigating for prolactin-secreting pituitary tumours.
  • Prolactinomas are mainly diagnosed in women aged 20-40 years.
  • Pituitary surgery and radiotherapy currently have very limited indications.
  • Pregnancies in patients with prolactinomas need careful planning and close monitoring.
  • [MeSH-minor] Adult. Antineoplastic Agents / therapeutic use. Dopamine Agonists / therapeutic use. Drug Resistance. Female. Humans. Pituitary Neoplasms / complications. Pituitary Neoplasms / drug therapy. Pregnancy. Pregnancy Complications / drug therapy. Prolactinoma / complications. Prolactinoma / drug therapy

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17889620.001).
  • [ISSN] 1521-6934
  • [Journal-full-title] Best practice & research. Clinical obstetrics & gynaecology
  • [ISO-abbreviation] Best Pract Res Clin Obstet Gynaecol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Dopamine Agonists
  • [Number-of-references] 85
  •  go-up   go-down


54. Samson WK: Putting the brakes on lactotrope hyperplasia. Trends Endocrinol Metab; 2006 Jan-Feb;17(1):2-3
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Putting the brakes on lactotrope hyperplasia.
  • Although much is known about the mechanisms by which dopamine, the major regulator of lactotrope function, controls hormone production and secretion, its growth inhibiting actions have remained less well characterized.
  • Recent research has uncovered an important role for endogenously produced transforming growth factor beta (TGFbeta) and TGFbeta receptors in dopamine's ability to put the brakes on lactotrope proliferation.
  • These novel findings promise increased knowledge of the genesis and potential therapeutic control of human prolactinomas.
  • [MeSH-major] Dopamine / metabolism. Pituitary Gland, Anterior / pathology. Pituitary Neoplasms / pathology. Prolactin / metabolism. Proteins / metabolism

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. DOPAMINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16307891.001).
  • [ISSN] 1043-2760
  • [Journal-full-title] Trends in endocrinology and metabolism: TEM
  • [ISO-abbreviation] Trends Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proteins; 0 / Receptors, Transforming Growth Factor beta; 9002-62-4 / Prolactin; VTD58H1Z2X / Dopamine
  •  go-up   go-down


55. Vallette S, Serri K, Serri O: Cabergoline therapy for prolactinomas: is valvular heart disease a real safety concern? Expert Rev Cardiovasc Ther; 2010 Jan;8(1):49-54
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cabergoline therapy for prolactinomas: is valvular heart disease a real safety concern?
  • Recent studies reported cardiac valve regurgitations in patients with Parkinson's disease treated with high doses of DA, raising concerns about the safety of cabergoline in patients with hyperprolactinemia.
  • Patients in all the studies were asymptomatic without clinical signs of cardiac disease.
  • [MeSH-minor] Adult. Case-Control Studies. Clinical Trials as Topic. Female. Humans. Male. Middle Aged. Pituitary Neoplasms / drug therapy. Prolactinoma / drug therapy. Receptors, Dopamine D2 / agonists

  • Genetic Alliance. consumer health - Heart Disease.
  • MedlinePlus Health Information. consumer health - Heart Valve Diseases.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20014934.001).
  • [ISSN] 1744-8344
  • [Journal-full-title] Expert review of cardiovascular therapy
  • [ISO-abbreviation] Expert Rev Cardiovasc Ther
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Dopamine Agonists; 0 / Ergolines; 0 / Receptors, Dopamine D2; LL60K9J05T / cabergoline
  •  go-up   go-down


56. Verma S, Shah D, Faridi MM: Breastfeeding a baby with mother on Bromocripine. Indian J Pediatr; 2006 May;73(5):435-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Prolactinomas, the most common pituitary adenomas, are important causes of infertility.
  • [MeSH-minor] Adult. Counseling. Female. Humans. Infant, Newborn. Pituitary Neoplasms / complications. Prolactinoma / complications

  • MedlinePlus Health Information. consumer health - Breastfeeding.
  • MedlinePlus Health Information. consumer health - Infant and Newborn Nutrition.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Pituitary. 2002;5(2):55-65 [12675502.001]
  • [Cites] Nihon Sanka Fujinka Gakkai Zasshi. 1985 May;37(5):758-62 [3998551.001]
  • [Cites] J Neurooncol. 2001 Sep;54(2):139-50 [11761431.001]
  • [Cites] Drug Saf. 1996 Apr;14(4):228-38 [8713691.001]
  • [Cites] J Fam Pract. 1994 Jul;39(1):56-64 [8027734.001]
  • [Cites] Zentralbl Gynakol. 1996;118(11):610-5 [9082694.001]
  • [Cites] Zhonghua Fu Chan Ke Za Zhi. 1996 Sep;31(9):537-9 [9275425.001]
  • [Cites] J Endocrinol Invest. 2003 Jan;26(1):96-9 [12602544.001]
  • [Cites] Midwifery. 1993 Dec;9(4):197-209 [8283952.001]
  • [Cites] Obstet Gynecol. 1981 Jun;57(6):725-9 [7231824.001]
  • [Cites] Acta Endocrinol (Copenh). 1979 Nov;92(3):407-12 [517046.001]
  • (PMID = 16741332.001).
  • [ISSN] 0973-7693
  • [Journal-full-title] Indian journal of pediatrics
  • [ISO-abbreviation] Indian J Pediatr
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Hormone Antagonists; 3A64E3G5ZO / Bromocriptine
  •  go-up   go-down


57. Pisarek H, Pawlikowski M, Kunert-Radek J, Radek M: Expression of somatostatin receptor subtypes in human pituitary adenomas -- immunohistochemical studies. Endokrynol Pol; 2009 Jul-Aug;60(4):240-51
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of somatostatin receptor subtypes in human pituitary adenomas -- immunohistochemical studies.
  • BACKGROUND: The highly variable expression of SSTR subtypes in pituitary adenomas (PA) may partially explain why the subgroup of somatotropinomas or other adenomas do not respond to the therapeutic action of currently used long-acting somatostatin analogues like octreotide or lanreotide.
  • RESULTS: The pattern of SSTR immunostaining (estimated according to the percentage frequency of appearance) was in acromegaly: SSTR 5 > SSTR 1 > SSTR 2A = SSTR 3 > SSTR 2B, in prolactinomas: SSTR 2B = SSTR 3 = SSTR 5 > SSTR 1 = SSTR 2A, in gonadotropinomas: SSTR 3 > SSTR 2B > SSTR 1 = SSTR 2A > SSTR 5, in corticotropinomas: SSTR 2A > SSTR 1 = SSTR 3 > SSTR 5 > SSTR 2B.
  • In PA immunonegative for pituitary hormones, we noticed only a weak staining of all receptor subtypes including SSTR 4.
  • In plurihormonal adenomas with positive GH phenotype the staining pattern was: SSTR 5 > SSTR 1 = SSTR 2B and in plurihormonal PA with negative GH phenotype: SSTR 1 = SSTR 5 > SSTR 2A = SSTR 2B = SSTR 3.
  • In plurihormonal adenoma with ACTH immunopositivity, the staining pattern was: SSTR = SSTR 2A = SSTR 3 = SSTR 5.
  • SSTR 1 and SSTR 5 were the most frequent subtypes of somatostatin receptor in plurihormonal adenomas without ACTH expression.
  • [MeSH-major] Adenoma / metabolism. Pituitary Neoplasms / metabolism. Receptors, Somatostatin / metabolism

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19753537.001).
  • [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 / Peptides, Cyclic; 0 / Protein Isoforms; 0 / Receptors, Somatostatin; 0G3DE8943Y / lanreotide; 51110-01-1 / Somatostatin; RWM8CCW8GP / Octreotide
  •  go-up   go-down


58. Vilar L, Czepielewsk MA, Naves LA, Rollin GA, Casulari LA, Coelho CE: Substantial shrinkage of adenomas cosecreting growth hormone and prolactin with use of cabergoline therapy. Endocr Pract; 2007 Jul-Aug;13(4):396-402
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Substantial shrinkage of adenomas cosecreting growth hormone and prolactin with use of cabergoline therapy.
  • RESULTS: A 48-year-old man (case 1) and a 26-year-old woman (case 2) were found to have acromegaly associated with very high levels of serum prolactin (2,700 and 5,250 ng/mL, respectively).
  • These patients received first line therapy with cabergoline that resulted not only in clinical improvement and normalization of growth hormone, prolactin, and insulin-like growth factor-I levels but also in a substantial reduction in the size of their somatotroph macroadenomas.
  • CONCLUSION: Our findings demonstrate that cabergoline should be considered for medical treatment of adenomas cosecreting growth hormone and prolactin, even in the presence of large tumors with appreciable suprasellar extension, because substantial tumor shrinkage is possible with this therapy.
  • [MeSH-major] Adenoma / drug therapy. Antineoplastic Agents / administration & dosage. Ergolines / administration & dosage. Growth Hormone-Secreting Pituitary Adenoma / drug therapy. Pituitary Neoplasms / drug therapy. Prolactinoma / drug therapy

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17669717.001).
  • [ISSN] 1934-2403
  • [Journal-full-title] Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists
  • [ISO-abbreviation] Endocr Pract
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Ergolines; LL60K9J05T / cabergoline
  •  go-up   go-down


59. Fedele M, De Martino I, Pivonello R, Ciarmiello A, Del Basso De Caro ML, Visone R, Palmieri D, Pierantoni GM, Arra C, Schmid HA, Hofland L, Lombardi G, Colao A, Fusco A: SOM230, a new somatostatin analogue, is highly effective in the therapy of growth hormone/prolactin-secreting pituitary adenomas. Clin Cancer Res; 2007 May 1;13(9):2738-44
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] SOM230, a new somatostatin analogue, is highly effective in the therapy of growth hormone/prolactin-secreting pituitary adenomas.
  • PURPOSE: We have previously shown that transgenic mice ubiquitously overexpressing the HMGA2 gene develop growth hormone/prolactin-secreting pituitary adenomas.
  • This animal model has been used to evaluate the therapeutic efficacy of SOM230, a somatostatin analogue with high affinity for the somatostatin receptor subtypes 1, 2, 3, and 5, on the growth of the pituitary adenomas.
  • The development of the tumor before and after therapy was monitored by magnetic resonance imaging of the pituitary region and evaluation of the serum prolactin levels.
  • CONCLUSIONS: These results clearly support the efficacy of the SOM230 treatment in human pituitary adenomas secreting prolactin based on the dramatic tumor shrinkage and fall in prolactin levels.
  • [MeSH-major] Growth Hormone-Secreting Pituitary Adenoma / drug therapy. Pituitary Neoplasms / drug therapy. Somatostatin / analogs & derivatives
  • [MeSH-minor] Animals. Cell Proliferation / drug effects. Female. HMGA2 Protein / genetics. Mice. Mice, Transgenic. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17473207.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HMGA2 Protein; 51110-01-1 / Somatostatin; 98H1T17066 / pasireotide
  •  go-up   go-down


60. Sharma A, Sharma MS, De Padua M, Jha UP, Jha AN: Synchronous endometrial carcinoma and a macroprolactinoma: exploring a causal relationship. Oncology; 2007;72(1-2):139-42
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: While unopposed estrogen hormone secretion is most commonly implicated in the pathogenesis of endometrial carcinoma, the role of prolactin has only recently been highlighted.
  • The authors present a case of a synchronous endometrial carcinoma in a patient with a prolactin-secreting macroadenoma.
  • Hormonal evaluation revealed elevated prolactin and subnormal luteinizing hormone and follicle-stimulating hormone (FSH) serum concentrations.
  • The MRI of the brain confirmed a pituitary macroadenoma.
  • The patient underwent a resectoscopic polypectomy and dilation and curettage followed by transnasal transsphenoidal excision of the pituitary macroadenoma.
  • RESULTS: The biopsy of the endometrium revealed a well-differentiated endometrioid carcinoma while that of the pituitary tumor confirmed a prolactinoma.
  • Patients with prolactinomas and irregular menstrual bleeding should undergo endometrial sampling to rule out this possibility.
  • [MeSH-major] Carcinoma / etiology. Endometrial Neoplasms / etiology. Neoplasms, Multiple Primary. Pituitary Neoplasms / complications. Prolactinoma / complications
  • [MeSH-minor] Adult. Drosophila Proteins / blood. Egg Proteins / blood. Female. Gonadotropin-Releasing Hormone / blood. Humans. Prolactin / secretion

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2007 S. Karger AG, Basel.
  • (PMID = 18025806.001).
  • [ISSN] 1423-0232
  • [Journal-full-title] Oncology
  • [ISO-abbreviation] Oncology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Drosophila Proteins; 0 / Egg Proteins; 0 / dec-1 protein, Drosophila; 33515-09-2 / Gonadotropin-Releasing Hormone; 9002-62-4 / Prolactin
  •  go-up   go-down


61. Jamjoom BA, Sharab MA, Nasser TA, Jamjoom AB: Pseudotumor cerebri and prolactin secreting pituitary adenoma. Association or coincidence? Neurosciences (Riyadh); 2010 Jul;15(3):200-3
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pseudotumor cerebri and prolactin secreting pituitary adenoma. Association or coincidence?
  • The occurrence of pseudotumor cerebri (PTC) and hyperprolactinemia related to a prolactinoma are extremely rare, and the link between these pathologies has not been examined adequately in the post-MRI era.
  • We report a patient with a small intrasellar prolactinoma who also developed PTC.
  • However 9 months later, her PTC symptoms recurred despite a normal serum prolactin level and a mild reduction of the pituitary tumor size on MRI.
  • We conclude that the findings in our patient do not support an association between PTC and hyperprolactinemia or prolactinoma.
  • However, the case supports the need for clinicians to consider the diagnosis of PTC when patients with small pituitary lesions exhibit raised intracranial pressure features.
  • [MeSH-major] Pituitary Neoplasms / complications. Prolactinoma / complications. Pseudotumor Cerebri / complications

  • Genetic Alliance. consumer health - Pseudotumor cerebri.
  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20831031.001).
  • [ISSN] 1319-6138
  • [Journal-full-title] Neurosciences (Riyadh, Saudi Arabia)
  • [ISO-abbreviation] Neurosciences (Riyadh)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Saudi Arabia
  •  go-up   go-down


62. Jennings JE, Georgitsi M, Holdaway I, Daly AF, Tichomirowa M, Beckers A, Aaltonen LA, Karhu A, Cameron FJ: Aggressive pituitary adenomas occurring in young patients in a large Polynesian kindred with a germline R271W mutation in the AIP gene. Eur J Endocrinol; 2009 Nov;161(5):799-804
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aggressive pituitary adenomas occurring in young patients in a large Polynesian kindred with a germline R271W mutation in the AIP gene.
  • OBJECTIVE: Mutations in the aryl hydrocarbon receptor-interacting protein (AIP) were recently shown to confer a pituitary adenoma predisposition in patients with familial isolated pituitary adenomas (FIPA).
  • We report a large Samoan FIPA kindred from Australia/New Zealand with an R271W mutation that was associated with aggressive pituitary tumors.
  • RESULTS: This previously unreported kindred consisted of three affected individuals that either presented with or had first symptoms of a pituitary macroadenoma in late childhood or adolescence.
  • The index case, a 15-year-old male with incipient gigantism and his maternal aunt, had somatotropinomas, and the maternal uncle of the index case had a prolactinoma.
  • CONCLUSIONS: This kindred exemplifies the aggressive features of pituitary adenomas associated with AIP mutations, while genetic analyses among three R271W FIPA families indicate that R271W represents a mutational hotspot that should be studied further in functional studies.

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • ORBi (University of Liege). Free full Text at ORBi .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19684062.001).
  • [ISSN] 1479-683X
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / aryl hydrocarbon receptor-interacting protein; 9007-49-2 / DNA
  •  go-up   go-down


63. Machado AL, Nomikos P, Kiesewetter F, Fahlbusch R, Buchfelder M: DNA-flow cytometry of 207 pituitary adenomas: ploidy, proliferation, and prognosis. J Endocrinol Invest; 2005 Oct;28(9):795-801
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] DNA-flow cytometry of 207 pituitary adenomas: ploidy, proliferation, and prognosis.
  • The principal factors involved in pituitary adenoma formation are unknown.
  • DNA-flow cytometry is a useful study providing an estimation of a tumor proliferative rate.
  • Two hundred and seven fresh pituitary adenoma specimens were assessed by flow cytometry.
  • Endocrinologically inactive pituitary adenomas were predominantly euploids (50.8%).
  • The highest proliferation rates occurred in Nelson's syndrome and the lowest in Cushing's disease.
  • A significant difference in proliferation was observed with prolactinomas and acromegaly when a medical treatment was performed before primary surgery.
  • In conclusion, DNA-flow cytometry was found to be useful for determining ploidy and obtaining an overview of cell cycle status.
  • It was helpful in identifying patients requiring closer follow-up, such as those with invasive adenomas and Nelson's syndrome.
  • [MeSH-major] Adenoma / pathology. Adenoma / therapy. DNA, Neoplasm / analysis. Flow Cytometry / methods. Pituitary Neoplasms / pathology. Pituitary Neoplasms / therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Antineoplastic Protocols. Cell Proliferation. Female. Follow-Up Studies. Humans. Male. Middle Aged. Neoplasm Invasiveness. Ploidies. Predictive Value of Tests

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Anal Cell Pathol. 1998;17(2):103-10 [10052634.001]
  • [Cites] Horm Res. 1994;42(6):262-6 [7698721.001]
  • [Cites] Clin Lab Med. 2001 Dec;21(4):779-94 [11770287.001]
  • [Cites] Br J Biomed Sci. 1997 Jun;54(2):140-8 [9231461.001]
  • [Cites] Rev Med Chil. 1999 Nov;127(11):1385-97 [10835727.001]
  • [Cites] Urologe A. 1987 May;26(3):162-7 [3603902.001]
  • [Cites] Oncology. 1997 Mar-Apr;54(2):112-7 [9075781.001]
  • [Cites] Neurol India. 2001 Jun;49(2):124-7 [11447429.001]
  • [Cites] MMW Fortschr Med. 2001 Nov 1;143(44):40-2 [11732395.001]
  • [Cites] Surg Neurol. 2001 Jul;56(1):27-32 [11546567.001]
  • [Cites] J Tongji Med Univ. 1998;18(3):161-3 [10806816.001]
  • [Cites] J Neurosurg. 1986 Apr;64(4):588-93 [3950742.001]
  • [Cites] Clin Endocrinol (Oxf). 1995 Jul;43(1):79-85 [7641414.001]
  • [Cites] Int Rev Cytol. 2001;204:239-98 [11243596.001]
  • [Cites] Mol Biotechnol. 1999 Feb;11(1):37-53 [10367281.001]
  • [Cites] Methods Cell Biol. 2001;63:19-50 [11060835.001]
  • [Cites] J Neurol Neurosurg Psychiatry. 1979 Nov;42(11):973-82 [501374.001]
  • [Cites] Pituitary. 1999 Aug;2(2):117-22 [11081161.001]
  • [Cites] Clin Genet. 2001 Jul;60(1):1-8 [11531961.001]
  • [Cites] Acta Neurochir Suppl. 1996;65:18-21 [8738487.001]
  • [Cites] Cancer. 1988 Oct 15;62(8):1556-60 [3048631.001]
  • [Cites] Cancer. 1984 Apr 15;53(8):1708-13 [6697308.001]
  • [Cites] Clin Sci (Lond). 1998 Aug;95(2):129-35 [9680493.001]
  • [Cites] Acta Neurochir (Wien). 1985;76(1-2):18-22 [2988290.001]
  • [Cites] Am J Dermatopathol. 1989 Dec;11(6):549-54 [2604022.001]
  • [Cites] J Neurosurg. 1986 Mar;64(3):402-7 [3950720.001]
  • [Cites] Curr Issues Mol Biol. 2001 Apr;3(2):37-8 [11471974.001]
  • [Cites] Clin Neurosurg. 1969;16:185-217 [5811707.001]
  • [Cites] J Neurosurg. 1986 Dec;65(6):733-44 [3095506.001]
  • [Cites] J Neurosurg. 2002 Feb;96(2):195-208 [11838791.001]
  • [Cites] J Pathol. 1992 Sep;168(1):7-13 [1360498.001]
  • [Cites] Cell Vis. 1998 Jan-Feb;5(1):56-61 [9660728.001]
  • [Cites] Am J Clin Pathol. 1981 May;75(5):734-8 [6165237.001]
  • [Cites] Radiat Environ Biophys. 1975 Jun 13;12(1):31-9 [1101288.001]
  • (PMID = 16370557.001).
  • [ISSN] 0391-4097
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / DNA, Neoplasm
  •  go-up   go-down


64. Mezosi E, Nemes O: [Treatment of pituitary adenomas]. Orv Hetil; 2009 Sep 27;150(39):1803-10
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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.
  • Neurosurgery is the primary therapy of GH-, ACTH-, TSH-producing and inactive adenomas.
  • 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.
  • 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

  • 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 = 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
  •  go-up   go-down


65. Schwartz TH, Stieg PE, Anand VK: Endoscopic transsphenoidal pituitary surgery with intraoperative magnetic resonance imaging. Neurosurgery; 2006 Feb;58(1 Suppl):ONS44-51; discussion ONS44-51
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Endoscopic transsphenoidal pituitary surgery with intraoperative magnetic resonance imaging.
  • OBJECTIVE: The two most recent significant advances in pituitary surgery have been the endonasal endoscopic approach and intraoperative magnetic resonance imaging (IMRI).
  • METHODS: We performed endoscopic, endonasal resection of pituitary macroadenomas in 15 patients using the Polestar N-10 (0.12T) IMRI (Odin Medical Technologies, Inc., Newton, MA).
  • Eleven patients had nonfunctioning tumors, three had acromegaly, and one had a medication-resistant prolactinoma.
  • This was overcome with the use of a wall-mounted plasma screen.
  • [MeSH-major] Adenoma / surgery. Endoscopy / methods. Hypophysectomy / methods. Monitoring, Intraoperative / instrumentation. Pituitary Neoplasms / surgery. Sphenoid Sinus / surgery
  • [MeSH-minor] Adult. Aged. Female. Humans. Image Processing, Computer-Assisted / methods. Magnetic Resonance Imaging / methods. Male. Middle Aged. Neuronavigation / methods. Operating Rooms. Pituitary Gland / pathology. Pituitary Gland / surgery. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Endoscopy.
  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16479628.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


66. O'Toole D, Saveanu A, Couvelard A, Gunz G, Enjalbert A, Jaquet P, Ruszniewski P, Barlier A: The analysis of quantitative expression of somatostatin and dopamine receptors in gastro-entero-pancreatic tumours opens new therapeutic strategies. Eur J Endocrinol; 2006 Dec;155(6):849-57
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Cell lines derived from GEP express dopaminergic receptors D(2).
  • New chimeric analogues simultaneously recognising sst(2) and sst(5) or sst(2) and D(2) have additive effects in inhibition of GH and prolactin secretion in pituitary adenomas.
  • Levels of expression were compared with a group of 13 somatotroph adenomas.

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17132755.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen; 0 / RNA, Messenger; 0 / Receptors, Dopamine D2; 0 / Receptors, Somatostatin; 0 / Vascular Endothelial Growth Factor A; 0 / somatostatin receptor 2; 0 / somatostatin receptor 3; 0 / somatostatin receptor 5
  •  go-up   go-down


67. Basu A, Brabant G, Gnanalingham KK: More than a prolactinoma. Pituitary; 2010;13(1):87-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] More than a prolactinoma.
  • [MeSH-major] Meningioma / diagnosis. Prolactinoma / diagnosis

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18461461.001).
  • [ISSN] 1573-7403
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dopamine Agonists; 0 / Ergolines; LL60K9J05T / cabergoline
  •  go-up   go-down


68. Freeman B, Levy W, Gorman JM: Successful monotherapy treatment with aripiprazole in a patient with schizophrenia and prolactinoma. J Psychiatr Pract; 2007 Mar;13(2):120-4
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Successful monotherapy treatment with aripiprazole in a patient with schizophrenia and prolactinoma.
  • [MeSH-major] Antipsychotic Agents / therapeutic use. Piperazines / therapeutic use. Pituitary Neoplasms / complications. Pituitary Neoplasms / drug therapy. Prolactinoma / complications. Prolactinoma / drug therapy. Quinolones / therapeutic use. Schizophrenia / complications. Schizophrenia / drug therapy
  • [MeSH-minor] Administration, Oral. Adult. Aripiprazole. Clonazepam / adverse effects. Clonazepam / therapeutic use. Dopamine Agonists / adverse effects. Dopamine Agonists / therapeutic use. Drug Therapy, Combination. Ergolines / adverse effects. Ergolines / therapeutic use. Female. Follow-Up Studies. Humans. Patient Care Team. Prolactin / blood

  • Genetic Alliance. consumer health - Schizophrenia.
  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • MedlinePlus Health Information. consumer health - Schizophrenia.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CLONAZEPAM .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17414690.001).
  • [ISSN] 1527-4160
  • [Journal-full-title] Journal of psychiatric practice
  • [ISO-abbreviation] J Psychiatr Pract
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antipsychotic Agents; 0 / Dopamine Agonists; 0 / Ergolines; 0 / Piperazines; 0 / Quinolones; 5PE9FDE8GB / Clonazepam; 82VFR53I78 / Aripiprazole; 9002-62-4 / Prolactin; LL60K9J05T / cabergoline
  •  go-up   go-down


69. Howell DL, Wasilewski K, Mazewski CM, Hudgins RJ, Meacham LR: The use of high-dose daily cabergoline in an adolescent patient with macroprolactinoma. J Pediatr Hematol Oncol; 2005 Jun;27(6):326-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Prolactinomas are rare in children and adolescents but well studied in adults.
  • Cabergoline, a second-generation ergot derivative with a longer half-life, has been used in resistant prolactinomas and as first-line treatment in adults.
  • The authors describe an adolescent boy with a pituitary macroadenoma with an initial prolactin level of 73,777 ng/mL.
  • After failing to respond to bromocriptine and standard-dose cabergoline, he responded well to very high daily doses of cabergoline (1.5 mg daily), with a current prolactin level of 726 ng/mL and notable reduction in tumor size.
  • Escalating doses of cabergoline should be considered in pediatric patients with dopamine-resistant prolactinomas.
  • [MeSH-major] Dopamine Agonists / therapeutic use. Ergolines / therapeutic use. Pituitary Neoplasms / drug therapy. Prolactinoma / drug therapy

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15956887.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dopamine Agonists; 0 / Ergolines; 3A64E3G5ZO / Bromocriptine; LL60K9J05T / cabergoline
  •  go-up   go-down


70. Provenzale JM: Morphology predicts oncology: a commentary on Vezina and Sutton's article, "Prolactin-secreting pituitary microadenomas: roentgenologic diagnosis". AJR Am J Roentgenol; 2007 Jan;188(1):9-10
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Morphology predicts oncology: a commentary on Vezina and Sutton's article, "Prolactin-secreting pituitary microadenomas: roentgenologic diagnosis".
  • [MeSH-major] Adenoma, Chromophobe / radiography. Craniopharyngioma / radiography. Craniopharyngioma / secretion. Lactation Disorders / etiology. Pituitary Neoplasms / complications. Pituitary Neoplasms / secretion. Prolactin / secretion

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentOn] Am J Roentgenol Radium Ther Nucl Med. 1974 Jan;120(1):46-54 [4855697.001]
  • (PMID = 17179340.001).
  • [ISSN] 1546-3141
  • [Journal-full-title] AJR. American journal of roentgenology
  • [ISO-abbreviation] AJR Am J Roentgenol
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hormones, Ectopic; 9002-62-4 / Prolactin
  •  go-up   go-down


71. Vera-Lastra O, Jara LJ, Medina G, Rojas JL, Veláquez F, Ariza R, Normandía A, Fuentes M: Functional hyperprolactinemia and hypophyseal microadenoma in systemic sclerosis. J Rheumatol; 2006 Jun;33(6):1108-12
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • However, the association with pituitary adenoma and the status of hypothalamic dopaminergic tone using metoclopramide (MTC) test has not been studied.
  • We investigated the prevalence of prolactin (PRL)-secreting pituitary adenoma and evaluated production of PRL by dynamic testing with MTC in SSc.
  • Serum PRL concentrations were determined by radioimmunoassay in all subjects, and PRL response was measured 30, 60, 90, and 120 min after injection of 10 mg of MTC.
  • RESULTS: The mean basal serum PRL levels before and after stimulation with MTC in SSc patients versus controls were: basal 18.2 +/- 5.4 versus 8.7 +/- 1.6 ng/ml, p = NS; 30 min: 175.0 +/- 5.4 versus 61.0 +/- 42 ng/ml, p < 0.001; 60 min: 160 +/- 64 versus 52 +/- 30 ng/ml, p < 0.001; 90 min: 125 +/- 57 versus 42 +/- 21.0 ng/ml, p < 0.05; 120 min: 108.0 +/- 57 versus 30.0 +/- 10 ng/ml, p < 0.005.
  • PRL may have a role in the pathogenesis of SSc.
  • [MeSH-major] Adenoma / blood. Hyperprolactinemia / blood. Pituitary Neoplasms / blood. Scleroderma, Diffuse / blood. Scleroderma, Limited / blood


72. Passos VQ, Fortes MA, Giannella-Neto D, Bronstein MD: Genes differentially expressed in prolactinomas responsive and resistant to dopamine agonists. Neuroendocrinology; 2009;89(2):163-70
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genes differentially expressed in prolactinomas responsive and resistant to dopamine agonists.
  • BACKGROUND/AIMS: Prolactin (PRL) secretion and its gene expression are inhibited by dopamine.
  • Prolactinomas are the most common secreting pituitary adenomas, and dopamine agonists (DA) are the first choice for their treatment.
  • As the mechanisms involved in DA resistance are not fully understood, the aim of this study was to obtain new insights regarding the molecular differences between the prolactinomas that are responsive to DA and those that are resistant.
  • METHODS: Tumor tissue samples were collected from 17 patients who harbored prolactinomas, which were classified as responsive or resistant according to their clinical and laboratorial reaction to DA.
  • The expression of 6 genes was evaluated by real-time polymerase chain reaction: dopamine receptor type 2 (DRD(2)), nerve growth factor-beta (NGFB) and its receptor (NGFR), estrogen receptor-alpha (ERA), estrogen receptor-beta (ERB) and the pituitary tumor transforming gene (PTTG).
  • Moreover, the expressions of DRD(2) and NGFR were positively correlated with PRL decrease during treatment (r = 0.66, p = 0.005 and r = 0.57, p = 0.044, respectively).
  • CONCLUSIONS: DRD(2) and NGFR expressions are related to the responsiveness of prolactinoma to DA.
  • Furthermore, the response of prolactinomas to DA should be viewed as a spectrum ranging from the most responsive to the most resistant ones.
  • [MeSH-major] Dopamine Agonists / therapeutic use. Pituitary Neoplasms / drug therapy. Pituitary Neoplasms / metabolism. Prolactinoma / drug therapy. Prolactinoma / metabolism
  • [MeSH-minor] Adult. Drug Resistance, Neoplasm / genetics. Female. Gene Expression. Humans. Male. RNA, Messenger / metabolism

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2008 S. Karger AG, Basel.
  • (PMID = 18791324.001).
  • [ISSN] 1423-0194
  • [Journal-full-title] Neuroendocrinology
  • [ISO-abbreviation] Neuroendocrinology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Dopamine Agonists; 0 / RNA, Messenger
  •  go-up   go-down


73. Liao CC, Lin SY, Lin HW, Chen KH, Chang LH, Chen ST, Wang J: Menstrual abnormalities in a woman with ACTH-dependent pituitary macroadenoma mimicking polycystic ovary syndrome. Taiwan J Obstet Gynecol; 2006 Jun;45(2):176-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Menstrual abnormalities in a woman with ACTH-dependent pituitary macroadenoma mimicking polycystic ovary syndrome.
  • OBJECTIVE: Here, we present a case of ACTH-dependent pituitary macroadenoma (Cushing's disease) resulting in secondary amenorrhea mimicking polycystic ovary syndrome (PCOS).
  • She visited a gynecologic clinic where PCOS was impressed according to the clinical manifestation and ultrasound finding.
  • Endocrine studies revealed: serum prolactin 21 ng/mL (3.0-20 ng/mL), FSH 5.69 mIU/mL (3.4-10.0 mIU/mL), LH 1.01 mIU/mL (1.1-11.6 mIU/mL), E2 < 20 pg/mL (follicular phase 53-258 pg/mL), ACTH 110 pg/mL (0-46.0 pg/mL), cortisol 26.7 microg/dL at 8 a.m. (5.0-25 microg/dL), cortisol 21.3 microg/dL at 11 p.m. (half of normal morning value).
  • Right pituitary macroadenoma was diagnosed through a series of dexamethasone tests and MRI.
  • CONCLUSION: PCOS is a common disease resulting in secondary amenorrhea.
  • However, Cushing's syndrome resulting from pituitary macroadenoma should also be considered.
  • Therefore, a careful history, observation, physical examination, and endocrine studies can differentiate between patients with PCOS and Cushing's disease.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / complications. ACTH-Secreting Pituitary Adenoma / diagnosis. Amenorrhea / etiology. Pituitary Neoplasms / complications. Pituitary Neoplasms / diagnosis. Polycystic Ovary Syndrome / diagnosis
  • [MeSH-minor] Adult. Craniotomy. Diagnosis, Differential. Female. Humans. Magnetic Resonance Imaging

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • MedlinePlus Health Information. consumer health - Polycystic Ovary Syndrome.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17197364.001).
  • [ISSN] 1875-6263
  • [Journal-full-title] Taiwanese journal of obstetrics & gynecology
  • [ISO-abbreviation] Taiwan J Obstet Gynecol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China
  •  go-up   go-down


74. Vilar L, Moura E, Canadas V, Gusmão A, Campos R, Leal E, Teixeira L, Santos V, Gomes B, Lima M, Paiva R, Albuquerque JL, Egito CS, Botelho CA, Azevedo M, Casulari LA, Naves LA: [Prevalence of macroprolactinemia among 115 patients with hyperprolactinemia]. Arq Bras Endocrinol Metabol; 2007 Feb;51(1):86-91
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Macroprolactinemia is characterized by the predominance in the serum of macroprolactin, a prolactin (PRL) with high molecular mass and low biological activity that does not need treatment.
  • Among them, 19 (16.5%) had solely macroprolactinemia, 4 (3.5%) polycystic ovary syndrome, 7 (6.1%) acromegaly, 8 (6.9%) idiopathic hyperprolactinemia, 10 (8.6%) primary hypothyroidism, 14 (12.2%) clinically non-functioning pituitary adenomas, 20 (17.4%) drug-induced hyperprolactinemia and 33 (28.7%) prolactinomas.
  • The diagnosis of macroprolactinemia was established by the demonstration of a PRL recovery < 30% after treatment of sera with polyethylene glycol.
  • Prolactin levels in cases of macroprolactin ranged from 45.1 to 404 ng/mL (mean 113.3 +/- 94.5) but in 15 (78.9%) were < 100 ng/mL.
  • [MeSH-major] Hyperprolactinemia / epidemiology. Prolactin / blood

  • Genetic Alliance. consumer health - Galactorrhoea-Hyperprolactinaemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17435860.001).
  • [ISSN] 0004-2730
  • [Journal-full-title] Arquivos brasileiros de endocrinologia e metabologia
  • [ISO-abbreviation] Arq Bras Endocrinol Metabol
  • [Language] por
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Biomarkers; 0 / prolactin, polymeric; 30IQX730WE / Polyethylene Glycols; 9002-62-4 / Prolactin
  •  go-up   go-down


75. Horiguchi K, Yamada M, Umezawa R, Satoh T, Hashimoto K, Tosaka M, Yamada S, Mori M: Somatostatin receptor subtypes mRNA in TSH-secreting pituitary adenomas: a case showing a dramatic reduction in tumor size during short octreotide treatment. Endocr J; 2007 Jun;54(3):371-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Somatostatin receptor subtypes mRNA in TSH-secreting pituitary adenomas: a case showing a dramatic reduction in tumor size during short octreotide treatment.
  • TSH-secreting adenoma is a rare pituitary adenoma, and the expression levels of the specific subtypes of somatostatin receptors (sstr) mRNAs have remained obscure.
  • To determine the quantitative expression of the sstr1-5 mRNAs in TSH-secreting adenomas that may be related to the efficacy of treatment with a somatostatin analogue, expression of the sstr1-5 mRNAs was examined and compared in TSH-secreting adenomas and other pituitary adenomas.
  • The pituitary adenomas were obtained at transsphenoidal surgery from 4 cases of TSH-secreting adenoma, including 1 patient showing a significant shrinkage of the tumor size after only 10 days of octreotide treatment, 2 patients without tumor size reduction and 1 patient without treatment, and 5 GH-secreting adenomas, 6 prolactinomas, 5 nonfunctioning adenomas, 4 ACTH-secreting adenomas and normal pituitaries at autopsy from 4 normal subjects.
  • In comparison to the normal pituitary, sstr2A>sstr1>sstr5>sstr3 mRNAs were expressed in the TSH-secreting adenomas examined.
  • The expression level of sstr2 mRNA was significantly higher than those in normal pituitary, prolactinomas, ACTH-secreting and nonfunctioning pituitary adenomas.
  • The patient with marked shrinkage of the tumor showed the highest expression of both sstr2 and sstr5 mRNAs among all the cases of pituitary adenoma.
  • A TSH-secreting tumor without shrinkage showed a similar expression level of sstr2 mRNA.
  • These findings demonstrated that TSH-secreting adenomas express sstr1, 2A, 3 and 5 mRNAs, predominantly sstr2A, and in addition to the expression of sstr2 mRNA, the expression level of sstr5 mRNA may be a factor affecting the tumor shrinkage by somatostatin analogues against TSH-secreting adenomas.
  • [MeSH-major] Adenoma / drug therapy. Adenoma / genetics. Octreotide / therapeutic use. Pituitary Neoplasms / drug therapy. Pituitary Neoplasms / genetics. Receptors, Somatostatin / genetics. Thyrotrophs / pathology. Tumor Burden / drug effects

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17420609.001).
  • [ISSN] 0918-8959
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Case Reports; Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / Receptors, Somatostatin; RWM8CCW8GP / Octreotide
  •  go-up   go-down


76. Morita S, Otsuki M, Izumi M, Asanuma N, Izumoto S, Saitoh Y, Yoshimine T, Kasayama S: Reduced epinephrine reserve in response to insulin-induced hypoglycemia in patients with pituitary adenoma. Eur J Endocrinol; 2007 Sep;157(3):265-70
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Reduced epinephrine reserve in response to insulin-induced hypoglycemia in patients with pituitary adenoma.
  • Insulin-induced hypoglycemia is used for evaluating GH-IGF-I and ACTH-adrenal axes in patients with pituitary disorders.
  • The aim of this study was to determine whether the response of catecholamine secretion to hypoglycemia is disrupted in patients with pituitary adenoma.
  • METHODS: The study population comprised 23 patients with pituitary adenoma (non-functioning adenoma or prolactinoma).
  • CONCLUSIONS: Impaired epinephrine secretion in response to insulin-induced hypoglycemia was frequently observed in patients with pituitary adenoma.
  • This disorder was especially severe in patients with secondary adrenal insufficiency.

  • Genetic Alliance. consumer health - Hypoglycemia.
  • MedlinePlus Health Information. consumer health - Hypoglycemia.
  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • Hazardous Substances Data Bank. Norepinephrine .
  • Hazardous Substances Data Bank. EPINEPHRINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17766707.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Hypoglycemic Agents; 0 / Insulin; X4W3ENH1CV / Norepinephrine; YKH834O4BH / Epinephrine
  •  go-up   go-down


77. Molitch ME: Pharmacologic resistance in prolactinoma patients. Pituitary; 2005;8(1):43-52
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pharmacologic resistance in prolactinoma patients.
  • Pharmacologic resistance to dopamine agonists is defined here as failure to normalize PRL levels and failure to decrease macroprolactinoma size by >or=50%.
  • Failure to normalize PRL levels is found in about one-quarter of patients treated with bromocriptine and 10-15% of those treated with pergolide or cabergoline.
  • [MeSH-major] Dopamine Agonists / therapeutic use. Pituitary Neoplasms / drug therapy. Prolactinoma / drug therapy
  • [MeSH-minor] Bromocriptine / pharmacology. Bromocriptine / therapeutic use. Cell Proliferation / drug effects. Dose-Response Relationship, Drug. Drug Resistance. Ergolines / pharmacology. Ergolines / therapeutic use. Estrogens / therapeutic use. Female. Humans. Male. Pergolide / pharmacology. Pergolide / therapeutic use. Prolactin / secretion. Receptors, Dopamine D2 / analysis. Receptors, Dopamine D2 / drug effects

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Horm Res. 1998;49(5):250-3 [9568811.001]
  • [Cites] J Clin Endocrinol Metab. 1986 Dec;63(6):1342-7 [3782422.001]
  • [Cites] Nature. 1975 Jun 5;255(5508):497-8 [1138203.001]
  • [Cites] Ann Endocrinol (Paris). 2000 Nov;61(5):411-7 [11084391.001]
  • [Cites] J Clin Endocrinol Metab. 1987 Feb;64(2):391-4 [3793856.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Oct;87(10):4447-51 [12364416.001]
  • [Cites] Acta Endocrinol (Copenh). 1992 Jun;126(6):489-94 [1642081.001]
  • [Cites] Endocrinology. 1986 Dec;119(6):2484-9 [3780536.001]
  • [Cites] Clin Endocrinol (Oxf). 1977;6 Suppl:91S-99S [617073.001]
  • [Cites] Ann Endocrinol (Paris). 2002 Dec;63(6 Pt 1):524-31 [12527854.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Mar;82(3):876-83 [9062500.001]
  • [Cites] Arch Pathol Lab Med. 1994 May;118(5):562-5 [8192565.001]
  • [Cites] N Engl J Med. 1983 Sep 22;309(12 ):704-9 [6888442.001]
  • [Cites] Clin Endocrinol (Oxf). 1986 Feb;24(2):127-33 [3708872.001]
  • [Cites] Lancet. 2004 Apr 10;363(9416):1179-83 [15081648.001]
  • [Cites] Neurology. 1996 Sep;47(3):785-8 [8797480.001]
  • [Cites] Clin Endocrinol (Oxf). 1991 Jan;34(1):25-9 [1672268.001]
  • [Cites] Gynecol Endocrinol. 1992 Sep;6(3):183-8 [1442163.001]
  • [Cites] Neurosci Lett. 2001 Oct 5;311(3):149-52 [11578816.001]
  • [Cites] Mayo Clin Proc. 2003 Jun;78(6):684-6 [12934776.001]
  • [Cites] Neuroendocrinology. 1982;34(5):339-42 [7078703.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Feb 4;100(3):1034-9 [12552124.001]
  • [Cites] Int J Fertil Menopausal Stud. 1994 Jul-Aug;39(4):202-7 [7951402.001]
  • [Cites] Endocrinology. 1985 Jun;116(6):2456-62 [3996322.001]
  • [Cites] J Neuroendocrinol. 1996 Oct;8(10):737-46 [8910802.001]
  • [Cites] N Engl J Med. 1994 Oct 6;331(14):904-9 [7915824.001]
  • [Cites] Fertil Steril. 1986 Aug;46(2):312-4 [3089843.001]
  • [Cites] Gynecol Endocrinol. 1994 Sep;8(3):175-81 [7847102.001]
  • [Cites] Neuroendocrinology. 1980 Jun;30(6):389-95 [7383277.001]
  • [Cites] Clin Endocrinol (Oxf). 1999 Nov;51(5):643-51 [10594527.001]
  • [Cites] Fertil Steril. 1979 Aug;32(2):187-92 [467699.001]
  • [Cites] Endocrinology. 1981 Mar;108(3):903-7 [7460850.001]
  • [Cites] J Clin Endocrinol Metab. 1982 Dec;55(6):1178-83 [6752167.001]
  • [Cites] Pituitary. 2003;6(1):19-27 [14674720.001]
  • [Cites] J Endocrinol. 1980 Jul;86(1):109-16 [7430882.001]
  • [Cites] Maturitas. 1982 Apr;4(1):19-26 [6285153.001]
  • [Cites] Mayo Clin Proc. 2002 Dec;77(12 ):1280-6 [12479512.001]
  • [Cites] Acta Endocrinol (Copenh). 1983 Aug;103(4):441-5 [6412498.001]
  • [Cites] Eur J Endocrinol. 1996 Oct;135(4):413-20 [8921822.001]
  • [Cites] JAMA. 2000 Nov 1;284(17):2215-21 [11056593.001]
  • [Cites] Endocr Pathol. 2000 Winter;11(4):341-352 [12114758.001]
  • [Cites] Contraception. 1991 Aug;44(2):155-61 [1832628.001]
  • [Cites] Fertil Steril. 1982 Jan;37(1):61-7 [7199483.001]
  • [Cites] Endocrinology. 1982 Oct;111(4):1057-60 [7117191.001]
  • [Cites] J Reprod Med. 1995 Aug;40(8):556-60 [7473451.001]
  • [Cites] J Biol Chem. 1982 Mar 10;257(5):2133-6 [7061411.001]
  • [Cites] Horm Res. 1993;39(5-6):218-22 [7906243.001]
  • [Cites] Eur J Obstet Gynecol Reprod Biol. 1991 Jul 1;40(2):111-8 [1676973.001]
  • [Cites] Neurology. 1997 Feb;48(2):363-8 [9040722.001]
  • [Cites] J Clin Endocrinol Metab. 1992 Mar;74(3):577-84 [1346788.001]
  • [Cites] J Biol Chem. 1994 Sep 16;269(37):23120-7 [7916015.001]
  • [Cites] Fertil Steril. 1987 May;47(5):785-91 [3569555.001]
  • [Cites] Obstet Gynecol. 1981 Dec;58(6):708-13 [6796919.001]
  • [Cites] Br J Cancer. 1995 Dec;72(6):1397-9 [8519650.001]
  • [Cites] Curr Opin Obstet Gynecol. 1994 Aug;6(4):393-7 [7742506.001]
  • [Cites] J Reprod Med. 1999 Dec;44(12 Suppl):1121-6 [10649822.001]
  • [Cites] Isr J Med Sci. 1991 Jul;27(7):375-9 [2071373.001]
  • [Cites] Horm Res. 1992;38(1-2):84-9 [1306523.001]
  • [Cites] Fertil Steril. 1979 Feb;31(2):124-9 [570131.001]
  • [Cites] J Endocrinol Invest. 1995 Jun;18(6):450-5 [7594240.001]
  • [Cites] Histochem Cell Biol. 2001 Sep;116(3):215-22 [11685549.001]
  • [Cites] N Engl J Med. 1985 Sep 12;313(11):656-9 [4022058.001]
  • [Cites] Clin Endocrinol (Oxf). 1984 Apr;20(4):427-34 [6609028.001]
  • [Cites] Clin Endocrinol (Oxf). 1986 Apr;24(4):421-6 [3742834.001]
  • [Cites] J Biol Chem. 2002 Sep 27;277(39):35819-25 [12121979.001]
  • [Cites] Endocrinology. 1980 Apr;106(4):1108-13 [6766855.001]
  • [Cites] Eur J Endocrinol. 2002 Oct;147(4):461-5 [12370106.001]
  • [Cites] Endocrinology. 2002 Mar;143(3):747-54 [11861492.001]
  • [Cites] J Biol Chem. 1988 Jul 25;263(21):10127-34 [2839476.001]
  • [Cites] J Endocrinol Invest. 1983 Feb;6(1):47-50 [6841916.001]
  • [Cites] Neuroendocrinology. 1994 Sep;60(3):314-22 [7969790.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Oct 29;99(22):14530-5 [12391292.001]
  • [Cites] Neurology. 2001 Oct 9;57(7):1313-6 [11591856.001]
  • [Cites] Nature. 1989 Dec 21-28;342(6252):926-9 [2480527.001]
  • [Cites] Endocrinol Metab Clin North Am. 2001 Sep;30(3):585-610 [11571932.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Sep;82(9):2962-5 [9284727.001]
  • [Cites] Gynecol Obstet Invest. 1997;44(2):124-6 [9286727.001]
  • [Cites] Presse Med. 1995 Apr 29;24(16):753-7 [7784413.001]
  • [Cites] AJNR Am J Neuroradiol. 1983 May-Jun;4(3):415-7 [6410759.001]
  • [Cites] No Shinkei Geka. 1987 Jan;15(1):65-72 [3822068.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Sep;85(9):3053-7 [10999785.001]
  • [Cites] Intern Med. 2001 Sep;40(9):857-61 [11579944.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Jan;85(1):8-13 [10634356.001]
  • [Cites] Eur J Endocrinol. 1996 Apr;134(4):454-6 [8640297.001]
  • [Cites] Mol Endocrinol. 2002 Feb;16(2):353-66 [11818506.001]
  • [Cites] Nouv Presse Med. 1976 Jul 3-10;5(27):1687-91 [986640.001]
  • [Cites] J Clin Endocrinol Metab. 1984 Feb;58(2):268-73 [6693536.001]
  • [Cites] Horm Res. 1985;22(3):153-63 [3932176.001]
  • [Cites] Fertil Steril. 1993 Mar;59(3):671-3 [8458475.001]
  • [Cites] J Clin Endocrinol Metab. 1985 Apr;60(4):698-705 [3882737.001]
  • [Cites] Arch Gynecol. 1980;229(3):177-90 [6998384.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Jun;85(6):2247-52 [10852458.001]
  • [Cites] Acta Endocrinol (Copenh). 1982 Dec;101(4):491-500 [7158226.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Nov;86(11):5256-61 [11701688.001]
  • [Cites] Nature. 1979 Mar 15;278(5701):252-4 [423973.001]
  • [Cites] Contraception. 1976 Jan;13(1):79-85 [1245120.001]
  • [Cites] J Clin Endocrinol Metab. 1989 Sep;69(3):500-9 [2760167.001]
  • [Cites] J Endocrinol Invest. 1999 Apr;22(4):306-9 [10342366.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Sep 1;90(17):7961-5 [8367448.001]
  • [Cites] Obstet Gynecol. 1985 Apr;65(4):506-10 [3982724.001]
  • [Cites] Mayo Clin Proc. 2003 Jun;78(6):730-1 [12934784.001]
  • [Cites] J Clin Endocrinol Metab. 1989 Jun;68(6):1201-6 [2656736.001]
  • [Cites] J Clin Endocrinol Metab. 1980 Jun;50(6):1026-33 [7189523.001]
  • [Cites] Contraception. 1998 Aug;58(2):69-73 [9773260.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Jul;84(7):2518-22 [10404830.001]
  • [Cites] Science. 1978 Jun 9;200(4346):1173-5 [418505.001]
  • [Cites] Acta Endocrinol (Copenh). 1978 Jul;88(3):435-51 [354299.001]
  • [Cites] Clin Neuropharmacol. 1996 Jun;19(3):202-12 [8726539.001]
  • [Cites] Obstet Gynecol. 1980 Jan;55(1):8-11 [7352067.001]
  • [Cites] J Endocrinol Invest. 1997 Oct;20(9):537-46 [9413808.001]
  • (PMID = 16411068.001).
  • [ISSN] 1386-341X
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dopamine Agonists; 0 / Ergolines; 0 / Estrogens; 0 / Receptors, Dopamine D2; 24MJ822NZ9 / Pergolide; 3A64E3G5ZO / Bromocriptine; 9002-62-4 / Prolactin; LL60K9J05T / cabergoline
  • [Number-of-references] 111
  •  go-up   go-down


78. Fleseriu M, Lee M, Pineyro MM, Skugor M, Reddy SK, Siraj ES, Hamrahian AH: Giant invasive pituitary prolactinoma with falsely low serum prolactin: the significance of 'hook effect'. J Neurooncol; 2006 Aug;79(1):41-3
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Giant invasive pituitary prolactinoma with falsely low serum prolactin: the significance of 'hook effect'.
  • The authors report a case of a patient with giant, invasive skull base tumor extending to the parasellar area discovered incidentally during the work-up for decreased memory.
  • Given the large size of the tumor, the elevated prolactin (PRL) was interpreted to be secondary to stalk effect and patient underwent debulking surgery through a transcranial approach.
  • Immunostaining of the excised tumor tissue was strongly positive for prolactin.
  • His prolactin was found to be 13,144 ng/ml in our lab after surgery confirming the diagnosis of invasive giant prolactinoma.
  • He was started on Cabergoline with normalization of his prolactin level and more than 50% decrease in residual tumor size over 9 months periods.
  • This case highlights the importance of 'Hook Effect' resulting in falsely low prolactin level, which may have significant therapeutic implication.
  • [MeSH-major] Diagnostic Errors. Hyperprolactinemia / etiology. Pituitary Neoplasms / diagnosis. Prolactin / blood. Prolactinoma / diagnosis
  • [MeSH-minor] Abducens Nerve Diseases / etiology. Diagnosis, Differential. Dopamine Agonists / therapeutic use. Ergolines / therapeutic use. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Neurosurgical Procedures / adverse effects. Oculomotor Nerve Diseases / etiology. Skull Base Neoplasms / pathology. Trochlear Nerve Diseases / etiology

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Clin Endocrinol (Oxf). 1996 Oct;45(4):506-7 [8959094.001]
  • [Cites] Saudi Med J. 2004 May;25(5):656-9 [15138537.001]
  • [Cites] Clin Endocrinol (Oxf). 1996 Mar;44(3):305-9 [8729527.001]
  • [Cites] Clin Chem. 1992 Mar;38(3):437-8 [1547570.001]
  • [Cites] Pituitary. 2002;5(4):261-5 [14558675.001]
  • [Cites] Clin Chem. 1991 May;37(5):771-2 [1709597.001]
  • [Cites] Clin Chem Lab Med. 1999 Apr;37(4):471-6 [10369120.001]
  • [Cites] Clin Chem. 2000 Oct;46(10):1719-21 [11017960.001]
  • [Cites] Clin Chem. 1986 Nov;32(11):2102 [3779958.001]
  • [Cites] Ann Biol Clin (Paris). 1998 Jan-Feb;56(1):41-7 [9754221.001]
  • [Cites] Ann Intern Med. 1993 Jul 15;119(2):173 [8512176.001]
  • [Cites] Neurol India. 2001 Mar;49(1):78-80 [11303248.001]
  • [Cites] Neurosurgery. 1998 Apr;42(4):913-5; discussion 915-6 [9574657.001]
  • [Cites] J Endocrinol Invest. 1998 Mar;21(3):184-8 [9591215.001]
  • (PMID = 16598425.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dopamine Agonists; 0 / Ergolines; 9002-62-4 / Prolactin; LL60K9J05T / cabergoline
  •  go-up   go-down


79. Cheung D, Heaney A: Dopamine agonists and valvular heart disease. Curr Opin Endocrinol Diabetes Obes; 2009 Aug;16(4):316-20
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dopamine agonists and valvular heart disease.
  • PURPOSE OF REVIEW: Dopamine agonists are first-line therapy for prolactinomas, normalizing serum prolactin and reducing tumor size in the majority of cases.
  • Recent studies reporting cardiac valvular abnormalities in dopamine agonist-treated Parkinson's disease patients have raised concerns regarding potential cardiac effects in dopamine agonist-treated prolactinoma patients.
  • This article reviews the current literature regarding dopamine agonist use and cardiac valve disease and provides guidance for clinical practice.
  • RECENT FINDINGS: Off-target action of dopamine agonists at 5-hydroxytryptamine 2B receptors is now recognized to cause cardiac valve disease in several studies in Parkinson's disease patients who received high daily dopamine agonist doses, including cabergoline and pergolide.
  • Generally, dopamine agonist doses in prolactinoma therapy are 10-fold lower than those employed in Parkinson's disease, although occasionally dopamine agonist-resistant patients require higher doses.
  • Most studies of dopamine agonist use in prolactinoma have not observed valvular abnormalities.
  • SUMMARY: Dopamine agonists are effective in treating prolactinomas.
  • [MeSH-minor] Humans. Pituitary Neoplasms / drug therapy. Prolactinoma / drug therapy

  • Genetic Alliance. consumer health - Heart Disease.
  • MedlinePlus Health Information. consumer health - Heart Valve Diseases.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19506475.001).
  • [ISSN] 1752-2978
  • [Journal-full-title] Current opinion in endocrinology, diabetes, and obesity
  • [ISO-abbreviation] Curr Opin Endocrinol Diabetes Obes
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Dopamine Agonists
  • [Number-of-references] 27
  •  go-up   go-down


80. Sicilia V, Earle J, Mezitis SG: Multiple ovarian cysts and oligomenorrhea as the initial manifestations of a gonadotropin-secreting pituitary macroadenoma. Endocr Pract; 2006 Jul-Aug;12(4):417-21
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Multiple ovarian cysts and oligomenorrhea as the initial manifestations of a gonadotropin-secreting pituitary macroadenoma.
  • OBJECTIVE: To report a case of a follicle-stimulating hormone (FSH)-secreting pituitary adenoma, which manifested with oligomenorrhea, dysmenorrhea, and multiple bilateral ovarian cysts.
  • METHODS: We present a case report of a 29-year-old woman, including detailed laboratory, radiologic, and pathologic findings, who was diagnosed as having an FSH-secreting pituitary tumor.
  • Relevant laboratory data were as follows: serum FSH 6.8 mIU/mL, luteinizing hormone 0.1 mIU/mL, prolactin 67 ng/mL, human chorionic gonadotropin <2 mIU/mL, progesterone 3.5 ng/dL, estradiol 237 pg/mL, thyrotropin 1.8 microIU/mL, testosterone <4 ng/dL, insulin 8.0 microIU/mL, and fasting plasma glucose 87 mg/dL.
  • Magnetic resonance imaging (MRI) of the brain revealed a 2.5-cm pituitary mass, although the patient had no symptoms of pituitary dysfunction.
  • Transsphenoidal removal of the mass was performed, and pathology studies were positive for FSH-secreting adenoma.
  • Almost 3 years after treatment, the patient remained asymptomatic, results of pituitary function tests were normal, and follow-up MRI showed no signs of tumor regrowth.
  • CONCLUSION: Although very uncommon, gonadotropin-secreting pituitary adenomas should be considered in the differential diagnosis of new-onset oligomenorrhea and dysmenorrhea, especially if associated with multicystic ovaries on ultrasound study, even in the absence of elevated levels of serum gonadotropins.
  • [MeSH-major] Gonadotropins / secretion. Oligomenorrhea / etiology. Ovarian Cysts / etiology. Pituitary Neoplasms / diagnosis. Pituitary Neoplasms / secretion
  • [MeSH-minor] Adenoma / complications. Adult. Female. Follicle Stimulating Hormone / secretion. Humans. Immunohistochemistry. Luteinizing Hormone / secretion

  • MedlinePlus Health Information. consumer health - Ovarian Cysts.
  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • Hazardous Substances Data Bank. MENOTROPINS .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16901798.001).
  • [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 / Gonadotropins; 9002-67-9 / Luteinizing Hormone; 9002-68-0 / Follicle Stimulating Hormone
  •  go-up   go-down


81. Ferone D, de Herder WW, Pivonello R, Kros JM, van Koetsveld PM, de Jong T, Minuto F, Colao A, Lamberts SW, Hofland LJ: Correlation of in vitro and in vivo somatotropic adenoma responsiveness to somatostatin analogs and dopamine agonists with immunohistochemical evaluation of somatostatin and dopamine receptors and electron microscopy. J Clin Endocrinol Metab; 2008 Apr;93(4):1412-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Correlation of in vitro and in vivo somatotropic adenoma responsiveness to somatostatin analogs and dopamine agonists with immunohistochemical evaluation of somatostatin and dopamine receptors and electron microscopy.
  • OBJECTIVE AND PATIENTS: Twenty-four pituitary adenomas from acromegalic patients (13 females, 11 males; age range 19-65 yr) were characterized for somatostatin receptor subtype 2A (sst(2A)), dopamine D(2) receptor (D(2)R), GH, and prolactin (PRL) expression by immunohistochemistry, and results correlated with the in vitro and in vivo hormone responses to octreotide and quinagolide.
  • In nine cases, GH and PRL content was further studied by immunoelectron microscopy.
  • Sst(2A) was scored as 2 in 13 cases, 1 in 10, and 0 in one; D(2)R was scored as 2 in 13 cases, 1 in nine, and 0 in 2; GH was 2 in 15 cases and 1 in nine; PRL was 2 in six cases, 1 in 13, and 0 in 5.
  • D(2)R was positively correlated with in vitro percent GH (P =0.000) and PRL (P =0.005) suppression by quinagolide.
  • Electron microscopy revealed two pure somatotroph adenomas, five somatomammotrophs with a variable coexpression of GH and PRL in the same cells, and two tumors consisting of mixed cell types, which were less sensitive to quinagolide and octreotide.
  • CONCLUSION: Sst(2A) and D(2)R are frequently coexpressed in adenomas from acromegalic patients, and immunohistochemistry may be helpful in characterizing receptor expression in pituitary adenomas to select patients responsive to different treatments.
  • [MeSH-major] Adenoma / drug therapy. Aminoquinolines / therapeutic use. Dopamine Agonists / therapeutic use. Growth Hormone-Secreting Pituitary Adenoma / drug therapy. Octreotide / therapeutic use. Receptors, Dopamine D2 / analysis. Receptors, Somatostatin / analysis
  • [MeSH-minor] Adult. Female. Human Growth Hormone / blood. Humans. Immunohistochemistry. Male. Microscopy, Electron. Middle Aged. Prolactin / blood

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18211974.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminoquinolines; 0 / Dopamine Agonists; 0 / Receptors, Dopamine D2; 0 / Receptors, Somatostatin; 0 / somatostatin receptor sst2A; 12629-01-5 / Human Growth Hormone; 80Q9QWN15M / quinagolide; 9002-62-4 / Prolactin; RWM8CCW8GP / Octreotide
  •  go-up   go-down


82. Wang H, Wang MD, Ma WB, Yang D, Shi YF, Kong YG, Li SF, Li ZH, Wang RZ: [Expression of galectin-3 in invasive prolactinomas]. Zhongguo Yi Xue Ke Xue Yuan Xue Bao; 2005 Jun;27(3):380-1
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Expression of galectin-3 in invasive prolactinomas].
  • OBJECTIVE: To investigate the expression of galectin-3 (Gal-3) in prolactinomas.
  • METHODS: Expressions of Gal-3 were evaluated by immunohistochemistry using polyclonal antibody in 16 invasive prolactinomas and 16 prolactinomas.
  • RESULTS: Gal-3 was expressed both in invasive prolactinomas and noninvasive prolactinomas while significantly higher expression seen in the invasive prolactinomas (P < 0.05).
  • CONCLUSION: Gal-3 expression may be used as a useful indicator to determine the invasiveness and prognosis of prolactinomas.
  • [MeSH-major] Galectin 3 / biosynthesis. Pituitary Neoplasms / metabolism. Prolactinoma / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Female. Humans. Male. Middle Aged. Neoplasm Invasiveness. Prognosis

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16038281.001).
  • [ISSN] 1000-503X
  • [Journal-full-title] Zhongguo yi xue ke xue yuan xue bao. Acta Academiae Medicinae Sinicae
  • [ISO-abbreviation] Zhongguo Yi Xue Ke Xue Yuan Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Galectin 3
  •  go-up   go-down


83. Buchfelder M, Schlaffer S: Surgical treatment of pituitary tumours. Best Pract Res Clin Endocrinol Metab; 2009 Oct;23(5):677-92
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Surgical treatment of pituitary tumours.
  • The surgical treatment of pituitary tumours underwent considerable evolution during the past centennial.
  • To date, transsphenoidal surgery is the approach of choice for over 90% of pituitary tumours, but still transcranial operations are needed even in experienced hands when asymmetrical and large pituitary tumours with minor intrasellar components present.
  • Generally speaking, patients with non-functioning pituitary adenomas, acromegaly, thyrotropinomas and Cushing's disease are excellent candidates for primary surgical treatment.
  • In prolactinomas, the primary therapy is medical; however, when dopamine agonists are not well tolerated or inefficient, an operative treatment should be considered.
  • [MeSH-major] Adenoma / surgery. Neurosurgical Procedures / methods. Pituitary Neoplasms / surgery

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19945031.001).
  • [ISSN] 1878-1594
  • [Journal-full-title] Best practice & research. Clinical endocrinology & metabolism
  • [ISO-abbreviation] Best Pract. Res. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 59
  •  go-up   go-down


84. De Bellis A, Colao A, Pivonello R, Savoia A, Battaglia M, Ruocco G, Tirelli G, Lombardi G, Bellastella A, Bizzarro A: Antipituitary antibodies in idiopathic hyperprolactinemic patients. Ann N Y Acad Sci; 2007 Jun;1107:129-35
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • To clarify the possible autoimmune pituitary involvement in patients with apparently idiopathic hyperprolactinemia we investigated the presence of antipituitary antibodies (APA) in hyperprolactinemic patients with idiopathic hyperprolactinemia and in those with prolactinoma.
  • APA, by immunofluorescence method, and anterior pituitary function were evaluated in both groups of patients.
  • With regard to the function of other pituitary hormones, all APA-negative patients in group 1 and in group 2 showed a normal pituitary function; instead, a partial anterior pituitary impairment was observed in 6 out of 17 (35.3%) APA-positive patients.
  • [MeSH-major] Autoantibodies / immunology. Hyperprolactinemia / immunology. Pituitary Gland / immunology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17804540.001).
  • [ISSN] 0077-8923
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Autoantibodies
  •  go-up   go-down


85. Vourliotaki I, Bonapart IE, Stamataki C, Tsapakis EM, Saridaki C: A case of a prolactinoma resistant to dopamine agonists. Hormones (Athens); 2005 Jul-Sep;4(3):165-70
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A case of a prolactinoma resistant to dopamine agonists.
  • Dopamine agonists are the drugs of choice in the treatment of prolactinomas, the most common type of pituitary adenomas.
  • However, up to 25% of prolactinomas do not respond to these drugs and alternative treatments have to be considered.
  • We describe a 37-year old female with a microprolactinoma who, although having received all available formulations of dopamine agonists over a period of 11 years, did not respond either clinically--diminution of galactorrhea and restoration of her menstrual cycle--or hormonally through normalisation of the elevated prolactin levels.
  • Throughout the same period, the size of the adenoma remained unchanged.
  • [MeSH-major] Dopamine Agonists / therapeutic use. Drug Resistance, Neoplasm. Pituitary Neoplasms / drug therapy. Prolactinoma / drug therapy

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16613827.001).
  • [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 / Dopamine Agonists
  •  go-up   go-down


86. Karavitaki N, Thanabalasingham G, Shore HC, Trifanescu R, Ansorge O, Meston N, Turner HE, Wass JA: Do the limits of serum prolactin in disconnection hyperprolactinaemia need re-definition? A study of 226 patients with histologically verified non-functioning pituitary macroadenoma. Clin Endocrinol (Oxf); 2006 Oct;65(4):524-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Do the limits of serum prolactin in disconnection hyperprolactinaemia need re-definition? A study of 226 patients with histologically verified non-functioning pituitary macroadenoma.
  • BACKGROUND: The differentiation of a pituitary non-functioning macroadenoma from a macroprolactinoma is important for planning appropriate therapy.
  • Serum PRL levels have been suggested as a useful diagnostic indicator.
  • OBJECTIVE: We wished therefore, to investigate the serum PRL values in a large series of patients presenting with apparently non-functioning pituitary macroadenomas.
  • PATIENTS AND METHODS: All patients presenting to the Department of Endocrinology in Oxford with clinically non-functioning pituitary macroadenomas (later histologically verified) between 1990 and 2005 were studied.
  • Information documented in the notes on the medications and on the presence of conditions capable of affecting the serum PRL levels at the time of blood sampling was also collected.
  • RESULTS: Two hundred and twenty-six patients were identified (median age at diagnosis 55 years, range 18-88 years; 146 males/80 females; 143 gonadotroph, 46 null cell, 25 plurihormonal and 12 silent ACTH adenomas).
  • At the time of blood sampling 41 subjects were taking medications capable of increasing serum PRL.
  • The median serum PRL values in the total group were 386 mU/l (range 16-3257) (males: median 299 mU/l, range 16-1560; females: median 572 mU/l, range 20-3257) and in those not taking drugs capable of increasing serum PRL 363 mU/l (range 16-2565) (males: median 299 mU/l, range 16-1560; females: median 572 mU/l, range 20-2565).
  • Serum PRL < 2000 mU/l was found in 98.7% (223/226) of the total group and in 99.5% (184/185) of those not taking drugs.
  • Among the three subjects with serum PRL > 2000 mU/l, two were taking oestrogen preparations.
  • CONCLUSIONS: Based on a large series of histologically confirmed cases, serum PRL > 2000 mU/l is almost never encountered in nonfunctioning pituitary macroadenomas.
  • Values above this limit in the presence of a macroadenoma should not be surrounded by diagnostic uncertainty (after acromegaly or Cushing's disease have been excluded); a prolactinoma is the most likely diagnosis and a dopamine agonist should be considered as the treatment of choice.
  • [MeSH-major] Adenoma / blood. Biomarkers, Tumor / blood. Pituitary Neoplasms / blood. Prolactin / blood. Prolactinoma / blood
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Diagnosis, Differential. Female. Humans. Immunohistochemistry / methods. Male. Middle Aged. Reference Values. Statistics, Nonparametric

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • 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
  • (PMID = 16984247.001).
  • [ISSN] 0300-0664
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 9002-62-4 / Prolactin
  •  go-up   go-down


87. Bussade I, Naliato EC, Mendonça LM, Violante AH, Farias ML: [Decreased bone mineral density in pre-menopause women with prolactinoma]. Arq Bras Endocrinol Metabol; 2007 Dec;51(9):1522-7
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Decreased bone mineral density in pre-menopause women with prolactinoma].
  • [Transliterated title] Redução da densidade mineral óssea em mulheres na menacme com prolactinoma.
  • Bone mineral density (BMD) was measured by dual-energy RX absorptiometry in 24 patients with prolactinoma (15 macro and 9 micro adenomas; age range = 18 to 49 years).
  • No difference was found in densitometric parameters for the comparison between macro and microprolactinoma, or those with normal prolactin versus hyperprolactinemia.
  • CONCLUSIONS: Decreased bone mineral density was detected in 20.83% of our young patients with prolactinoma.
  • The great involvement of trabecular bone skeletal regions, such as vertebrae, suggests the participation of hypogonadism in the pathogenesis of bone disease.
  • Irrespective of prolactin levels, return to normal menses seems the best index of good control.
  • [MeSH-major] Bone Density / physiology. Hyperprolactinemia / physiopathology. Osteoporosis / physiopathology. Pituitary Neoplasms / physiopathology. Premenopause / physiology. Prolactinoma / physiopathology

  • MedlinePlus Health Information. consumer health - Bone Density.
  • MedlinePlus Health Information. consumer health - Osteoporosis.
  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18209896.001).
  • [ISSN] 0004-2730
  • [Journal-full-title] Arquivos brasileiros de endocrinologia e metabologia
  • [ISO-abbreviation] Arq Bras Endocrinol Metabol
  • [Language] por
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Brazil
  •  go-up   go-down


88. Colao A, Loche S: Prolactinomas in children and adolescents. Endocr Dev; 2010;17:146-59
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prolactinomas in children and adolescents.
  • Prolactinomas are the most common pituitary adenomas in children and adolescents followed by adrenocorticotropic hormone-secreting and growth hormone-secreting adenomas.
  • Diagnosis is generally based on clinical symptoms of primary or secondary gonadal failure, growth delay and/or tumor compressive symptoms.
  • Treatment is based on medical therapy with dopamine agonists, to control prolactin levels and reduce tumor size.
  • Surgery is indicated in patients with tumors resistant to dopamine agonists as well as in those showing severe neurological symptoms at diagnosis.
  • [MeSH-major] Pituitary Neoplasms / therapy. Prolactinoma / therapy

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 S. Karger AG, Basel.
  • (PMID = 19955764.001).
  • [ISSN] 1662-2979
  • [Journal-full-title] Endocrine development
  • [ISO-abbreviation] Endocr Dev
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Ergolines; LL60K9J05T / cabergoline
  •  go-up   go-down


89. Rosário PW, Purisch S: Biochemical acromegaly in patients with prolactinoma during treatment with dopaminergic agonists. Arq Bras Endocrinol Metabol; 2010 Aug;54(6):546-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Biochemical acromegaly in patients with prolactinoma during treatment with dopaminergic agonists.
  • OBJECTIVE: To evaluate the frequency of subclinical acromegaly (in the absence of clinical phenotype but biochemically uncontrolled) in patients with prolactinoma during treatment with dopaminergic agonists.
  • RESULTS: Initially, the laboratory diagnosis of acromegaly was unequivocal (elevated IGF-1 for gender and age with nadir GH > 1 μg/L) in two patients, and likely (elevated IGF-1 with nadir GH > cut-off but < 1 μg/L) in another patient.
  • In two other patients, this diagnosis was possible (normal IGF-1 with nadir GH > 1 μg/L).
  • Repetition of the tests 6 months after withdrawal of the dopaminergic agonist confirmed the diagnosis of subclinical acromegaly (elevated IGF-1 for gender and age with nadir GH > 1 μg/L) in these 5 patients.
  • CONCLUSION: In patients with prolactinomas, acromegaly should be investigated not only in cases with a clinical phenotype.
  • [MeSH-major] Acromegaly / diagnosis. Dopamine Agonists / therapeutic use. Pituitary Neoplasms / drug therapy. Prolactinoma / drug therapy

  • 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 = 20857059.001).
  • [ISSN] 1677-9487
  • [Journal-full-title] Arquivos brasileiros de endocrinologia e metabologia
  • [ISO-abbreviation] Arq Bras Endocrinol Metabol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Dopamine Agonists; 12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I
  •  go-up   go-down


90. Coiré CI, Smyth HS, Rosso D, Horvath E, Kovacs K: A double pituitary adenoma presenting as a prolactin-secreting tumor with partial response to medical therapy. Case report. Endocr Pathol; 2010 Jun;21(2):135-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A double pituitary adenoma presenting as a prolactin-secreting tumor with partial response to medical therapy. Case report.
  • Double pituitary adenomas are difficult to recognize pre-operatively as only a single mass may be appreciated on imaging.
  • We present herein a giant prolactin-secreting pituitary adenoma in a middle-aged man that had responded partially to dopamine agonist therapy.
  • The excised specimen demonstrated a double adenoma.
  • The prolactin-producing one displayed the expected morphological changes resulting from medical therapy, while the other, a gonadotroph adenoma, did not.
  • The failure of tumor shrinkage can be attributed to the presence of a double adenoma, a previously unreported cause of failure of medical therapy in prolactinoma.
  • [MeSH-major] Adenoma / pathology. Gonadotrophs / pathology. Neoplasms, Multiple Primary / pathology. Prolactinoma / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Endocr Pathol. 2005 Fall;16(3):187-94 [16299401.001]
  • [Cites] J Neurosurg. 2000 Feb;92(2):361 [10659029.001]
  • [Cites] Pathology. 2002 Feb;34(1):57-60 [11902447.001]
  • [Cites] Virchows Arch A Pathol Anat Histopathol. 1991;418(5):439-46 [2035258.001]
  • [Cites] Pituitary. 2000 Nov;3(3):159-68 [11383480.001]
  • [Cites] Magn Reson Imaging. 1999 May;17(4):633-6 [10231191.001]
  • [Cites] Treat Endocrinol. 2003;2(1):23-32 [15871552.001]
  • [Cites] J Endocrinol Invest. 2000 Jan;23(1):37-41 [10698050.001]
  • [Cites] Clin Endocrinol (Oxf). 2004 Jul;61(1):26-30 [15212641.001]
  • [Cites] J Neurosurg. 1991 Feb;74(2):243-7 [1988594.001]
  • [Cites] Pituitary. 1999 May;1(3-4):243-50 [11081204.001]
  • [Cites] Nat Clin Pract Endocrinol Metab. 2006 Apr;2(4):200-10 [16932285.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Sep;85(9):3053-7 [10999785.001]
  • [Cites] J Neurosurg. 2000 Nov;93(5):753-61 [11059654.001]
  • [Cites] Neurosurgery. 1992 Nov;31(5):840-9; discussion 849 [1331847.001]
  • [Cites] Neurol Med Chir (Tokyo). 1996 Nov;36(11):818-21 [9420436.001]
  • [Cites] Eur J Endocrinol. 2006 May;154(5):753-8 [16645024.001]
  • (PMID = 20058099.001).
  • [ISSN] 1559-0097
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Ergolines; LL60K9J05T / cabergoline
  •  go-up   go-down


91. Larner AJ: Headache induced by dopamine agonists prescribed for prolactinoma: think SUNCT! Int J Clin Pract; 2006 Mar;60(3):360-1
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Headache induced by dopamine agonists prescribed for prolactinoma: think SUNCT!
  • Short-lasting unilateral neuralgiform headache with conjunctival injection and tearing (SUNCT) syndrome may be associated with pituitary prolactinoma and may be induced by treatment of prolactinoma with dopamine agonists.
  • Endocrinologists treating patients with prolactinoma need to be aware of this syndrome as its pathophysiology and treatment differ from that of other headache syndromes.
  • [MeSH-major] Dopamine Agonists / adverse effects. Ergolines / adverse effects. Headache / chemically induced. Prolactinoma / drug therapy

  • Genetic Alliance. consumer health - SUNCT headache.
  • MedlinePlus Health Information. consumer health - Headache.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16494654.001).
  • [ISSN] 1368-5031
  • [Journal-full-title] International journal of clinical practice
  • [ISO-abbreviation] Int. J. Clin. Pract.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Dopamine Agonists; 0 / Ergolines; LL60K9J05T / cabergoline
  •  go-up   go-down


92. Pollock BE, Brown PD, Nippoldt TB, Young WF Jr: Pituitary tumor type affects the chance of biochemical remission after radiosurgery of hormone-secreting pituitary adenomas. Neurosurgery; 2008 Jun;62(6):1271-6; discussion 1276-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pituitary tumor type affects the chance of biochemical remission after radiosurgery of hormone-secreting pituitary adenomas.
  • OBJECTIVE: Reported biochemical remission rates have ranged widely after stereotactic radiosurgery for patients with hormone-secreting pituitary adenomas.
  • Confounding variables include histology, radiation dose, use of pituitary-suppressive medications, and length of follow-up.
  • METHODS: A retrospective review of 46 patients with pituitary adenomas (growth hormone-secreting, n = 27; prolactin-secreting, n = 11; adrenocorticotropin-secreting, n = 8) undergoing radiosurgery between January 1990 and December 2003 was conducted.
  • All received a tumor margin dose of 18 Gy or more and were off pituitary-suppressive medications for at least 1 month before radiosurgery.
  • RESULTS: The 4-year remission rates were 87% for patients with Cushing's disease, 67% for patients with acromegaly, and 18% for patients with prolactinomas.
  • Patients with oversecretion of adrenocorticotropin or growth hormone were more likely to achieve remission after radiosurgery than patients with prolactinomas (hazard ratio, 4.4; 95% confidence interval, 1.1-18.2; P = 0.04).
  • Of 44 patients with normal or partial anterior pituitary function before radiosurgery, 16 (36%) developed one or more new anterior pituitary deficits.
  • The incidence of new anterior pituitary deficits was 26% at 4 years.
  • CONCLUSION: There seems to be a differential sensitivity after radiosurgery for hormone-secreting pituitary adenomas.
  • Remission rates are greater for patients with Cushing's disease and acromegaly, whereas radiosurgery is less effective in achieving biochemical remission for patients with prolactinomas.
  • [MeSH-major] Adenoma / metabolism. Adenoma / surgery. Pituitary Hormones / metabolism. Pituitary Neoplasms / metabolism. Pituitary Neoplasms / surgery. Radiosurgery

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Neurosurgery. 2010 May;66(5):E1030; author reply E1030 [20404679.001]
  • (PMID = 18824993.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Pituitary Hormones
  •  go-up   go-down


93. Quentien MH, Barlier A, Franc JL, Pellegrini I, Brue T, Enjalbert A: Pituitary transcription factors: from congenital deficiencies to gene therapy. J Neuroendocrinol; 2006 Sep;18(9):633-42
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pituitary transcription factors: from congenital deficiencies to gene therapy.
  • Despite the existence of interspecies phenotypic variability, animal models have yielded valuable insights into human pituitary diseases.
  • Studies on Snell and Jackson mice known to have growth hormone, prolactin and thyroid-stimulating hormone deficiencies involving the hypoplastic pituitary gland have led to identifying alterations of the pituitary specific POU homeodomain Pit-1 transcription factor gene.
  • Terminal differentiation of lactotroph cells and direct regulation of the prolactin gene both require interactions between Pit-1 and cell type specific partners, including panpituitary transcriptional regulators such as Pitx1 and Pitx2.
  • Synergistic activation of the prolactin promoter by Pitx factors and Pit-1 is involved not only in basal condition, but also in responsiveness to forskolin, thyrotrophin-releasing-hormone and epidermal growth factor.
  • This finding supports the idea that Tpit plays an essential role in the differentiation of the pro-opiomelanocortin pituitary lineage.
  • The effects of Pit-1 are not restricted to hormone gene regulation because this factor also contributes to cell division and protects the cell from programmed cell death.
  • Lentiviral vectors expressing a Pit-1 dominant negative mutant induced time- and dose-dependent cell death in somatotroph and lactotroph adenomas in vitro.
  • Gene transfer by lentiviral vectors should provide a promising step towards developing an efficient specific therapeutic approach by which a gene therapy programme for treating human pituitary adenomas could be based.
  • [MeSH-major] Gene Expression Regulation / physiology. Genetic Therapy. Pituitary Diseases / genetics. Pituitary Gland, Anterior / metabolism. Pituitary Hormones / metabolism. Transcription Factor Pit-1 / metabolism
  • [MeSH-minor] Animals. Gene Transfer Techniques. Growth Hormone / metabolism. Homeodomain Proteins / genetics. Homeodomain Proteins / metabolism. Humans. Mice, Neurologic Mutants. Mutation / genetics. Pituitary Neoplasms / genetics. Pituitary Neoplasms / physiopathology. Pituitary Neoplasms / therapy. Prolactin / metabolism. T-Box Domain Proteins. Thyrotropin / metabolism. Transcription Factors / genetics. Transcription Factors / metabolism

  • MedlinePlus Health Information. consumer health - Genes and Gene Therapy.
  • MedlinePlus Health Information. consumer health - Pituitary Disorders.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16879162.001).
  • [ISSN] 0953-8194
  • [Journal-full-title] Journal of neuroendocrinology
  • [ISO-abbreviation] J. Neuroendocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Pituitary Hormones; 0 / T-Box Domain Proteins; 0 / TBX19 protein, human; 0 / Transcription Factor Pit-1; 0 / Transcription Factors; 184787-43-7 / homeobox protein PITX2; 9002-62-4 / Prolactin; 9002-71-5 / Thyrotropin; 9002-72-6 / Growth Hormone
  • [Number-of-references] 98
  •  go-up   go-down


94. Salehi F, Kovacs K, Scheithauer BW, Cantelmi D, Horvath E, Lloyd RV, Cusimano M: Immunohistochemical expression of pituitary tumor transforming gene (PTTG) in pituitary adenomas: a correlative study of tumor subtypes. Int J Surg Pathol; 2010 Feb;18(1):5-13
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunohistochemical expression of pituitary tumor transforming gene (PTTG) in pituitary adenomas: a correlative study of tumor subtypes.
  • OBJECTIVE: We investigated the correlation between immunohistochemical expression of the pituitary tumor transforming gene (PTTG) and pituitary adenoma subtype.
  • METHODS: Pituitary adenomas (n = 89) were stained for PTTG using the streptavidin-biotin-peroxidase complex method and a monoclonal PTTG antibody.
  • Reactivity was highest in growth hormone (GH) adenomas as compared with other tumors, including prolactin (PRL), follicle-stimulating hormone/luteinizing hormone/alpha subunit, as well as adrenocorticotrophic hormone-secreting adenomas.
  • PRL adenomas exhibited the lowest expression levels.
  • Among GH adenomas, untreated tumors demonstrated significantly higher PTTG levels than octreotide-treated examples.
  • Although dopamine agonist-treated PRL adenomas tended to show lower expression levels, statistical significance was not reached.
  • CONCLUSIONS: Our finding that PTTG was differentially expressed in pituitary adenoma subtypes suggests a cell-specific function for PTTG.
  • Moreover, treatment of GH adenomas with somatostatin analogues lowered PTTG expression.
  • Further investigation into mechanisms mediating cell-specific expression of PTTG is warranted.
  • [MeSH-major] Neoplasm Proteins / metabolism. Pituitary Neoplasms / metabolism

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20106827.001).
  • [ISSN] 1940-2465
  • [Journal-full-title] International journal of surgical pathology
  • [ISO-abbreviation] Int. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Biomarkers, Tumor; 0 / Hormone Antagonists; 0 / Neoplasm Proteins; 0 / Securin; 0 / pituitary tumor-transforming protein 1, human; 3A64E3G5ZO / Bromocriptine; RWM8CCW8GP / Octreotide
  •  go-up   go-down


95. López-Arbolay O, Morales-Sabina O, González-González JL, Valdés-Lorenzo N: [Transsphenoidal approach to prolactinomas]. Neurocirugia (Astur); 2006 Jun;17(3):226-31
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Transsphenoidal approach to prolactinomas].
  • [Transliterated title] Cirugia transeptoesfenoidal en adenomas hipofisarios productores de prolactina.
  • INTRODUCTION: Transeptal transsphenoidal surgery for pituitary tumors is a well established surgical technique.
  • In particular the use of medical treatment in patient with prolactinomas has induced the control of hiperprolactinemia and the shrinkage of the tumor in the great majority of the patients, for that reason the treatment of the prolactinomas is controversial.
  • OBJECTIVE: We evaluate the results of transsphenoidal microsurgical treatment of prolactin secreting adenomas at our Unit.
  • METHODS: We made a retrospective analysis of 63 patients operated on via transsphenoidal microsurgical technique for prolactin secreting adenomas between 1996 and 2003.
  • Prolactin levels were reduced to non tumoral values in 90.6% of microadenomas (29 cases) and in 67.7% of macroadenomas (21 cases).
  • CONCLUSIONS: Transsphenoidal adenomectomy is a safe treatment option for patients with prolactin secreting adenomas with surgical indication.
  • [MeSH-major] Hyperprolactinemia / surgery. Neurosurgical Procedures / methods. Pituitary Neoplasms / surgery. Prolactinoma / surgery. Sphenoid Bone / surgery

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16855780.001).
  • [ISSN] 1130-1473
  • [Journal-full-title] Neurocirugía (Asturias, Spain)
  • [ISO-abbreviation] Neurocirugia (Astur)
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Spain
  •  go-up   go-down


96. Fedele M, Visone R, De Martino I, Troncone G, Palmieri D, Battista S, Ciarmiello A, Pallante P, Arra C, Melillo RM, Helin K, Croce CM, Fusco A: HMGA2 induces pituitary tumorigenesis by enhancing E2F1 activity. Cancer Cell; 2006 Jun;9(6):459-71
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HMGA2 induces pituitary tumorigenesis by enhancing E2F1 activity.
  • HMGA2 gene amplification and overexpression in human prolactinomas and the development of pituitary adenomas in HMGA2 transgenic mice showed that HMGA2 plays a crucial role in pituitary tumorigenesis.
  • Here we show that HMGA2 interacts with pRB and induces E2F1 activity in mouse pituitary adenomas by displacing HDAC1 from the pRB/E2F1 complex-a process that results in E2F1 acetylation.
  • We found that loss of E2F1 function (obtained by mating HMGA2 and E2F1(-/-) mice) suppressed pituitary tumorigenesis in HMGA2 mice.
  • Thus, HMGA2-mediated E2F1 activation is a crucial event in the onset of these tumors in transgenic mice and probably also in human prolactinomas.
  • [MeSH-major] E2F1 Transcription Factor / physiology. HMGA2 Protein / physiology. Pituitary Neoplasms / metabolism
  • [MeSH-minor] Acetylation. Animals. Cell Line. Cell Proliferation. Cell Transformation, Neoplastic. DNA / metabolism. Enzyme Activation. Histone Deacetylase 1. Histone Deacetylases / metabolism. Histones / metabolism. Humans. Mice. Mice, Knockout. Mice, Mutant Strains. Mice, Transgenic. Promoter Regions, Genetic. Protein Binding. Response Elements. Retinoblastoma Protein / metabolism. Signal Transduction


97. Levy MJ, Matharu MS, Meeran K, Powell M, Goadsby PJ: The clinical characteristics of headache in patients with pituitary tumours. Brain; 2005 Aug;128(Pt 8):1921-30
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The clinical characteristics of headache in patients with pituitary tumours.
  • The clinical characteristics of 84 patients with pituitary tumour who had troublesome headache were investigated.
  • SUNCT-like headache was only seen in patients with acromegaly and prolactinoma.
  • Headache appears to be a significant problem in pituitary disease and is associated with a range of headache phenotypes.
  • A proposed modification of the current classification of pituitary-associated headache is given.
  • [MeSH-major] Adenoma / physiopathology. Headache / physiopathology. Pituitary Neoplasms / physiopathology. Somatostatin / analogs & derivatives

  • MedlinePlus Health Information. consumer health - Headache.
  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15888539.001).
  • [ISSN] 1460-2156
  • [Journal-full-title] Brain : a journal of neurology
  • [ISO-abbreviation] Brain
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoquinolines; 0 / Antineoplastic Agents, Hormonal; 0 / Dopamine Agonists; 0 / Ergolines; 0 / Peptides, Cyclic; 118992-92-0 / lanreotide; 3A64E3G5ZO / Bromocriptine; 51110-01-1 / Somatostatin; 80Q9QWN15M / quinagolide; LL60K9J05T / cabergoline; RWM8CCW8GP / Octreotide
  •  go-up   go-down


98. Kars M, Delgado V, Holman ER, Feelders RA, Smit JW, Romijn JA, Bax JJ, Pereira AM: Aortic valve calcification and mild tricuspid regurgitation but no clinical heart disease after 8 years of dopamine agonist therapy for prolactinoma. J Clin Endocrinol Metab; 2008 Sep;93(9):3348-56
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aortic valve calcification and mild tricuspid regurgitation but no clinical heart disease after 8 years of dopamine agonist therapy for prolactinoma.
  • OBJECTIVE: Treatment with ergot-derived dopamine agonists, pergolide, and cabergoline has been associated with an increased frequency of valvular heart disease in Parkinson's disease.
  • The aim of the present study was to assess the prevalence of valvular heart disease in patients treated with dopamine agonists for prolactinomas.
  • PATIENTS: We performed two-dimensional and Doppler echocardiography in 78 consecutive patients with prolactinoma (mean age 47 +/- 1.4 yr, 26% male, 31% macroprolactinoma) treated with dopamine agonists for at least 1 yr (mean 8 +/- 0.6 yr) and 78 control subjects.
  • RESULTS: Clinically relevant valvular heart disease was present in 12% of patients (nine of 78) vs. 17% of controls (13 of 78) (P = 0.141) and 17% (eight of 47) of patients treated with cabergoline vs. 3% (one of 31) of patients not treated with cabergoline (P = 0.062).
  • CONCLUSION: Several years of dopamine agonist treatment in patients with prolactinomas is associated with increased prevalence of aortic valve calcification and mild tricuspid regurgitation but not with clinically relevant valvular heart disease.
  • Therefore, additional studies on the adverse cardiac effects of dopaminergic drugs in prolactinoma are warranted, especially in patients with much longer use of these drugs.
  • [MeSH-major] Calcinosis / chemically induced. Dopamine Agonists / adverse effects. Dopamine Agonists / therapeutic use. Heart Valve Diseases / chemically induced. Pituitary Neoplasms / drug therapy. Prolactinoma / drug therapy. Tricuspid Valve Insufficiency / chemically induced
  • [MeSH-minor] Adult. Aortic Valve / drug effects. Aortic Valve / pathology. Case-Control Studies. Cross-Sectional Studies. Disease Progression. Ergolines / adverse effects. Ergolines / therapeutic use. Female. Humans. Male. Middle Aged. Prevalence. Time Factors

  • Genetic Alliance. consumer health - Heart Disease.
  • MedlinePlus Health Information. consumer health - Heart Valve Diseases.
  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18559921.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dopamine Agonists; 0 / Ergolines; LL60K9J05T / cabergoline
  •  go-up   go-down


99. Ren SG, Melmed S: Pyridoxal phosphate inhibits pituitary cell proliferation and hormone secretion. Endocrinology; 2006 Aug;147(8):3936-42
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pyridoxal phosphate inhibits pituitary cell proliferation and hormone secretion.
  • Pyridoxal phosphate (PLP), a bioactive form of pyridoxine, dose-dependently (10-1000 microm) inhibited cell proliferation in rat pituitary MMQ and GH3 cells and in mouse AtT-20 cells.
  • After 4 d, MMQ cell numbers were reduced by up to 81%, GH3 cell numbers were reduced by up to 64% (P < 0.05), and AtT-20 cell numbers were reduced by up to 90%.
  • Cell proliferation rates recovered and dose-dependently reverted to control levels after PLP withdrawal.
  • PLP (400-1000 microm) reduced GH3 cell GH and prolactin secretion and AtT-20 cell ACTH secretion (adjusted for cell number) by approximately 70% after 2 d.
  • The 100 microm PLP also inhibited prolactin secretion (65%, P < 0.05) in primary rat pituitary cells treated for 2 d.
  • Furthermore, PLP induced AtT-20 and GH3 cell apoptosis (28 vs. 6, P < 0.05; 26 vs. 3, P < 0.05, respectively) and dose-dependently reduced content of the antiapoptosis gene Bcl-2.
  • These results indicate that pharmacological doses of PLP inhibit pituitary cell proliferation and hormone secretion, in part mediated through PLP-induced cell-cycle arrest and apoptosis.
  • Pyridoxine may therefore be appropriate for testing as a relatively safe drug for adjuvant treatment of hormone-secreting pituitary adenomas.

  • MedlinePlus Health Information. consumer health - B Vitamins.
  • 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).
  • 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
  • [Cites] J Natl Cancer Inst. 1987 May;78(5):951-9 [3472003.001]
  • [Cites] Am J Clin Nutr. 1987 Oct;46(4):659-64 [3499066.001]
  • [Cites] Anticancer Res. 1988 Nov-Dec;8(6):1313-8 [3218963.001]
  • [Cites] J Clin Lab Anal. 1989;3(2):95-100 [2732845.001]
  • [Cites] J Biol Chem. 1990 Jul 25;265(21):12424-33 [2373699.001]
  • [Cites] J Biol Chem. 1992 Feb 25;267(6):3819-24 [1310983.001]
  • [Cites] J Nutr. 1995 Sep;125(9):2370-8 [7666255.001]
  • [Cites] Recent Prog Horm Res. 1996;51:189-215; discussion 215-6 [8701079.001]
  • [Cites] J Clin Invest. 1997 Feb 15;99(4):789-98 [9045884.001]
  • [Cites] Endocr Rev. 1997 Apr;18(2):206-28 [9101137.001]
  • [Cites] Nutr Cancer. 1997;28(2):206-11 [9290129.001]
  • [Cites] J Clin Invest. 1997 Nov 1;100(9):2386-92 [9410919.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Apr;83(4):1275-83 [9543156.001]
  • [Cites] J Natl Cancer Inst. 2005 May 4;97(9):684-92 [15870439.001]
  • [Cites] Oncol Rep. 2005 Jul;14(1):265-9 [15944799.001]
  • [Cites] J Nutr. 2001 Aug;131(8):2204-7 [11481418.001]
  • [Cites] Endocrinology. 2001 Sep;142(9):3756-63 [11517151.001]
  • [Cites] Nutr Cancer. 2000;38(2):281-6 [11525607.001]
  • [Cites] Neoplasma. 2001;48(4):307-12 [11712684.001]
  • [Cites] J Steroid Biochem. 1986 Sep;25(3):359-65 [3773514.001]
  • [Cites] Nutr Cancer. 1985;7(1-2):43-52 [4070008.001]
  • [Cites] Neurology. 1985 Oct;35(10):1466-8 [2993949.001]
  • [Cites] JAMA. 2002 Jun 19;287(23):3116-26 [12069675.001]
  • [Cites] Urol Clin North Am. 2002 Feb;29(1):157-68 [12109342.001]
  • [Cites] J Nutr. 2002 Nov;132(11):3308-13 [12421844.001]
  • [Cites] Int J Oncol. 2003 Mar;22(3):499-508 [12579301.001]
  • [Cites] Nutr Cancer. 2002;43(2):152-8 [12588695.001]
  • [Cites] J Natl Cancer Inst. 2003 Mar 5;95(5):373-80 [12618502.001]
  • [Cites] Biochim Biophys Acta. 2003 Apr 11;1647(1-2):127-30 [12686121.001]
  • [Cites] Cancer Causes Control. 2003 Jun;14(5):477-84 [12946043.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2003 Nov;12(11 Pt 1):1271-2 [14652294.001]
  • [Cites] Am J Clin Nutr. 2004 May;79(5):805-11 [15113718.001]
  • [Cites] Int J Mol Med. 2004 Nov;14(5):819-23 [15492851.001]
  • [Cites] J Clin Endocrinol Metab. 1975 Feb;40(2):256-9 [1117978.001]
  • [Cites] J Clin Endocrinol Metab. 1976 Mar;42(3):603-6 [1254699.001]
  • [Cites] J Clin Endocrinol Metab. 1977 Jun;44(6):1197-9 [559690.001]
  • [Cites] Biomedicine. 1977 Jul;27(6):219-22 [20170.001]
  • [Cites] Biomedicine. 1978 Feb;29(1):13-5 [667280.001]
  • [Cites] Acta Endocrinol (Copenh). 1978 Oct;89(2):217-20 [358720.001]
  • [Cites] J Endocrinol Invest. 1979 Apr-Jun;2(2):117-24 [573769.001]
  • [Cites] J Clin Invest. 1980 Oct;66(4):688-95 [7419716.001]
  • [Cites] J Clin Endocrinol Metab. 1982 Apr;54(4):872-5 [6801073.001]
  • [Cites] N Engl J Med. 1982 Aug 12;307(7):444-5 [7088124.001]
  • [Cites] J Inorg Biochem. 1982 Nov;17(3):185-203 [6757388.001]
  • [Cites] J Clin Endocrinol Metab. 1978 Sep;47(3):689-90 [263321.001]
  • [Cites] N Engl J Med. 1983 Aug 25;309(8):445-8 [6308447.001]
  • [Cites] Horm Metab Res. 1985 Jan;17(1):46-7 [3967846.001]
  • (PMID = 16690808.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [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, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-bcl-2; 12001-76-2 / Vitamin B Complex; 5V5IOJ8338 / Pyridoxal Phosphate; 9002-62-4 / Prolactin; 9002-72-6 / Growth Hormone
  • [Other-IDs] NLM/ NIHMS10630; NLM/ PMC1513048
  •  go-up   go-down


100. Molino C, Fabbian F, Russo G, Cantelli S, Bortot A, Galdi A, Catizone L: [MEN type 1 and chronic renal failure: a rarely reported association]. G Ital Nefrol; 2007 Jan-Feb;24(1):79-82
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Multiple endocrine neoplasia type 1 (MEN 1), or Wermer's syndrome, is a rare autosomal dominant genetic syndrome characterized by tumors or hyperplasia involving the pituitary, parathyroid, and pancreatic islet cells.
  • CASE: A 70-year-old Caucasian female patient had a history of primitive hyperparathyroidism, prolactinoma, glucagonoma, adrenal adenoma and pulmonary neuroendocrine neoplasia.
  • Moreover, hyperparathyroidism in MEN 1 is clinically similar to the kidney failure condition; indeed, diffuse hyper-plasia of more than one gland is common.

  • MedlinePlus Health Information. consumer health - Kidney Failure.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17342698.001).
  • [ISSN] 0393-5590
  • [Journal-full-title] Giornale italiano di nefrologia : organo ufficiale della Società italiana di nefrologia
  • [ISO-abbreviation] G Ital Nefrol
  • [Language] ita
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Italy
  •  go-up   go-down






Advertisement