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1. Jiménez Caballero PE: SUNCT syndrome in a patient with prolactinoma and cabergoline-induced attacks. Cephalalgia; 2007 Jan;27(1):76-8
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  • [Title] SUNCT syndrome in a patient with prolactinoma and cabergoline-induced attacks.
  • We report a patient with prolactinoma and cabergoline-induced SUNCT attacks and the literature is reviewed for a better understanding of the pathophysiology.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Ergolines / adverse effects. Pituitary Neoplasms / drug therapy. Prolactinoma / drug therapy. SUNCT Syndrome / chemically induced. SUNCT Syndrome / diagnosis

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  • (PMID = 17212687.001).
  • [ISSN] 0333-1024
  • [Journal-full-title] Cephalalgia : an international journal of headache
  • [ISO-abbreviation] Cephalalgia
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Ergolines; LL60K9J05T / cabergoline
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2. Evans CO, Moreno CS, Zhan X, McCabe MT, Vertino PM, Desiderio DM, Oyesiku NM: Molecular pathogenesis of human prolactinomas identified by gene expression profiling, RT-qPCR, and proteomic analyses. Pituitary; 2008;11(3):231-45
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  • [Title] Molecular pathogenesis of human prolactinomas identified by gene expression profiling, RT-qPCR, and proteomic analyses.
  • The molecular pathogenesis of prolactinomas has resisted elucidation; with the exception of a RAS mutation in a single aggressive prolactinoma, no mutational changes have been identified.
  • In prolactinomas, a further obstacle has been the paucity of surgical specimens suitable for molecular analysis since prolactionomas are infrequently removed due to the availability and effectiveness of medical therapy.
  • Using high-throughput analysis from a large bank of human pituitary adenomas, we examined these tumors according to their molecular profiles rather than traditional immunohistochemistry.
  • We examined six prolactinomas and eight normal pituitary glands using oligonucleotide GeneChip microarrays, reverse transcription-real time quantitative polymerase chain reaction using 10 prolactinomas, and proteomic analysis to examine protein expression in four prolactinomas.
  • Microarray analyses identified 726 unique genes that were statistically significantly different between prolactinomas and normal glands, whereas proteomic analysis identified four differently up-regulated and 19 down-regulated proteins.
  • Several components of the Notch pathway were altered in prolactinomas, and there was an increased expression of the Pit-1 transcription factor, and the survival factor BAG1 but decreased E-cadherin and N-cadherin expression.
  • Taken together, expression profiling and proteomic analyses have identified molecular features unique to prolactinomas that may contribute to their pathogenesis.
  • In the current era of molecular medicine, these findings greatly enhance our understanding and supercede immunohistochemical diagnosis.
  • [MeSH-major] Adenoma / diagnosis. Gene Expression Profiling. Molecular Diagnostic Techniques. Oligonucleotide Array Sequence Analysis. Pituitary Neoplasms / diagnosis. Prolactinoma / diagnosis. Proteomics. Reverse Transcriptase Polymerase Chain Reaction
  • [MeSH-minor] Adult. Cluster Analysis. DNA, Neoplasm / analysis. Female. Gene Expression Regulation, Neoplastic. Humans. Male. Middle Aged. Neoplasm Proteins / analysis. RNA, Neoplasm / analysis. Reproducibility of Results

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  • (PMID = 18183490.001).
  • [ISSN] 1386-341X
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 2R01-CA077337; United States / NCI NIH HHS / CA / K22-CA96560; United States / NINDS NIH HHS / NS / NS 42843; United States / NCI NIH HHS / CA / R01-CA106826; United States / NCRR NIH HHS / RR / RR-10522; United States / NCRR NIH HHS / RR / RR-14593
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Neoplasm Proteins; 0 / RNA, Neoplasm
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3. Trivedi P, Gupta A, Pasricha S, Patel D: Malignant prolactinoma: a rare case report. Neurol India; 2010 Sep-Oct;58(5):778-80
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  • [Title] Malignant prolactinoma: a rare case report.
  • Pituitary carcinomas are rare adenohypophyseal tumors with cerebrospinal or extracranial metastasis.
  • None of the histologic findings distinguish pituitary adenoma from carcinoma.
  • We describe clinico-pathological and immunohistological features of malignant prolactinoma.
  • The patient initially presented with a prolactin-secreting pituitary adenoma.
  • MIB-1 and p53 labeling indices were also compared in primary adenoma, recurrent invasive adenoma and metastatic tumor.
  • [MeSH-major] Carcinoma / pathology. Pituitary Neoplasms / pathology. Prolactinoma / pathology. Spinal Neoplasms / secondary

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  • (PMID = 21045511.001).
  • [ISSN] 0028-3886
  • [Journal-full-title] Neurology India
  • [ISO-abbreviation] Neurol India
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Antibodies, Antinuclear; 0 / Antibodies, Monoclonal; 0 / MIB-1 antibody; 0 / Tumor Suppressor Protein p53
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4. Hoffer ZS, Roth RL, Mathews M: Evidence for the partial dopamine-receptor agonist aripiprazole as a first-line treatment of psychosis in patients with iatrogenic or tumorogenic hyperprolactinemia. Psychosomatics; 2009 Jul-Aug;50(4):317-24
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  • BACKGROUND: Antipsychotic drugs have many side effects, including elevation of prolactin levels through tuberoinfundibular dopamine-receptor blockade.
  • Although a number of studies claim that aripiprazole is a prolactin-sparing antipsychotic drug that may even lower prolactin levels, there has not been an exhaustive evaluation of this claim.
  • METHOD: The authors conducted a literature search for case studies, reports, and placebo-controlled trials that measured prolactin levels in adult patients taking aripiprazole.
  • RESULTS: The search identified 17 studies, in which 3,489 psychotic patients were given aripiprazole alone, as an adjuvant to haloperidol or risperidone, or to treat psychosis with a concomitant prolactinoma.
  • Across all studies, aripiprazole lowered prolactin levels an average of 74.3%, even in psychotic patients with prolactinoma, whereas haloperidol and risperidone increased prolactin levels by as much as 272%.
  • CONCLUSION: These findings suggest that aripiprazole may play an important niche role in treating psychotic patients sensitive to elevated prolactin and patients with prolactin-secreting pituitary tumors.

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  • (PMID = 19687170.001).
  • [ISSN] 1545-7206
  • [Journal-full-title] Psychosomatics
  • [ISO-abbreviation] Psychosomatics
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antipsychotic Agents; 0 / Dopamine Antagonists; 0 / Piperazines; 0 / Quinolones; 82VFR53I78 / Aripiprazole; J6292F8L3D / Haloperidol; L6UH7ZF8HC / Risperidone
  • [Number-of-references] 39
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5. Bulayeva NN, Wozniak AL, Lash LL, Watson CS: Mechanisms of membrane estrogen receptor-alpha-mediated rapid stimulation of Ca2+ levels and prolactin release in a pituitary cell line. Am J Physiol Endocrinol Metab; 2005 Feb;288(2):E388-97
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  • [Title] Mechanisms of membrane estrogen receptor-alpha-mediated rapid stimulation of Ca2+ levels and prolactin release in a pituitary cell line.
  • The role of membrane estrogen receptor-alpha (mERalpha) in rapid nongenomic responses to 17beta-estradiol (E(2)) was tested in sublines of GH3/B6 rat prolactinoma cells selected for high (GH3/B6/F10) and low (GH3/B6/D9) mERalpha expression.
  • [Ca(2+)](i) elevation was correlated with prolactin (PRL) release in the F10 cell line in as little as 3 min.
  • E(2) caused a much higher PRL release than KCl treatment (which caused maximal Ca(2+) elevation), suggesting that secretion was also controlled by additional mechanisms.
  • Participation of mERalpha in these effects was confirmed by the ability of E(2)-peroxidase (a cell-impermeable analog of E(2)) to cause these responses, blockage of the responses with the ER antagonist ICI 182 780, and the inability of the E(2) stereoisomer 17alpha-E(2) to elicit a response.
  • Thus rapid exocytosis of PRL is regulated in these cells by mERalpha signaling to specific Ca(2+) channels utilizing extracellular Ca(2+) sources and additional signaling mechanisms.
  • [MeSH-major] Calcium / metabolism. Calcium Signaling. Cell Membrane / metabolism. Estrogen Receptor alpha / metabolism. Pituitary Neoplasms / metabolism. Prolactin / pharmacokinetics. Prolactinoma / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Dose-Response Relationship, Drug. Estradiol / pharmacology. Nifedipine / pharmacology. Rats

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  • (PMID = 15494610.001).
  • [ISSN] 0193-1849
  • [Journal-full-title] American journal of physiology. Endocrinology and metabolism
  • [ISO-abbreviation] Am. J. Physiol. Endocrinol. Metab.
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / ES 010987; United States / NIEHS NIH HHS / ES / R01 ES010987-02; United States / NIEHS NIH HHS / ES / R01 ES010987-03
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Estrogen Receptor alpha; 4TI98Z838E / Estradiol; 9002-62-4 / Prolactin; I9ZF7L6G2L / Nifedipine; SY7Q814VUP / Calcium
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6. Elston MS, Gill AJ, Conaglen JV, Clarkson A, Cook RJ, Little NS, Robinson BG, Clifton-Bligh RJ, McDonald KL: Nuclear accumulation of e-cadherin correlates with loss of cytoplasmic membrane staining and invasion in pituitary adenomas. J Clin Endocrinol Metab; 2009 Apr;94(4):1436-42
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  • [Title] Nuclear accumulation of e-cadherin correlates with loss of cytoplasmic membrane staining and invasion in pituitary adenomas.
  • CONTEXT: Loss of the cell adhesion protein E-cadherin is associated with invasion and metastasis in a number of malignancies.
  • Recent studies have highlighted that loss of E-cadherin cell membrane expression may be accompanied by its detection in the nucleus, suggesting cellular redistribution during neoplasia.
  • Pituitary tumors, although typically benign, may be locally invasive, and loss of membranous E-cadherin has been reported as a marker of invasion in prolactinomas.
  • OBJECTIVE: Our objective was to study E-cadherin expression in pituitary adenomas, specifically whether nuclear redistribution occurs in this setting.
  • RESULTS: Strong cytoplasmic membrane staining was present in all eight normal samples but completely absent in 21 of 44 adenomas (48%) with weak staining in an additional 11 adenomas using an antibody against the extracellular domain of E-cadherin.
  • Nuclear staining was present in 38 of 44 adenomas (86%) and absent in normal tissue.
  • CONCLUSIONS: E-cadherin was frequently lost at the cytoplasmic membrane but detected in the nucleus, suggesting that cleavage of the extracellular domain and nuclear translocation of E-cadherin is a common event that may determine local invasion in pituitary adenomas.
  • [MeSH-major] Cadherins / genetics. Pituitary Neoplasms / genetics. Prolactinoma / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. DNA Primers. DNA, Neoplasm / genetics. DNA, Neoplasm / isolation & purification. Female. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Invasiveness. Pituitary Gland / physiology. RNA, Neoplasm / genetics. RNA, Neoplasm / isolation & purification. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 19158195.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cadherins; 0 / DNA Primers; 0 / DNA, Neoplasm; 0 / RNA, Neoplasm
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7. Lévêque M, Dimitriu C, Gustin T, Jamart J, Gilliard C, Bojanowski MW: [Evaluation of neuro-oncology information for French speaking patients on the Internet]. Neurochirurgie; 2007 Nov;53(5):343-55
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  • [Transliterated title] Evaluation de l'information sur Internet destinée aux patients francophones en neuro-oncologie.
  • OBJECTIVE: Internet has become the first place where patients go to when seeking information about their disease.
  • MATERIALS AND METHODS: We entered six key words "glioblastome", "méningiome", "métastase cérébrale", "neurinome de l'acoustique", "adénome à prolactine" and "lymphome primitif cérébral" into 2 different search engines and, for each key word, the first fifty websites were reviewed using the tool "DISCERN", and with the help of two neuro-oncologists, we rated their content in terms of quality and comprehension.

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  • (PMID = 17881014.001).
  • [ISSN] 0028-3770
  • [Journal-full-title] Neuro-Chirurgie
  • [ISO-abbreviation] Neurochirurgie
  • [Language] fre
  • [Publication-type] English Abstract; Evaluation Studies; Journal Article
  • [Publication-country] France
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8. Grottoli S, Gasco V, Broglio F, Baldelli R, Ragazzoni F, Gallenca F, Mainolfi A, Prodam F, Muccioli G, Ghigo E: Cortistatin-17 and somatostatin-14 display the same effects on growth hormone, prolactin, and insulin secretion in patients with acromegaly or prolactinoma. J Clin Endocrinol Metab; 2006 Apr;91(4):1595-9
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  • [Title] Cortistatin-17 and somatostatin-14 display the same effects on growth hormone, prolactin, and insulin secretion in patients with acromegaly or prolactinoma.
  • OBJECTIVE: We compared the endocrine effects of cortistatin-17 with those of somatostatin-14 in patients with acromegaly (ACRO) or prolactinoma (PRLOMA).
  • Cortistatin-17 and somatostatin-14 inhibited PRL secretion in PRLOMA (P < 0.05), to some extent in ACRO (P value not significant), but not in NS.
  • CONCLUSIONS: Cortistatin-17 and somatostatin-14 display the same effects on GH, PRL, and insulin secretion in patients with ACRO or PRLOMA.
  • [MeSH-major] Acromegaly / blood. Human Growth Hormone / blood. Insulin / blood. Pituitary Neoplasms / blood. Prolactin / blood. Prolactinoma / blood. Somatostatin / pharmacology

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  • (PMID = 16449338.001).
  • [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; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / CORT protein, human; 0 / Carrier Proteins; 0 / Insulin; 0 / Neuropeptides; 12629-01-5 / Human Growth Hormone; 51110-01-1 / Somatostatin; 9002-62-4 / Prolactin; EC 1.1.3.4 / Glucose Oxidase
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9. 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
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  • [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

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  • (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
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10. Zidverc-Trajkovic J, Vujovic S, Sundic A, Radojicic A, Sternic N: Bilateral SUNCT-like headache in a patient with prolactinoma responsive to lamotrigine. J Headache Pain; 2009 Dec;10(6):469-72
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  • [Title] Bilateral SUNCT-like headache in a patient with prolactinoma responsive to lamotrigine.
  • We have reported a case of bilateral SUNCT-like headache secondary to a prolactinoma and responsive to lamotrigine treatment.
  • [MeSH-major] Pituitary Neoplasms / complications. Prolactinoma / complications. SUNCT Syndrome / drug therapy. SUNCT Syndrome / etiology. Triazines / administration & dosage
  • [MeSH-minor] Bromocriptine / administration & dosage. Calcium Channel Blockers / administration & dosage. Female. Functional Laterality / physiology. Hormone Antagonists / administration & dosage. Humans. Magnetic Resonance Imaging. Pituitary Gland / pathology. Pituitary Gland / physiopathology. Pituitary Gland / secretion. Treatment Outcome. Young Adult

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  • (PMID = 19763771.001).
  • [ISSN] 1129-2377
  • [Journal-full-title] The journal of headache and pain
  • [ISO-abbreviation] J Headache Pain
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Calcium Channel Blockers; 0 / Hormone Antagonists; 0 / Triazines; 3A64E3G5ZO / Bromocriptine; U3H27498KS / lamotrigine
  • [Other-IDs] NLM/ PMC3476218
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11. Zhen JR, Yu Q, Zhang YH, Ma WB, Lin SQ: [Cost-effectiveness analysis of two therapeutic methods for prolactinoma]. Zhonghua Fu Chan Ke Za Zhi; 2008 Apr;43(4):257-61
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  • [Title] [Cost-effectiveness analysis of two therapeutic methods for prolactinoma].
  • OBJECTIVE: To evaluate the therapeutic responses to transsphenoidal surgery and medical therapy in terms of normalization of prolactin (PRL), mortality, morbidity and the cost-effectiveness of PRL normalization in order to establish an individualized therapeutic protocol for the patients with prolactinoma.
  • METHODS: A retrospective study was undertaken of a consecutive series of patients with prolactinoma who were followed for at least 1 year after transsphenoidal surgery or medical treatment.
  • The clinical characteristics and the long-term outcomes (normalization of PRL, morbidity or mortality) were assessed.
  • (1) The success rate of normalizing serum PRL through surgical treatment in microadenoma was 85% (22/26), and that of medical treatment was 95% (19/20).
  • The success rate of normalizing serum PRL through surgical treatment in macroadenoma was 45% (19/42), and that of medical treatment was 5/5.
  • There was a statistical difference between the two therapies (P < 0.05). (2) According to the Markov model, it would cost a microprolactinoma patient 25,129.25 yuan to normalize serum PRL by surgical treatment.
  • CONCLUSIONS: Medical therapy is superior to surgical treatment in regard to complication rate and cost-effectiveness for macro- and extra big prolactinomas.
  • [MeSH-major] Hypophysectomy / economics. Pituitary Neoplasms / economics. Pituitary Neoplasms / therapy. Prolactinoma / economics. Prolactinoma / therapy
  • [MeSH-minor] Adult. Bromocriptine / economics. Bromocriptine / therapeutic use. Cost-Benefit Analysis. Female. Humans. Markov Chains. Middle Aged. Prolactin / blood. Prospective Studies. Retrospective Studies. Treatment Outcome. Young Adult

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  • (PMID = 18843964.001).
  • [ISSN] 0529-567X
  • [Journal-full-title] Zhonghua fu chan ke za zhi
  • [ISO-abbreviation] Zhonghua Fu Chan Ke Za Zhi
  • [Language] chi
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 3A64E3G5ZO / Bromocriptine; 9002-62-4 / Prolactin
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12. Maciá-Bobes C, Ronzón-Fernández A, Castaño-Fernández G, Botas-Cervero P: [Incidentally discovered pituitary macroadenoma. Neurosurgical treatment indications illustrated by two cases]. Neurocirugia (Astur); 2006 Dec;17(6):538-41
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  • [Title] [Incidentally discovered pituitary macroadenoma. Neurosurgical treatment indications illustrated by two cases].
  • [Transliterated title] Macroadenoma de hipófisis descubierto incidentalmente. Indicaciones del tratamiento quirúrgico a propósito de dos casos.
  • Pituitary macroadenomas (more than 10 mm in diameter) are infrequent as casual findings and optimal management strategy for these tumours has not been established.
  • Neurosurgical approach must be always considered in patients with visual field defects or with hormone-secreting adenomas (but prolactinoma), and in those with evidence of lesion's growth or if clinical pituitary apoplexy occurs.
  • We also discuss the benefits of including such unusual indications for neurosurgical treatment into the incidentally discovered pituitary macroadenomas evaluation strategy.
  • [MeSH-major] Adenoma / diagnosis. Hypophysectomy. Pituitary Neoplasms / diagnosis

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  • (PMID = 17242842.001).
  • [ISSN] 1130-1473
  • [Journal-full-title] Neurocirugía (Asturias, Spain)
  • [ISO-abbreviation] Neurocirugia (Astur)
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 3XMK78S47O / Testosterone
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13. Shirodkar M, Jabbour SA: Endocrine incidentalomas. Int J Clin Pract; 2008 Sep;62(9):1423-31
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  • Incidentalomas are discovered in the thyroid, pituitary and adrenal glands during imaging studies performed for non-endocrine reasons.
  • Pituitary incidentalomas are also common, with a prevalence of 10-20%.
  • All patients with pituitary masses should have a workup for hormonal hypersecretion.
  • All hyperfunctioning adenomas are resected except prolactinomas which are treated medically.
  • [MeSH-major] Endocrine Gland Neoplasms / diagnosis. Incidental Findings
  • [MeSH-minor] Biopsy, Fine-Needle. Diagnosis, Differential. Diagnostic Imaging. Humans. Physical Examination. Risk Factors. Tumor Burden

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  • (PMID = 18657198.001).
  • [ISSN] 1742-1241
  • [Journal-full-title] International journal of clinical practice
  • [ISO-abbreviation] Int. J. Clin. Pract.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 34
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14. Yamaguchi M, Yamada Y, Hosokawa Y, Iwamoto R, Tamba S, Ihara A, Yamamoto K, Hoshida Y, Matsuzawa Y: Long-term suppressive effect of octreotide on progression of metastatic gastrinoma with multiple endocrine neoplasia type 1: seven-year follow up. Intern Med; 2010;49(15):1557-63
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  • A 30-year-old woman had a history of prolactinoma and primary hyperparathyroidism.
  • [MeSH-minor] Adult. Disease Progression. Female. Follow-Up Studies. Humans. Time Factors


15. Marek J: [Quo vadis, hypophysis? Some news and prospects]. Vnitr Lek; 2007 Jul-Aug;53(7-8):789-94
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  • Clinically relevant hypophysial adenomas affect approximately 1 per thousand of population.
  • Two thirds of the above number are prolactinomas.
  • Most prolactinomas can be cured without major difficulty, only those resistant to pharmacological treatment can become a problem.
  • We treat adenomas surgically, expose possible residua to Leksell gamma knife irradiation and apply pharmacological therapy until the effect of irradiation has been achieved.
  • Like in the case of acromegaly, also in that of Cushing's disease, new drugs are developed which promise greater therapeutic advantages.
  • [MeSH-major] Pituitary Gland / physiology
  • [MeSH-minor] Humans. Pituitary ACTH Hypersecretion / diagnosis. Pituitary ACTH Hypersecretion / physiopathology. Pituitary ACTH Hypersecretion / therapy. Pituitary Neoplasms / diagnosis. Pituitary Neoplasms / physiopathology. Pituitary Neoplasms / therapy

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  • (PMID = 17915419.001).
  • [ISSN] 0042-773X
  • [Journal-full-title] Vnitr̆ní lékar̆ství
  • [ISO-abbreviation] Vnitr Lek
  • [Language] cze
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Czech Republic
  • [Number-of-references] 41
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16. de Lourdes Figuerola M, Bruera O, Pozzo MJ, Leston J: SUNCT syndrome responding absolutely to steroids in two cases with different etiologies. J Headache Pain; 2009 Feb;10(1):55-7
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  • We are presenting now two cases absolutely responders to steroid therapy, one of them a SUNCT-like secondary to a prolactinoma and the other primary.
  • [MeSH-major] Conjunctiva / pathology. Prolactinoma / complications. Prolactinoma / physiopathology. SUNCT Syndrome / drug therapy. SUNCT Syndrome / etiology. Steroids / therapeutic use

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  • (PMID = 19020800.001).
  • [ISSN] 1129-2377
  • [Journal-full-title] The journal of headache and pain
  • [ISO-abbreviation] J Headache Pain
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Steroids
  • [Other-IDs] NLM/ PMC3451757
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17. Giacomini D, Acuña M, Gerez J, Nagashima AC, Silberstein S, Páez-Pereda M, Labeur M, Theodoropoulou M, Renner U, Stalla GK, Arzt E: Pituitary action of cytokines: focus on BMP-4 and gp130 family. Neuroendocrinology; 2007;85(2):94-100
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pituitary action of cytokines: focus on BMP-4 and gp130 family.
  • The anterior pituitary can develop benign tumors of different sizes, classified as micro- and macroadenomas, frequently associated with high levels of hormone production, leading to different associated syndromes like Cushing's disease, acromegaly or prolactinomas.
  • Much work has been done in order to understand the signaling pathways and the factors and hormones involved in the pituitary tumorigenic process.
  • In recent years, much evidence has been collected and it is now well documented that cytokines of the gp130 family, such as interleukin-6, that use gp130 as a common signaling protein stimulate not only the proliferation but also the hormone secretion of pituitary cells.
  • Experiments in vivo have shown that the overexpression of the gp130 receptor resulted in pituitary abnormal growth.
  • Moreover, it has been recently described that bone morphogenetic protein-4 (BMP-4), a member of the TGF-beta family, has a stimulatory role on lactosomatotropic cells promoting the development of prolactinomas but it has an inhibitory action on the corticotropic lineage.
  • This inhibitory action prevents Cushing's disease progression.
  • The present review highlights the most recent work about gp130 and TGF-beta cytokine families and their role in pituitary tumorigenesis.
  • [MeSH-major] Bone Morphogenetic Proteins / physiology. Cytokine Receptor gp130 / physiology. Cytokines / physiology. Pituitary Gland / physiology

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  • (PMID = 17337883.001).
  • [ISSN] 0028-3835
  • [Journal-full-title] Neuroendocrinology
  • [ISO-abbreviation] Neuroendocrinology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / BMP4 protein, human; 0 / Bone Morphogenetic Protein 4; 0 / Bone Morphogenetic Proteins; 0 / Cytokines; 133483-10-0 / Cytokine Receptor gp130
  • [Number-of-references] 53
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18. Ptasińska-Wnuk D, Lawnicka H, Fryczak J, Kunert-Radek J, Pawlikowski M: Angiotensin peptides regulate angiogenic activity in rat anterior pituitary tumour cell cultures. Endokrynol Pol; 2007 Nov-Dec;58(6):478-86
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Angiotensin peptides regulate angiogenic activity in rat anterior pituitary tumour cell cultures.
  • VEGF is one of the crucial pro-angiogenic cytokines produced by the cells of many of the tumours examined, including various types of anterior pituitary adenomas.
  • Moreover, an association of the renin-angiotensin system (RAS) with oestrogen-induced vascular changes during the development of rat pituitary PRL-secreting adenoma has already been demonstrated.
  • The aim of the study was to determine the in vitro effects of angiotensin peptides (Ang II, Ang III and Ang IV) on the secretion of VEGF in two anterior pituitary adenoma cell cultures: the culture of the rat pituitary lactosomatotrope tumour cell line (GH3) and the primary culture of rat PRL-secreting tumour induced by diethylstilbestrol (DES).
  • MATERIAL AND METHODS: GH3 and prolactinoma cells were cultured in an F10 and an F-12 medium respectively and then placed into 24 multiwell plates (10(5) of GH3 cells/well and 10(6) of rat prolactinoma cells/well).
  • RESULTS: The incubation of both GH3 cells and rat adenoma cells with Ang II, Ang III or Ang IV at concentrations of 10(-12) -10(-8)M resulted in a significant increase in VEGF concentration in the culture medium.
  • Exposure of GH3 cells to Ang III or Ang IV at concentrations of 10(-6)M led to a significant inhibition of cytokine release, and Pearson's correlation curve showed a tendency for Ang II at concentrations of more than 10(-6)M to inhibit VEGF secretion in primary prolactinoma cell culture.
  • The stimulatory influence of Ang II on VEGF secretion in GH3 cell culture was negated by losartan or by PD123319 in both concentrations tested.
  • CONCLUSIONS: Ang II, Ang III and Ang IV affect the secretion of VEGF in cultures of the rat lactosomatotrope GH3 cell line and primary rat prolactinoma cells.
  • Both AT1 and AT2 receptors mediate the stimulatory action of Ang II on the cytokine release in GH3 cell culture.
  • [MeSH-minor] Animals. In Vitro Techniques. Male. Pituitary Neoplasms / metabolism. Rats. Tumor Cells, Cultured / metabolism

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  • (PMID = 18205103.001).
  • [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 / Angiotensins; 0 / Receptor, Angiotensin, Type 1; 0 / Receptor, Angiotensin, Type 2; 0 / Vascular Endothelial Growth Factor A
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19. Saito T, Watanabe Y, Yuzawa M, Saito T, Tamemoto H, Suzuki H, Kusaka G, Omori Y, Shinoda S, Kawakami M, Ishikawa SE: SIADH is only an atypical clinical feature in a patient with prolactinoma. Intern Med; 2007;46(10):653-6
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  • [Title] SIADH is only an atypical clinical feature in a patient with prolactinoma.
  • Serum prolactin was 254 ng/ml, and anterior pituitary hormones of ACTH, TSH and GH were in the normal ranges.
  • Brain magnetic resonance imaging (MRI) showed a pituitary tumor with a size of 20 x 22 x 21 mm and it pushed a pituitary stalk upward.
  • Immunohistochemistry revealed prolactinoma.
  • The present study indicates that syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is manifested in association with pituitary macroadenoma of prolactinoma.
  • [MeSH-major] Inappropriate ADH Syndrome / etiology. Pituitary Neoplasms / complications. Prolactinoma / complications
  • [MeSH-minor] Humans. Hyponatremia / etiology. Magnetic Resonance Imaging. Male. Middle Aged. Pituitary-Adrenal System / physiology

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  • (PMID = 17527038.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
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20. Cónsole GM, Hereñú CB, Camihort GA, Luna GC, Ferese C, Goya RG: Effect of insulin-like growth factor-I gene therapy on the somatotropic axis in experimental prolactinomas. Cells Tissues Organs; 2009;190(1):20-6
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  • [Title] Effect of insulin-like growth factor-I gene therapy on the somatotropic axis in experimental prolactinomas.
  • Gene therapy was implemented in young female Sprague-Dawley rats which received 2 pituitary stereotaxic injections of a control recombinant adenoviral vector expressing green fluorescent protein (RAd-GFP) or IGF-I (RAd-IGF-I).
  • Morphometric analysis revealed that the somatotrope cells in estrogen-treated rats without stereotaxic injections showed a significant (p < 0.01) increase in the cell size compared with intact controls (59.9 +/- 1.1 vs. 42.9 +/- 1.2 microm(2)) and had a significant (p < 0.05) decrease in cell density with respect to intact animals (10.5 +/- 0.1 vs. 19.7 +/- 1.7).
  • The treatment of pituitary adenomas with RAd-IGF-I induced a significant (p < 0.05) decrease in cell size with respect to E(2) + RAd-GFP (51.3 +/- 0.3 vs. 58.9 +/- 0.3 microm(2)) and no changes in cell density compared with RAd-GFP-injected animals (12.8 +/- 1.7 vs. 10.5 +/- 0.1).
  • In rats carrying estrogen-induced adenomas, RAd-IGF-I injection induced a significant (p < 0.05) decrease in serum growth hormone compared to RAd-GFP-injected animals (107.5 +/- 7 vs. 142.4 +/- 9 ng/ml).
  • IGF-I gene therapy appears to be an effective approach for the treatment of experimental somatomammotropic pituitary tumors and could be potentially useful as an adjuvant of conventional therapies.
  • [MeSH-major] Genetic Therapy. Insulin-Like Growth Factor I / genetics. Insulin-Like Growth Factor I / therapeutic use. Pituitary Neoplasms / therapy. Prolactinoma / genetics. Prolactinoma / therapy. Somatotrophs / pathology
  • [MeSH-minor] Animals. Cell Count. Cell Size. Estrogens / administration & dosage. Estrogens / pharmacology. Female. Green Fluorescent Proteins / metabolism. Growth Hormone / blood. Implants, Experimental. Neoplasms, Experimental / blood. Neoplasms, Experimental / genetics. Neoplasms, Experimental / pathology. Neoplasms, Experimental / therapy. Prolactin / blood. Rats. Rats, Sprague-Dawley. Rats, Transgenic

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  • [Copyright] (c) 2008 S. Karger AG, Basel.
  • (PMID = 18957836.001).
  • [ISSN] 1422-6421
  • [Journal-full-title] Cells, tissues, organs
  • [ISO-abbreviation] Cells Tissues Organs (Print)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Estrogens; 147336-22-9 / Green Fluorescent Proteins; 67763-96-6 / Insulin-Like Growth Factor I; 9002-62-4 / Prolactin; 9002-72-6 / Growth Hormone
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21. Lamberts SW, Hofland LJ: Future treatment strategies of aggressive pituitary tumors. Pituitary; 2009;12(3):261-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Future treatment strategies of aggressive pituitary tumors.
  • While surgery remains the first-line treatment of most aggressive pituitary adenomas, medical therapy is important as second-line or adjunctive therapy in a large proportion of patients.
  • Dopamine agonists (DAs) are the best treatment for prolactinomas, but when DAs are not tolerated, new somatostatin receptor subtype 5 (SSTR(5)) inhibitors may offer an alternative in the future.
  • Unfortunately, these are unlikely to be effective in DA-resistant prolactinomas.
  • There is an urgent need for medical therapies in Cushing's disease, and the SSTR(5) analogs could offer an effective treatment in a proportion of patients within the next few years.
  • Finally, the medical management options for non-functioning pituitary adenomas are also very limited, and a new chimeric agent with activity towards dopamine receptors, SSTR(5) and SSTR(2) may help reduce adenoma recurrence in the future.
  • [MeSH-major] Dopamine Agonists / therapeutic use. Pituitary Neoplasms
  • [MeSH-minor] Acromegaly / drug therapy. Humans. Octreotide / therapeutic use. Peptides, Cyclic / therapeutic use. Pituitary ACTH Hypersecretion / drug therapy. Pituitary ACTH Hypersecretion / surgery. Prolactinoma / drug therapy. Prolactinoma / surgery. Receptors, Somatostatin / antagonists & inhibitors. Somatostatin / analogs & derivatives. Somatostatin / therapeutic use

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  • (PMID = 19003539.001).
  • [ISSN] 1573-7403
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dopamine Agonists; 0 / Peptides, Cyclic; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 5; 118992-92-0 / lanreotide; 51110-01-1 / Somatostatin; RWM8CCW8GP / Octreotide
  • [Number-of-references] 20
  • [Other-IDs] NLM/ PMC2712619
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22. Spada A, Mantovani G, Lania A: Pathogenesis of prolactinomas. Pituitary; 2005;8(1):7-15
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pathogenesis of prolactinomas.
  • In recent years the demonstration that human pituitary adenomas are monoclonal in origin provides further evidence that pituitary neoplasia arise from the replication of a single mutated cell in which growth advantage results from either activation of proto-oncogenes or inactivation of tumor suppressor genes.
  • However, with the exception of one RAS mutation identified in a single unusually aggressive prolactinoma resistant to dopaminergic inhibition that resulted to be lethal, no mutational changes have been so far detected in prolactinomas.
  • Indeed, our knowledge on the molecular events involved in lactotroph proliferation is even more limited in comparison to the other tumor types, since these tumors are very infrequently surgically removed and therefore available for molecular biology studies.
  • In this respect, it is worth noting that the molecular and biological abnormalities so far described in prolactinomas mainly concern aggressive and atypical tumors and likely do not apply to the typical prolactinomas, that are characterized by good response to medical treatment and a very low growth rate.
  • [MeSH-major] Pituitary Neoplasms / etiology. Prolactinoma / etiology
  • [MeSH-minor] Cell Cycle / genetics. Cell Cycle / physiology. Cell Proliferation. DNA, Neoplasm / genetics. Gene Expression Regulation, Neoplastic. Genes, Tumor Suppressor. Growth Substances / genetics. Growth Substances / physiology. Humans. Mutation. Proto-Oncogenes

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  • (PMID = 16411063.001).
  • [ISSN] 1386-341X
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Growth Substances
  • [Number-of-references] 102
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23. Honegger JB, Psaras T, Petrick M, Beuschlein F, Reincke M: Spontaneous cerebrospinal fluid rhinorrhea in untreated macroprolactinoma--an indication for primary surgical therapy. Zentralbl Neurochir; 2006 Aug;67(3):149-54
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  • BACKGROUND: Medical therapy is usually indicated as first-line treatment for prolactinomas.
  • Surgery is generally reserved as second-line therapy if prolactinomas are non-responsive to dopamine agonists (DA) or DA therapy is not tolerated.
  • Herein, we draw attention to the rare occurrence of spontaneous CSF rhinorrhea in prolactinomas requiring primary surgical therapy.
  • Only 8 cases of confirmed prolactinomas with spontaneous rhinorrhea have been reported in the literature so far.
  • CASE REPORTS: Two out of 267 surgical cases with pituitary adenomas presented with spontaneous rhinorrhea.
  • Both patients harbored invasive prolactinomas.
  • CONCLUSION: Certain clinical settings still require primary surgical therapy of prolactinomas.
  • Early detection and surgical repair of a CSF leak is crucial for a favorable clinical outcome.
  • [MeSH-major] Cerebrospinal Fluid Rhinorrhea / etiology. Cerebrospinal Fluid Rhinorrhea / surgery. Neurosurgical Procedures. Pituitary Neoplasms / complications. Pituitary Neoplasms / surgery. Prolactinoma / complications. Prolactinoma / surgery

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  • (PMID = 16958013.001).
  • [ISSN] 0044-4251
  • [Journal-full-title] Zentralblatt für Neurochirurgie
  • [ISO-abbreviation] Zentralbl. Neurochir.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Hormones
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24. Yin Z, Williams-Simons L, Parlow AF, Asa S, Kirschner LS: Pituitary-specific knockout of the Carney complex gene Prkar1a leads to pituitary tumorigenesis. Mol Endocrinol; 2008 Feb;22(2):380-7
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  • [Title] Pituitary-specific knockout of the Carney complex gene Prkar1a leads to pituitary tumorigenesis.
  • Among the endocrine tumors that comprise the syndrome, GH-producing pituitary tumors are seen in approximately 10% of patients, although biochemical abnormalities of the GH axis are much more common.
  • To explore the role of loss of the CNC gene PRKAR1A on pituitary tumorigenesis, we produced a tissue-specific knockout (KO) of this gene in the mouse.
  • For these studies, we generated a mouse line expressing the cre recombinase in pituitary cells using the rat GHRH receptor promoter.
  • Although prolactinomas were observed in KO and control mice, the KO mice exhibited a significantly increased frequency of pituitary tumors compared with wild-type or conventional Prkar1a(+/-) mice.
  • Characterization of the tumors demonstrated they were composed of cells of the Pit1 lineage that stained for GH, prolactin, and TSH.
  • At the biochemical level, levels of GH in the serum of KO animals were markedly elevated compared with controls, regardless of the presence of a frank tumor.
  • These data indicate that complete loss of Prkar1a is sufficient to allow the formation of pituitary tumors and abnormalities of the GH axis, in close analogy to human patients with CNC.

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  • (PMID = 17975024.001).
  • [ISSN] 0888-8809
  • [Journal-full-title] Molecular endocrinology (Baltimore, Md.)
  • [ISO-abbreviation] Mol. Endocrinol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016058; United States / NCI NIH HHS / CA / R01 CA112268; United States / NCI NIH HHS / CA / CA 112268; United States / NCI NIH HHS / CA / CA 16058
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit; 0 / Prkar1a protein, mouse; 9002-62-4 / Prolactin; 9002-71-5 / Thyrotropin; 9002-72-6 / Growth Hormone; EC 2.7.7.- / Cre recombinase; EC 2.7.7.- / Integrases
  • [Other-IDs] NLM/ PMC2234591
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25. Goffin V, Bernichtein S, Touraine P, Kelly PA: Development and potential clinical uses of human prolactin receptor antagonists. Endocr Rev; 2005 May;26(3):400-22
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  • [Title] Development and potential clinical uses of human prolactin receptor antagonists.
  • There is a large body of literature showing that prolactin (PRL) exerts growth-promoting activities in breast cancer, and possibly in prostate cancer and prostate hyperplasia.
  • In addition, increasing evidence argues for the involvement of locally produced (autocrine) PRL, perhaps even more than pituitary-secreted (endocrine) PRL, in tumor growth.
  • Because dopamine analogs are unable to inhibit PRL production in extrapituitary sites, alternative strategies need investigation.
  • To that end, several PRL receptor antagonists have been developed by introducing various mutations into its natural ligands.
  • For all but one of these analogs, the mechanism of action involves a competition with endogenous PRL for receptor binding.
  • Such compounds are thus candidates to counteract the undesired actions of PRL, not only in tumors, but also in dopamine-resistant prolactinomas.
  • We discuss to what extent this new molecule could be considered as a lead compound for inhibiting the actions of human PRL in the above-mentioned diseases.
  • We also speculate on the multiple questions that could be addressed with respect to the therapeutic use of PRL receptor antagonists in patients.
  • [MeSH-major] Receptors, Prolactin / antagonists & inhibitors
  • [MeSH-minor] Animals. Breast Neoplasms / drug therapy. Disease Models, Animal. Female. Humans. Male. Prostatic Neoplasms / drug therapy

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  • (PMID = 15814850.001).
  • [ISSN] 0163-769X
  • [Journal-full-title] Endocrine reviews
  • [ISO-abbreviation] Endocr. Rev.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Prolactin
  • [Number-of-references] 1553
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26. Vilar L, Naves LA, Freitas MC, Lima M, Canadas V, Albuquerque JL, Lyra R, Azevedo MF, Casulari LA: Clinical and laboratory features greatly overlap in patients with macroprolactinemia or monomeric hyperprolactinemia. Minerva Endocrinol; 2007 Jun;32(2):79-86
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  • METHODS: The study included 64 patients (54 women and 10 men) with macroprolactinemia and 96 patients (70 women and 26 men) with monomeric hyperprolactinemia (32 with prolactinomas).
  • RESULTS: Symptoms related to prolactin (PRL) excess were found in about 44% of individuals from the macroprolactinemia group and in 88.5% of patients with monomeric hyperprolactinemia (P<0.0001).
  • Although mean PRL levels were higher in patients with monomeric hyperprolactinemia (565.9+/-2726.4 vs 113.3+/-94.5 ng/mL, P<0.001), there was a great overlap between both groups.
  • Among macroprolactinemic patients, pituitary magnetic resonance imaging revealed an image suggestive of a microadenoma in 7 (10.9%) and a macroadenoma in 1 (1.6%).
  • Normalization of PRL levels during therapy with dopamine agonists was significantly more frequent in patients with monomeric hyperprolactinemia than in subjects with macroprolactinemia (78.6% vs 32%, P=0.0006).
  • CONCLUSION: Our data show that symptoms related to PRL excess are frequently found in subjects with macroprolactinemia.
  • [MeSH-major] Hyperprolactinemia / diagnosis. Pituitary Neoplasms / diagnosis. Prolactin / blood. Prolactinoma / diagnosis

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  • (PMID = 17557033.001).
  • [ISSN] 0391-1977
  • [Journal-full-title] Minerva endocrinologica
  • [ISO-abbreviation] Minerva Endocrinol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Dopamine Antagonists; 9002-62-4 / Prolactin
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27. Colao A, Di Sarno A, Guerra E, De Leo M, Mentone A, Lombardi G: Drug insight: Cabergoline and bromocriptine in the treatment of hyperprolactinemia in men and women. Nat Clin Pract Endocrinol Metab; 2006 Apr;2(4):200-10
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  • Prolactinoma is the most frequent pituitary tumor histotype.
  • The major objectives of treating prolactinomas are to suppress excessive hormone secretion and its clinical consequences, to remove the tumor mass while preserving the residual pituitary function, and possibly to prevent disease recurrence or progression.
  • Primary therapy of prolactinomas is based on use of dopamine-receptor agonists.
  • Bromocriptine induces normalization of prolactin levels in 80-90% of patients with microprolactinomas and approximately 70% of those with macroprolactinomas.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Bromocriptine / therapeutic use. Ergolines / therapeutic use. Hyperprolactinemia / blood. Prolactinoma / drug therapy
  • [MeSH-minor] Adenoma / drug therapy. Adenoma / etiology. Female. Humans. Male. Prolactin / blood. Sex Characteristics

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  • (PMID = 16932285.001).
  • [ISSN] 1745-8366
  • [Journal-full-title] Nature clinical practice. Endocrinology & metabolism
  • [ISO-abbreviation] Nat Clin Pract Endocrinol Metab
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Ergolines; 3A64E3G5ZO / Bromocriptine; 9002-62-4 / Prolactin; LL60K9J05T / cabergoline
  • [Number-of-references] 78
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28. Ke C, Deng Z, Lei T, Zhou S, Guo DS, Wan J, Wu S: Pituitary prolactin producing adenoma with ossification: a rare histological variant and review of literature. Neuropathology; 2010 Apr;30(2):165-9
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  • [Title] Pituitary prolactin producing adenoma with ossification: a rare histological variant and review of literature.
  • Pituitary adenoma with ossification is a rare histological variant.
  • Here a case of pituitary prolactin-producing adenoma with bone formation in a 21-year-old woman is described.
  • The pre-operative prolactin serum level was 258.78 ng/mL.
  • The cytoplasm of the adenoma cells was slightly eosinophilic and the myelo-adipose metaplastic foci were also found within the parenchyma.
  • Immunohistochemical staining of tumor cells showed positive expressions of prolactin, synaptophysin and chromogranin A in the cytoplasm of the tumor cells.
  • Meanwhile, negative expressions of S-100, epithelial membrane antigen, GFAP and other pituitary hormones were also demonstrated.
  • As a rare histological variant of pituitary adenoma, the current case of pituitary prolactin producing adenoma with ossification is reported.
  • It is speculated that the ossification may be derived from the osteo-metaplasia of mesenchymal fibroblasts resulting from the effects of both secondary ischemia by the outgrowth of the tumor and/or the autocrine effect of prolactin in this case.
  • The bony shell structure may limit the growth of pituitary adenoma.
  • [MeSH-major] Ossification, Heterotopic / pathology. Pituitary Gland / pathology. Pituitary Neoplasms / pathology. Prolactinoma / pathology

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  • (PMID = 19737358.001).
  • [ISSN] 1440-1789
  • [Journal-full-title] Neuropathology : official journal of the Japanese Society of Neuropathology
  • [ISO-abbreviation] Neuropathology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
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29. McSheehy PM, Port RE, Rodrigues LM, Robinson SP, Stubbs M, van der Borns K, Peters GJ, Judson IR, Leach MO, Griffiths JR: Investigations in vivo of the effects of carbogen breathing on 5-fluorouracil pharmacokinetics and physiology of solid rodent tumours. Cancer Chemother Pharmacol; 2005 Feb;55(2):117-28
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  • METHODS: Two different tumour models were used, rat GH3 prolactinomas xenografted s.c. into nude mice and rat H9618a hepatomas grown s.c. in syngeneic Buffalo rats.
  • [MeSH-minor] Animals. Liver Neoplasms, Experimental / metabolism. Magnetic Resonance Spectroscopy. Mice. Models, Biological. Neoplasm Transplantation. Prolactinoma / metabolism. Rats. Transplantation, Heterologous

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  • (PMID = 15592719.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 142M471B3J / Carbon Dioxide; 8063-77-2 / carbogen; S88TT14065 / Oxygen; U3P01618RT / Fluorouracil
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30. Heras M, Iglesias P, Fernández-Reyes MJ, Sánchez R, Jiménez MJ, Muñoz H, Tajada P, Duarte J: Nephrotic-range proteinuria in a patient with a giant prolactinoma. Am J Kidney Dis; 2008 Jun;51(6):1025-8
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  • [Title] Nephrotic-range proteinuria in a patient with a giant prolactinoma.
  • In the follow-up period, a giant prolactinoma was found by chance with extremely high prolactin (PRL) values.
  • After establishing cabergoline therapy, we achieved a remarkable decrease in both serum PRL levels and tumor mass, and surprisingly, proteinuria disappeared.
  • We discuss the possible pathogenic mechanisms of proteinuria that may correspond to PRL level in urine (prolactinuria) or another tumor-related protein.
  • [MeSH-major] Dopamine Agonists / therapeutic use. Ergolines / therapeutic use. Hyperprolactinemia / drug therapy. Hyperprolactinemia / etiology. Pituitary Neoplasms / complications. Prolactinoma / complications. Proteinuria / etiology

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  • (PMID = 18455849.001).
  • [ISSN] 1523-6838
  • [Journal-full-title] American journal of kidney diseases : the official journal of the National Kidney Foundation
  • [ISO-abbreviation] Am. J. Kidney Dis.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dopamine Agonists; 0 / Ergolines; LL60K9J05T / cabergoline
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31. Ribeiro RS, Abucham J: Recovery of persistent hypogonadism by clomiphene in males with prolactinomas under dopamine agonist treatment. Eur J Endocrinol; 2009 Jul;161(1):163-9
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  • [Title] Recovery of persistent hypogonadism by clomiphene in males with prolactinomas under dopamine agonist treatment.
  • CONTEXT: Persistence of hypogonadism is common in male patients with prolactinomas under dopamine agonist (DA) treatment.
  • OBJECTIVE: To evaluate the use of clomiphene as a treatment for persistent hypogonadism in males with prolactinomas.
  • PATIENTS: Fourteen adult hypogonadal males (testosterone <300 ng/dl and low/normal LH) with prolactinomas on DA, including seven with high prolactin (range: 29-1255 microg/l; median: 101 microg/l) despite maximal doses of DA.
  • MEASURES: Testosterone, estradiol, LH, FSH, and prolactin were measured before and 10 days, 4, 8, and 12 weeks after clomiphene.
  • Prolactin levels remained unchanged.
  • CONCLUSIONS: Clomiphene restores normal testosterone levels and improves sperm motility in most male patients with prolactinomas and persistent hypogonadism under DA therapy.
  • Recovery of gonadal function by clomiphene is independent of prolactin levels.

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  • (PMID = 19359408.001).
  • [ISSN] 1479-683X
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Dopamine Agonists; 0 / Estrogen Antagonists; 1HRS458QU2 / Clomiphene; 3XMK78S47O / Testosterone; 4TI98Z838E / Estradiol; 9002-62-4 / Prolactin; 9002-67-9 / Luteinizing Hormone; 9002-68-0 / Follicle Stimulating Hormone; EC 3.4.21.77 / Prostate-Specific Antigen
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32. Vlotides G, Cooper O, Chen YH, Ren SG, Greenman Y, Melmed S: Heregulin regulates prolactinoma gene expression. Cancer Res; 2009 May 15;69(10):4209-16
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  • [Title] Heregulin regulates prolactinoma gene expression.
  • To investigate the role of p185(her2/neu)/ErbB3 signaling in pituitary tumor function, we examined these receptors in human prolactinomas.
  • Immunofluorescent p185(her2/neu) was detected in almost all (seven of eight), and ErbB3 expression in a subset (four of eight) of tumors (seven adenomas and one carcinoma).
  • Quantitative PCR also showed abundant ErbB3 mRNA in tumor specimens derived from a rarely encountered prolactin-cell carcinoma.
  • Activation of p185(c-neu)/ErbB3 signaling with heregulin, the ErbB3 ligand, in rat lacto-somatotroph (GH4C1) tumor cells specifically induced prolactin (PRL) mRNA expression approximately 5-fold and PRL secretion approximately 4-fold, whereas growth hormone expression was unchanged.
  • Gefitinib, the tyrosine kinase inhibitor, suppressed heregulin-mediated p185(c-neu)/ErbB3 signaling to PRL.
  • Heregulin induction of PRL was also abrogated by transfecting cells with short interfering RNA directed against ErbB3.
  • Pharmacologic inhibition of heregulin-induced phosphoinositide-3-kinase/Akt (with LY294002) and ERK (with U0126) signaling, as well as short interfering RNA-mediated mitogen-activated protein kinase-1 down-regulation, showed ERK signaling as the primary transducer of heregulin signaling to PRL.
  • These results show ErbB3 expression in human prolactinomas and a novel ErbB3-mediated mechanism for PRL regulation in experimental lactotroph tumors.
  • Targeted inhibition of up-regulated p185(c-neu)/ErbB3 activity could be useful for the treatment of aggressive prolactinomas resistant to conventional therapy.

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  • (PMID = 19401448.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA075979-09; United States / NCI NIH HHS / CA / CA 075979; United States / NCI NIH HHS / CA / R01 CA075979-09; United States / NCI NIH HHS / CA / R01 CA075979; United States / NIDDK NIH HHS / DK / K23 DK085148
  • [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 / Actins; 0 / Neuregulin-1; 0 / RNA, Small Interfering; 0 / beta 2-Microglobulin; 9002-62-4 / Prolactin; 9002-72-6 / Growth Hormone; EC 1.2.1.- / Glyceraldehyde-3-Phosphate Dehydrogenases; EC 3.2.1.31 / Glucuronidase
  • [Other-IDs] NLM/ NIHMS112443; NLM/ PMC2688701
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33. Heinzlmann A, Köves K: The characteristic change in the distribution of S-100 immunoreactive folliculostellate cells in rat anterior pituitary upon long-term estrogen treatment is prevented by concomitant progesterone treatment. Endocrine; 2008 Jun;33(3):342-8
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  • [Title] The characteristic change in the distribution of S-100 immunoreactive folliculostellate cells in rat anterior pituitary upon long-term estrogen treatment is prevented by concomitant progesterone treatment.
  • The presence of folliculostellate cells in the anterior pituitary was described 49 years ago.
  • These cells give about 10% of the whole cell population and through their long processes they provide intrahypophyseal communication.
  • It was previously found that the diethylstilbestrol treatment basically influences the morphology and function of the trophic hormone secreting as well as the folliculostellate cells.
  • In the present experiment, we have studied whether a concomitant progesterone treatment can prevent or attenuate changes caused by diethylstilbestrol treatment in the distribution of folliculostellate, prolactin, and GH cells.
  • Diethylstilbestrol alone induced the appearance of prolactinomas.
  • Inside the prolactinomas, folliculostellate cells were scattered but outside the prolactinomas they formed a demarcation line.
  • Inside the prolactinomas, there were only a few growth hormone immunoreactive cells but they surrounded the prolactinomas in a ring-like pattern.
  • Concomitant progesterone influence prevented morphological changes in the anterior pituitary.
  • In accordance with the formation of prolactinomas, the plasma prolactin level was very high in diethylstilbestrol treated rats.
  • Progesterone alone did not influence the prolactin level.
  • [MeSH-major] Diethylstilbestrol / toxicity. Estrogens, Non-Steroidal / toxicity. Pituitary Gland, Anterior / drug effects. Pituitary Neoplasms / prevention & control. Progesterone / pharmacology. Prolactinoma / prevention & control. S100 Proteins / metabolism
  • [MeSH-minor] Animals. Biomarkers / metabolism. Drug Implants. Drug Interactions. Growth Hormone / metabolism. Immunohistochemistry. Male. Prolactin / metabolism. Radioimmunoassay. Rats. Rats, Sprague-Dawley

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  • (PMID = 19082791.001).
  • [ISSN] 1355-008X
  • [Journal-full-title] Endocrine
  • [ISO-abbreviation] Endocrine
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Drug Implants; 0 / Estrogens, Non-Steroidal; 0 / S100 Proteins; 4G7DS2Q64Y / Progesterone; 731DCA35BT / Diethylstilbestrol; 9002-62-4 / Prolactin; 9002-72-6 / Growth Hormone
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34. Wendell DL, Platts A, Land S: Global analysis of gene expression in the estrogen induced pituitary tumor of the F344 rat. J Steroid Biochem Mol Biol; 2006 Nov;101(4-5):188-96
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  • [Title] Global analysis of gene expression in the estrogen induced pituitary tumor of the F344 rat.
  • The F344 rat rapidly forms large prolactinomas in response to chronic estrogen treatment.
  • To identify genes expressed in the course of this estrogen induced pituitary tumor growth, we performed microarray analysis on the F344 rat pituitary after chronic estrogen treatment and on untreated controls.
  • Of those genes, 70 have not been reported previously as being affected by estrogen in the F344 rat pituitary.
  • Since many other investigators have studied the effect of estrogen on specific gene expression in rat pituitary, we also examined the mRNA expression of the 36 genes that have been previously reported as having their expression affected by estrogen in the rat pituitary.

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  • (PMID = 17005392.001).
  • [ISSN] 0960-0760
  • [Journal-full-title] The Journal of steroid biochemistry and molecular biology
  • [ISO-abbreviation] J. Steroid Biochem. Mol. Biol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R15 DK064675; United States / NIDDK NIH HHS / DK / R15 DK64675
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Estrogens; 731DCA35BT / Diethylstilbestrol
  • [Other-IDs] NLM/ NIHMS13691; NLM/ PMC1679906
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35. Kostrzak A, Warenik-Szymankiewicz A, Meczekalski B: The role of serum PRL bioactivity evaluation in hyperprolactinaemic women with different menstrual disorders. Gynecol Endocrinol; 2009 Dec;25(12):799-806
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  • [Title] The role of serum PRL bioactivity evaluation in hyperprolactinaemic women with different menstrual disorders.
  • OBJECTIVE: The objective of the study was to characterize the bioactivity of prolactin (PRL) in hyperprolactinaemic patients with prolactinomas, irregular menstrual cycles, regular menstrual cycles and PCOS.
  • METHODS: Serum PRL, biological activity of PRL (after polyethylene glycol (PEG) precipitation) and serum follicle stimulating hormone (FSH), luteinizing hormone (LH), estradiol (E2), testosterone (T), thyroid-stimulating hormone (TSH) concentrations were measured in all hyperprolactinaemic patients and control group (healthy subjects).
  • Correlations between active PRL (PRL-PEG) and serum FSH, LH, E2, T, TSH concentrations were also evaluated.
  • RESULTS: Prolactinoma is characterized by high serum PRL levels and its high biological activity.
  • Hyperprolactinaemic patients with irregular cycles were characterized by high biological activity of PRL.
  • Patients with hyperprolactinaemia and regular cycles had low biological activity of PRL.
  • CONCLUSIONS: Diagnosis of hyperprolactinaemia should be associated with estimation of PRL biological activity because it is important for type of hyperprolactinaemia management.
  • Low biological activity of PRL does not impair FSH and LH secretion and does not cause hypoestrogenism.
  • [MeSH-major] Hyperprolactinemia / blood. Menstrual Cycle / blood. Prolactin / metabolism
  • [MeSH-minor] Adult. Body Mass Index. Estradiol / blood. Female. Follicle Stimulating Hormone / blood. Humans. Luteinizing Hormone / blood. Magnetic Resonance Imaging. Oligomenorrhea / blood. Oligomenorrhea / complications. Pituitary Neoplasms / blood. Pituitary Neoplasms / complications. Polycystic Ovary Syndrome / blood. Polycystic Ovary Syndrome / complications. Prolactinoma / blood. Prolactinoma / complications. Testosterone / blood. Thyrotropin / blood

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  • (PMID = 19905999.001).
  • [ISSN] 1473-0766
  • [Journal-full-title] Gynecological endocrinology : the official journal of the International Society of Gynecological Endocrinology
  • [ISO-abbreviation] Gynecol. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 3XMK78S47O / Testosterone; 4TI98Z838E / Estradiol; 9002-62-4 / Prolactin; 9002-67-9 / Luteinizing Hormone; 9002-68-0 / Follicle Stimulating Hormone; 9002-71-5 / Thyrotropin
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36. Remick AK, Wood CE, Cann JA, Gee MK, Feiste EA, Kock ND, Cline JM: Histologic and immunohistochemical characterization of spontaneous pituitary adenomas in fourteen cynomolgus macaques (Macaca fascicularis). Vet Pathol; 2006 Jul;43(4):484-93
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  • [Title] Histologic and immunohistochemical characterization of spontaneous pituitary adenomas in fourteen cynomolgus macaques (Macaca fascicularis).
  • Pituitary adenomas were identified in 14 of 491 (2.9%) cynomolgus macaques evaluated from 1994 to 2004.
  • Seven of the pituitary adenomas caused gross enlargement of the pituitary gland that was visible on postmortem examination, whereas the remaining 7 were multifocal microadenomas identified on histologic examination.
  • A total of 35 adenomas were identified in the 14 macaques, 6 of which were being treated for diabetes mellitus.
  • Mean (+/- SD) pituitary weight was 0.31 +/- 0.42 g, compared with 0.07 +/- 0.02 g for 430 historical control animals (P < 0.0001).
  • Immunohistochemical staining for follicle-stimulating hormone, luteinizing hormone, prolactin, human growth hormone, thyroid-stimulating hormone, and adrenocorticotropic hormone was applied to pituitary tissue from all cases.
  • Immunostaining revealed 22 of 35 (62.9%) lactotroph adenomas, 5 of 35 (14.3%) plurihormonal cell adenomas, 3 of 35 (8.6%) corticotroph adenomas, 2 of 35 (5.7%) null cell adenomas, 1 of 35 (2.9%) somatotroph adenomas, 1 of 35 (2.9%) mixed corticotroph-somatotroph adenomas, 1 of 35 (2.9%) mixed lactotroph-corticotroph adenomas, 0 of 35 gonadotroph adenomas, and 0 of 35 thyrotroph adenomas.
  • This study represents the first extensive retrospective case series performed to evaluate the histologic and immunohistochemical characteristics of pituitary adenomas in cynomolgus macaques.
  • Our findings indicated that macaque pituitary adenomas frequently had mixed histologic appearance and hormone expression, and that, similar to human pituitary adenomas, prolactin-secreting neoplasms were the most prevalent type.
  • [MeSH-major] Macaca fascicularis. Monkey Diseases / pathology. Pituitary Neoplasms / veterinary. Prolactinoma / veterinary
  • [MeSH-minor] Adrenocorticotropic Hormone / biosynthesis. Animals. Female. Follicle Stimulating Hormone / biosynthesis. Human Growth Hormone / biosynthesis. Immunohistochemistry / veterinary. Luteinizing Hormone / biosynthesis. Male. Prevalence. Prolactin / biosynthesis. Retrospective Studies. Thyrotropin / biosynthesis

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  • (PMID = 16846990.001).
  • [ISSN] 0300-9858
  • [Journal-full-title] Veterinary pathology
  • [ISO-abbreviation] Vet. Pathol.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / T32 RR07009
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 12629-01-5 / Human Growth Hormone; 9002-60-2 / Adrenocorticotropic Hormone; 9002-62-4 / Prolactin; 9002-67-9 / Luteinizing Hormone; 9002-68-0 / Follicle Stimulating Hormone; 9002-71-5 / Thyrotropin
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37. Kobayashi T: Long-term results of stereotactic gamma knife radiosurgery for pituitary adenomas. Specific strategies for different types of adenoma. Prog Neurol Surg; 2009;22:77-95
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  • [Title] Long-term results of stereotactic gamma knife radiosurgery for pituitary adenomas. Specific strategies for different types of adenoma.
  • Long-term results of gamma knife radiosurgery for pituitary adenomas are presented and treatment strategies for different adenoma types are discussed.
  • Two hundred and sixty-seven patients with pituitary adenoma have been treated by gamma knife radiosurgery during the past 12 years.
  • There were 131 cases of nonfunctioning and 136 cases of functioning adenomas, in which 71 GH-producing, 33 PRL-producing and 32 ACTH-producing adenomas were included.
  • Micro- and small adenomas could be cured by gamma knife radiosurgery alone.
  • Nonfunctioning adenomas showed higher control rates than functioning adenomas even with lower dose treatment.
  • Cushing disease showed the best response because of the smallest tumor size with the highest dose treatment.
  • Acromegaly and prolactinoma were difficult to control because of larger tumors with lower dose treatment.
  • The rate of hormone normalization was also high in Cushing disease but lower in prolactinoma and lowest in acromegaly.
  • High-dose treatment was necessary for functioning adenomas to control tumor growth and oversecretion of hormones.
  • In conclusion, gamma knife radiosurgery was effective and safe for the treatment of pituitary adenomas.
  • However, the treatment strategies should be specific to each adenoma type according to the radiosensitivity, chemosensitivity and biological nature of the tumor.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / surgery. Acromegaly / surgery. Adenoma / surgery. Radiosurgery
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Child. Female. Follow-Up Studies. Growth Hormone-Secreting Pituitary Adenoma / pathology. Growth Hormone-Secreting Pituitary Adenoma / surgery. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Patient Satisfaction. Pituitary ACTH Hypersecretion / pathology. Pituitary ACTH Hypersecretion / surgery. Prolactinoma / pathology. Prolactinoma / surgery. Treatment Outcome. Young Adult

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  • (PMID = 18948721.001).
  • [ISSN] 0079-6492
  • [Journal-full-title] Progress in neurological surgery
  • [ISO-abbreviation] Prog Neurol Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
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38. Boikos SA, Stratakis CA: Molecular genetics of the cAMP-dependent protein kinase pathway and of sporadic pituitary tumorigenesis. Hum Mol Genet; 2007 Apr 15;16 Spec No 1:R80-7
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  • [Title] Molecular genetics of the cAMP-dependent protein kinase pathway and of sporadic pituitary tumorigenesis.
  • Pituitary tumors are among the most common human neoplasms.
  • The genetic causes of common pituitary tumors remain for the most part unknown; progress has been limited to the elucidation of the molecular etiology of four genetic syndromes predisposing to pituitary neoplasias: McCune-Albright syndrome, multiple endocrine neoplasia type 1, Carney complex and, most recently, familial acromegaly and prolactinomas and other tumors caused by mutations in the GNAS, menin, PRKAR1A, AIP, and p27 (CDKN1B) genes, respectively.
  • Intense molecular studies of sporadic pituitary tumors from patients with negative family histories and no other neoplasms have yielded interesting findings with abnormalities in growth factor expression and cell cycle control dysregulation.
  • To add to the difficulties in understanding pituitary tumorigenesis in man, good murine models of these neoplasms simply do not exist: pituitary tumors are common in rodents, but their histologic origin (mostly from the intermediate lobe), age of presentation (late in murine life) and clinical course make them hardly models of their human counterparts.
  • The present report reviews the clinical and molecular genetics of the cAMP-dependent protein kinase pathway in human pituitary tumors; it also reviews briefly other pathways that have been involved in sporadic pituitary neoplasms.
  • At the end, we attempt a unifying hypothesis for pituitary tumorigenesis, taking into account data that are also discussed elsewhere in this issue.
  • [MeSH-major] Cyclic AMP-Dependent Protein Kinases / genetics. Pituitary Neoplasms / enzymology. Pituitary Neoplasms / genetics
  • [MeSH-minor] Adenoma / enzymology. Adenoma / etiology. Adenoma / genetics. Adenoma / pathology. Animals. Cell Cycle / genetics. Growth Substances / genetics. Humans. Mice. Models, Biological. Molecular Biology. Neoplasm Proteins / genetics. Receptors, Growth Factor / genetics. Securin. Signal Transduction. Syndrome

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  • (PMID = 17613552.001).
  • [ISSN] 0964-6906
  • [Journal-full-title] Human molecular genetics
  • [ISO-abbreviation] Hum. Mol. Genet.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Growth Substances; 0 / Neoplasm Proteins; 0 / Receptors, Growth Factor; 0 / Securin; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases
  • [Number-of-references] 93
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39. Li M, Keiser HD, Peeva E: Prolactinoma and systemic lupus erythematosus: do serum prolactin levels matter? Clin Rheumatol; 2006 Jul;25(4):602-5
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  • [Title] Prolactinoma and systemic lupus erythematosus: do serum prolactin levels matter?
  • The lactogenic hormone prolactin is produced in part by cells of the immune system and serves as an upregulator of immune function.
  • Hyperprolactinemia is common in patients with systemic lupus erythematosus (SLE), raising the possibility that the hormone contributes to the excessive immune response in the disease.
  • The highest levels of circulating prolactin occur in association with prolactin-secreting tumors, but prolactinomas have only rarely been encountered in patients with SLE.
  • We present here three patients with SLE and prolactinomas.
  • As with the previously reported six patients, there was no consistency in the presence of findings related to prolactin excess or in the coincidence of hyperprolactinemia with flares of SLE disease activity.
  • We speculate that this may be due to genetic differences in the response to prolactin and/or to the presence of variant prolactin isoforms detected in the clinical immunoassay that have reduced or absent biologic activity.
  • [MeSH-major] Lupus Erythematosus, Systemic / complications. Pituitary Neoplasms / complications. Prolactin / blood. Prolactinoma / complications


40. Yoneoka Y, Isogawa M, Terumitsu M, Matsuzawa H, Fujii Y: Insidious extension of pituitary prolactinoma: two can't-miss findings depicted on a 3.0-T MR system. J Neuroimaging; 2010 Jul;20(3):267-71
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  • [Title] Insidious extension of pituitary prolactinoma: two can't-miss findings depicted on a 3.0-T MR system.
  • BACKGROUND: In this article, we present two can't-miss findings on preoperative magnetic resonance imaging (MRI) using a 3.0-T MR system resulting in a better surgical option in prolactinoma treatment after emergent of dopamine agonists.
  • METHODS: We reviewed six cases of pituitary prolactinoma; each had vague or occult bulk of adenoma on 1.5-T MR imaging, which were finally confirmed by surgery.
  • With the 3.0-T MR system, 3-dimension-anisotropy-contrast (3DAC) MR imaging and 3-dimension fast spoiled gradient recalled acquisition in the steady state (3D-FSPGR) imaging were used for depiction of the adenoma.
  • RESULTS: 3DAC imaging revealed cavernous sinus (CS) pathology in three cases, and multiplanar reconstruction of 3D-FSPGR imaging revealed normal pituitary gland and invasive adenoma into the CS in three cases and creeping extension up to the contralateral side of the CS invasion in four cases.
  • (1) intrasellar creeping extension up to the opposite side of the adenoma main body and (2) intracavernous-localized adenoma with indistinct intrasellar mass should be carefully considered when neurosurgeons perform adenomectomy for patients with prolactinoma, even in cases of microprolactinoma.
  • [MeSH-major] Image Processing, Computer-Assisted / methods. Magnetic Resonance Imaging / methods. Pituitary Neoplasms / pathology. Prolactinoma / pathology

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  • (PMID = 19453836.001).
  • [ISSN] 1552-6569
  • [Journal-full-title] Journal of neuroimaging : official journal of the American Society of Neuroimaging
  • [ISO-abbreviation] J Neuroimaging
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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41. Webb C, Prayson RA: Pediatric pituitary adenomas. Arch Pathol Lab Med; 2008 Jan;132(1):77-80
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  • [Title] Pediatric pituitary adenomas.
  • CONTEXT: Pituitary adenomas are relatively rare occurrences in the pediatric population, and there are few studies documenting the profile of these tumors in this age group.
  • OBJECTIVE: To study the clinical and pathologic features of pediatric pituitary adenomas in conjunction with a review of the available literature.
  • DESIGN: A retrospective clinicopathologic review of 20 pediatric patients (younger than 20 years of age) with pituitary adenomas resected during a 24.5-year period (1981-2005).
  • Tumor size based on radiographic data was known for 19 tumors; 12 adenomas were greater than 1 cm in greatest dimension, and 7 were less than 1 cm.
  • On follow-up, 2 patients with total gross tumor resections had recurrent adenomas; time to recurrence was 5 months and 17 months, respectively.
  • Nine adenomas stained solely for prolactin, 5 for adrenocorticotropic hormone, and 3 for growth hormone.
  • Two stained for growth hormone and prolactin.
  • CONCLUSIONS: Most pediatric pituitary adenomas present after the onset of puberty and present with frequent headaches, changes in visual acuity and, in females, menstrual dysfunction.
  • Most (19/20) were secretory, with prolactinomas being the most common type.
  • [MeSH-major] Pituitary Neoplasms / diagnosis
  • [MeSH-minor] Adolescent. Adrenocorticotropic Hormone / metabolism. Adult. Biomarkers, Tumor / metabolism. Child. Disease-Free Survival. Female. Growth Hormone / metabolism. Headache / diagnosis. Humans. Male. Menstruation Disturbances / diagnosis. Neoplasm Recurrence, Local. Prolactin / metabolism. Retrospective Studies. Vision Disorders / diagnosis

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  • (PMID = 18181678.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 9002-60-2 / Adrenocorticotropic Hormone; 9002-62-4 / Prolactin; 9002-72-6 / Growth Hormone
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42. Maclean FR, Hanley JP: Prolactinoma presenting as chronic anaemia with osteoporosis: a case report. J Med Case Rep; 2010;4:33
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  • [Title] Prolactinoma presenting as chronic anaemia with osteoporosis: a case report.
  • INTRODUCTION: Unexplained anaemia is a rare mode of presentation for prolactinoma.
  • We describe a case of a man, with chronic anaemia ascribed to old age.
  • Six years later, he was evaluated and diagnosed with a prolactinoma and resultant osteoporosis.
  • Prolactinoma in old people may present insidiously with chronic anaemia and osteoporosis with or without sexual dysfunction.
  • CASE PRESENTATION: We describe the case of a 70-year-old Caucasian man who presented with mild anaemia and tiredness.
  • His serum prolactin was massively increased and a magnetic resonance imaging (MRI) scan of the head demonstrated a pituitary mass consistent with a prolactinoma.
  • Treatment of the prolactinoma led to a reduction in his serum prolactin with a rise in his haemoglobin to normal levels.
  • This suggested that the prolactinoma was present during the initial presentation and was the cause of his anaemia.

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  • (PMID = 20205855.001).
  • [ISSN] 1752-1947
  • [Journal-full-title] Journal of medical case reports
  • [ISO-abbreviation] J Med Case Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2825518
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43. 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
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  • [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

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  • (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
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44. Furtado SV, Venkatesh PK, Ghosal N, Hegde AS: Coexisting intracranial tumors with pituitary adenomas: genetic association or coincidence? J Cancer Res Ther; 2010 Apr-Jun;6(2):221-3
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  • [Title] Coexisting intracranial tumors with pituitary adenomas: genetic association or coincidence?
  • The authors report three rare cases of intracranial tumors associated with pituitary adenomas.
  • Two of the pituitary tumors were functioning adenomas: a prolactinoma and a thyrotropin secreting adenoma.
  • We briefly discuss the presentation and treatment options of these cases and review the 19 previous publications in the literature of pituitary tumors occurring in association with other neoplasms and explore the possible links underlying these co-occurring neoplasms.
  • Our three cases represent 0.86% of all pituitary tumors operated at our institute over a 9-year period.
  • [MeSH-major] Adenoma / complications. Brain Neoplasms / complications. Genetic Predisposition to Disease. Pituitary Neoplasms / complications

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  • (PMID = 20622373.001).
  • [ISSN] 1998-4138
  • [Journal-full-title] Journal of cancer research and therapeutics
  • [ISO-abbreviation] J Cancer Res Ther
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
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45. McPhail LD, Griffiths JR, Robinson SP: Assessment of tumor response to the vascular disrupting agents 5,6-dimethylxanthenone-4-acetic acid or combretastatin-A4-phosphate by intrinsic susceptibility magnetic resonance imaging. Int J Radiat Oncol Biol Phys; 2007 Nov 15;69(4):1238-45
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  • METHODS AND MATERIALS: Multigradient echo MRI was used to quantify R(2)(*) in rat GH3 prolactinomas.

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  • (PMID = 17967313.001).
  • [ISSN] 0360-3016
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Biomarkers, Tumor; 0 / Hemoglobins; 0 / Stilbenes; 0 / Xanthones; 0829J8133H / vadimezan; 9008-02-0 / deoxyhemoglobin; I5590ES2QZ / fosbretabulin
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46. Acharya SV, Gopal RA, Bandgar TR, Joshi SR, Menon PS, Shah NS: Clinical profile and long term follow up of children and adolescents with prolactinomas. Pituitary; 2009;12(3):186-9
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  • [Title] Clinical profile and long term follow up of children and adolescents with prolactinomas.
  • We report clinical presentation, response to medical treatment, and long-term follow-up of 39 children and adolescents with prolactinoma (F:M; 30:9) (30 macro and 9 microadenoma) diagnosed at the age of 9-20 years.
  • Mean serum prolactin (PRL) concentration at the time of diagnosis was 322.50 ng/ml in patients with microadenoma, 522.38 ng/ml in patients with macroadenoma and 2,294.86 ng/ml in patients with macroadenoma with suprasellar extension.
  • In 25 patients, BC normalized PRL levels and caused variable, but significant, tumor shrinkage.
  • Cabergoline normalized PRL concentrations in 14 patients.
  • Impairment of other pituitary hormone secretion was documented at the time of diagnosis in only one patient.
  • Postoperatively six patients had other pituitary hormone deficiencies.
  • In conclusion, the medical treatment with dopaminergic compounds is effective and safe in patients with prolactinoma with onset in childhood, allowing preservation of the anterior pituitary function.
  • [MeSH-major] Prolactinoma / pathology
  • [MeSH-minor] Adolescent. Amenorrhea / pathology. Bromocriptine / therapeutic use. Child. Dopamine Agonists / therapeutic use. Ergolines / therapeutic use. Female. Galactorrhea / pathology. Humans. Male. Pregnancy. Prolactin / blood. Retrospective Studies. Treatment Outcome. Young Adult

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  • (PMID = 18946737.001).
  • [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; 0 / Ergolines; 3A64E3G5ZO / Bromocriptine; 9002-62-4 / Prolactin; LL60K9J05T / cabergoline
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47. Radaelli E, Arnold A, Papanikolaou A, Garcia-Fernandez RA, Mattiello S, Scanziani E, Cardiff RD: Mammary tumor phenotypes in wild-type aging female FVB/N mice with pituitary prolactinomas. Vet Pathol; 2009 Jul;46(4):736-45
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  • [Title] Mammary tumor phenotypes in wild-type aging female FVB/N mice with pituitary prolactinomas.
  • Prolactin-secreting pituitary adenomas are common spontaneous lesions in aging FVB females.
  • Prolactin-secreting pituitary proliferations play a significant role in mouse mammary tumorigenesis generally producing adenosquamous carcinomas.
  • Since genetically engineered FVB mice are frequently used to study mammary tumor biology, we have examined a cohort of 64 aging wild-type FVB/N females to establish the prevalence and the nature of spontaneous mammary and pituitary tumors.
  • Tissues from mammary and pituitary glands were studied by histopathology and immunohistochemistry.
  • Of the 64 examined mice, 20 had pituitary tumors and 20 had mammary tumors.
  • Mammary and pituitary tumors were associated in 17 mice.
  • All pituitary tumors were prolactin-positive by immunohistochemistry and classified as prolactinomas.
  • Fourteen mammary tumors, including 12 cases with and 2 without concurrent prolactinomas, were adenocarcinomas with different combinations of epithelial growth patterns.
  • Five mice with prolactinomas had mammary tumors characterized by the epithelial-mesenchymal transition (EMT) phenotype.
  • This study confirms that spontaneous prolactinomas and mammary tumors are both common and significantly associated lesions in FVB mice.
  • Compared with previous reports, prolactinoma-associated mammary tumors displayed a broader morphologic spectrum, including cases with the EMT phenotype.
  • The elevated number of prolactinoma-associated and ERalpha-positive mammary tumors opens intriguing possibilities concerning the role of ERalpha cytoplasmic localization during EMT tumorigenesis.

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  • (PMID = 19276050.001).
  • [ISSN] 1544-2217
  • [Journal-full-title] Veterinary pathology
  • [ISO-abbreviation] Vet. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA141582; United States / NCI NIH HHS / CA / CA55909
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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48. Platta CS, Mackay C, Welsh JS: Pituitary adenoma: a radiotherapeutic perspective. Am J Clin Oncol; 2010 Aug;33(4):408-19
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  • [Title] Pituitary adenoma: a radiotherapeutic perspective.
  • Pituitary adenomas comprise approximately 10% to 20% of all central nervous system neoplasms whereas autopsy series have suggested that the incidence of pituitary adenoma in the general population may approach 25%.
  • Several treatment modalities are used in the treatment of pituitary adenomas, including observation, surgery, medical intervention, and radiotherapy.
  • The treatment modality employed depends greatly on the type of pituitary adenoma and presenting symptoms.
  • This review will discuss the biology of pituitary adenomas and the current management principles for the treatment of prolactinomas, Cushing disease, acromegaly, and nonsecretory adenomas, with an emphasis on the published radiotherapeutic literature.
  • [MeSH-major] Adenoma / radiotherapy. Pituitary Neoplasms / radiotherapy
  • [MeSH-minor] Adult. Follow-Up Studies. Humans. Hypothalamus / physiology. Incidence. Organ Size. Pituitary Gland / anatomy & histology. Pituitary Gland / physiology. Retrospective Studies. United States / epidemiology

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  • (PMID = 19687730.001).
  • [ISSN] 1537-453X
  • [Journal-full-title] American journal of clinical oncology
  • [ISO-abbreviation] Am. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 155
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49. Tsinzerling N, Pirskanen R, Matell G, Zhulev NM, Chukhlovina ML, Lefvert AK: Raised prolactin levels in myasthenia gravis: two case reports and a study of two patient populations. Acta Neurol Scand; 2006 Nov;114(5):346-9
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  • [Title] Raised prolactin levels in myasthenia gravis: two case reports and a study of two patient populations.
  • OBJECTIVES: To describe two patients with myasthenia gravis (MG) and prolactinoma and analyze the associations between MG and prolactin (PRL) levels.
  • DESIGN: Two case reports and a case-control study of PRL levels in 192 patients with MG.
  • RESULTS: Two women with MG and thymic hyperplasia accompanied by prolactinomas are described.
  • The levels of plasma PRL were raised in 101 women with MG, but not in 91 men.
  • There was an association between high PRL levels and high levels of autoantibodies against the acetylcholine receptor.
  • CONCLUSIONS: There is an association of MG with raised levels of PRL in women.
  • PRL has stimulating effects on immune activation and the increased levels might thus be implied in the pathophysiology of MG.
  • [MeSH-major] Myasthenia Gravis / complications. Pituitary Neoplasms / complications. Prolactin / blood. Prolactinoma / complications. Thymoma / complications

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  • (PMID = 17022784.001).
  • [ISSN] 0001-6314
  • [Journal-full-title] Acta neurologica Scandinavica
  • [ISO-abbreviation] Acta Neurol. Scand.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Autoantibodies; 0 / Receptors, Cholinergic; 9002-62-4 / Prolactin
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50. Mikami S, Kameyama K, Takahashi S, Yoshida K, Kawase T, Sano T, Mukai M: Combined gangliocytoma and prolactinoma of the pituitary gland. Endocr Pathol; 2008;19(2):117-21
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  • [Title] Combined gangliocytoma and prolactinoma of the pituitary gland.
  • Gangliocytomas of the pituitary gland are rare lesions that often occur in combination with pituitary adenomas, which are frequently associated with the hypersecretion of pituitary hormones, particularly growth hormones.
  • We report a case of combined gangliocytoma and prolactinoma of the pituitary gland.
  • Histologically, the tumor was composed of adenoma cells, mature ganglion cells and cells with features intermediate between those of adenoma cells and ganglion cells (intermediate cells).
  • Immunohistochemical analysis revealed the ganglion cells and intermediate cells as well as adenoma cells to be positive for prolactin.
  • The first is that adenoma cells transform into ganglion cells, and the second is that both components originate from the embryonal pituitary cell rests, showing intermediate features between ganglion cells and adenoma cells.
  • [MeSH-major] Ganglioneuroma / pathology. Pituitary Neoplasms / pathology. Prolactinoma / pathology
  • [MeSH-minor] Coloring Agents. Eosine Yellowish-(YS). Fluorescent Dyes. Headache / etiology. Hematoxylin. Humans. Immunohistochemistry. Magnetic Resonance Imaging. Male. Middle Aged. Paraffin Embedding. Pituitary Hormones / blood. Tissue Fixation. Vertigo / etiology

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  • (PMID = 18651251.001).
  • [ISSN] 1046-3976
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Coloring Agents; 0 / Fluorescent Dyes; 0 / Pituitary Hormones; TDQ283MPCW / Eosine Yellowish-(YS); YKM8PY2Z55 / Hematoxylin
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51. Molitch ME: The cabergoline-resistant prolactinoma patient: new challenges. J Clin Endocrinol Metab; 2008 Dec;93(12):4643-5
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  • [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

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  • [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
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52. Pawlikowski M: Immunohistochemical detection of dopamine D2 receptors in human pituitary adenomas. Folia Histochem Cytobiol; 2010 Sep 30;48(3):394-7
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  • [Title] Immunohistochemical detection of dopamine D2 receptors in human pituitary adenomas.
  • Thirty one pituitary adenomas and 3 samples of peritumoral anterior pituitary tissue were immunostained with an antibody raised against dopamine D2 receptor protein.
  • The positive reactions were found in cell cytoplasm, a subpopulation of cell nuclei and the intratumoral blood vessels walls.
  • As expected, the positive immunostaining was shown in cytoplasm and/or cell nuclei of all examined prolactinomas (7/7).
  • In acromegaly the positive D2 staining occurred in 5/7 samples, in gonadotropinomas in 6/8 and in plurihormonal adenomas 2/4.
  • These findings corroborate with the well known efficacy of D2 agonists in the treatment of prolactinomas and somatotropinomas, and support the rationale of the therapeutic trials with these compounds in gonadotropinomas.
  • Moreover, the presence of D2 receptors in intratumoral blood vessels walls constitutes the possibility of the anti-angiogenic action of D2 agonists in pituitary adenomas.

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  • (PMID = 21071344.001).
  • [ISSN] 1897-5631
  • [Journal-full-title] Folia histochemica et cytobiologica
  • [ISO-abbreviation] Folia Histochem. Cytobiol.
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Receptors, Dopamine D2
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53. Siddiqui A, Chew N, Miszkiel K: Case report: Unusual orbital invasion by a giant prolactinoma. Br J Radiol; 2008 Nov;81(971):e259-62
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  • [Title] Case report: Unusual orbital invasion by a giant prolactinoma.
  • Intra-orbital extension of giant pituitary adenomas is an extremely uncommon event.
  • We describe the imaging appearances of a giant prolactinoma presenting with proptosis owing to an unusual pattern of intraorbital extension and extensive skull base involvement.
  • The CT and MRI findings of a middle-aged man presenting with proptosis are described.
  • In conclusion, radiologists should be wary of such an unusual pattern of intraorbital extension of giant pituitary adenomas, which may mimic an enlarged superior ophthalmic vein on axial CT imaging.
  • [MeSH-major] Orbital Neoplasms / diagnosis. Pituitary Neoplasms / diagnosis. Prolactinoma / diagnosis
  • [MeSH-minor] Adult. Exophthalmos / etiology. Humans. Magnetic Resonance Imaging. Male. Neoplasm Invasiveness. Prolactin / blood. Retinal Vein / radiography. Tomography, X-Ray Computed

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  • (PMID = 18941037.001).
  • [ISSN] 1748-880X
  • [Journal-full-title] The British journal of radiology
  • [ISO-abbreviation] Br J Radiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 9002-62-4 / Prolactin
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54. Harzallah F, Harzallah L, Ben Brahim A, Mekaouer A, Slimane H: [Macroprolactinoma revealed by an exophthalmos]. J Fr Ophtalmol; 2009 Feb;32(2):133.e1-3
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  • [Transliterated title] Macroadénome à prolactine révélé par une exophtalmie.
  • With the purpose of illustrating a particular circumstance of giant macroprolactinoma diagnosis, we report the case of a 54-year-old woman who was seen in the Endocrinology department with the suspected diagnosis of hyperthyroidism in presence of unilateral exophthalmos.
  • The hormonal investigation confirmed the diagnosis of prolactinoma, with a level of 8723 ng/ml, and revealed hypopituitarism.
  • The start of bromocriptin treatment was followed by a fall in the prolactin level to less then 200 ng/ml in 1 month.
  • [MeSH-major] Exophthalmos / etiology. Pituitary Neoplasms / complications. Prolactinoma / complications

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  • (PMID = 20579476.001).
  • [ISSN] 1773-0597
  • [Journal-full-title] Journal français d'ophtalmologie
  • [ISO-abbreviation] J Fr Ophtalmol
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
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55. Buchbinder S, Bierhaus A, Zorn M, Nawroth PP, Humpert P, Schilling T: Aryl hydrocarbon receptor interacting protein gene (AIP) mutations are rare in patients with hormone secreting or non-secreting pituitary adenomas. Exp Clin Endocrinol Diabetes; 2008 Nov;116(10):625-8
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  • [Title] Aryl hydrocarbon receptor interacting protein gene (AIP) mutations are rare in patients with hormone secreting or non-secreting pituitary adenomas.
  • OBJECTIVE: Recent data suggest that mutations in the aryl hydrocarbon receptor interacting protein gene (AIP) are associated with pituitary adenomas.
  • METHODS: 110 Caucasian patients living in Germany with pituitary adenoma (55 hormone secreting, 55 non-functioning) were examined for AIP mutations.
  • All three patients suffered from non-functioning adenoma.
  • Additionally, a silent polymorphism, D172D (c.516C>T), was found in 3 patients with non-functioning adenoma, in 2 patients with prolactinoma and in one patient with acromegaly.
  • CONCLUSIONS: AIP mutations are rare in sporadic pituitary adenomas in the German population and occur independently from a hormone secretion of the adenoma.
  • [MeSH-major] Adenoma / genetics. Adenoma / secretion. Chromosomes, Human, Pair 11. Intracellular Signaling Peptides and Proteins / genetics. Mutation. Pituitary Neoplasms / genetics. Pituitary Neoplasms / secretion
  • [MeSH-minor] Adult. Age of Onset. Aged. Amino Acid Substitution. Chromosome Mapping. Female. Humans. Male. Middle Aged. Pedigree. Pituitary Hormones / secretion

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  • (PMID = 18484068.001).
  • [ISSN] 0947-7349
  • [Journal-full-title] Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association
  • [ISO-abbreviation] Exp. Clin. Endocrinol. Diabetes
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / Pituitary Hormones; 0 / aryl hydrocarbon receptor-interacting protein
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56. Naliato EC, Farias ML, Braucks GR, Costa FS, Zylberberg D, Violante AH: Prevalence of osteopenia in men with prolactinoma. J Endocrinol Invest; 2005 Jan;28(1):12-7
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  • [Title] Prevalence of osteopenia in men with prolactinoma.
  • The aim of this cross-sectional study was to analyze bone mineral density (BMD) and prevalence of osteopenia and osteoporosis in 30 men with prolactinoma, and compare them to 22 control subjects.
  • PRL, testosterone, estradiol, sexual hormone-binding globulin and free androgen and estrogen indexes (FAI and FEI, respectively) were measured in all the subjects.
  • In patients with prolactinoma, mean values of PRL and testosterone were calculated for the 12-month period that preceded the study.
  • The mean T-score of the four sites analyzed by bone densitometry was lower in men with prolactinoma than in controls (p-values: lumbar spine=0.015, femoral neck <0.0001, trochanter=0.037, total femur=0.036), and 55.6% of the former presented osteopenia or osteoporosis at one or more sites (p =0.035).
  • The lumbar spine was the most seriously affected site, where 29.6% had osteopenia and 14.8% had osteoporosis.
  • By the time of BMD determination, significant associations were found between BMD and PRL, testosterone, FAI, estradiol, FEI, and duration of hypogonadism.
  • Considering the period of 12 months that preceded BMD evaluation, trochanter BMD was associated with mean PRL levels, while there was an association between lumbar spine BMD and mean testosterone levels.
  • In conclusion, men with prolactinoma have high prevalence of osteopenia and osteoporosis.
  • [MeSH-major] Bone Diseases, Metabolic / epidemiology. Bone Diseases, Metabolic / etiology. Osteoporosis / epidemiology. Osteoporosis / etiology. Prolactinoma / complications

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  • (PMID = 15816365.001).
  • [ISSN] 0391-4097
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Estrogens; 0 / Hormones
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57. Manuchehri AM, Sathyapalan T, Lowry M, Turnbull LW, Rowland-Hill C, Atkin SL: Effect of dopamine agonists on prolactinomas and normal pituitary assessed by dynamic contrast enhanced magnetic resonance imaging (DCE-MRI). Pituitary; 2007;10(3):261-6
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  • [Title] Effect of dopamine agonists on prolactinomas and normal pituitary assessed by dynamic contrast enhanced magnetic resonance imaging (DCE-MRI).
  • CONTEXT: Dopamine agonists (DA) may act on prolactinoma size and secretion through additional effects on adenoma vascularity that can be visualized using dynamic contrast enhanced magnetic resonance imaging (DCE-MRI).
  • OBJECTIVE: We hypothesized that DAs may exert their effect through a change in tumour functional vascularity leading to a reduction of prolactin (PRL) levels and tumour size.
  • Data were analysed using the Brix model, producing a measure of vascular permeability and leakage space.
  • RESULTS: PRL levels were significantly reduced in all patients and volunteers.
  • CONCLUSION: Functional prolactinoma vascularity differs from non-lesion hyperprolactinemic pituitary and normal pituitary, and is responsive to DA therapy.
  • [MeSH-major] Dopamine Agonists / therapeutic use. Pituitary Gland / drug effects. Pituitary Gland / metabolism. Pituitary Neoplasms / drug therapy. Prolactinoma / drug therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Aminoquinolines / pharmacokinetics. Aminoquinolines / therapeutic use. Contraceptives, Oral, Hormonal / adverse effects. Ergolines / pharmacokinetics. Ergolines / therapeutic use. Female. Humans. Immunoglobulin G / analysis. Magnetic Resonance Imaging. Male. Middle Aged. Prolactin / blood

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  • (PMID = 17557207.001).
  • [ISSN] 1386-341X
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminoquinolines; 0 / Contraceptives, Oral, Hormonal; 0 / Dopamine Agonists; 0 / Ergolines; 0 / Immunoglobulin G; 80Q9QWN15M / quinagolide; 9002-62-4 / Prolactin; LL60K9J05T / cabergoline
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58. Kars M, Pereira AM, Smit JW, Romijn JA: Long-term outcome of patients with macroprolactinomas initially treated with dopamine agonists. Eur J Intern Med; 2009 Jul;20(4):387-93
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: Dopamine agonists are the first line therapy for the treatment of prolactinomas.
  • Median prolactin level of the untreated patients was 460 microg/L (range 96-35,398 microg/L) at presentation.
  • During long-term follow-up, normoprolactinemia was present in 85% of the patients, but biochemical remission (normal prolactin levels in the absence of dopamine agonists) was present in only 22% of the patients.
  • CONCLUSION: Dopamine agonists are effective in normalizing prolactin values, and inducing tumor shrinkage.
  • [MeSH-major] Dopamine Agonists / administration & dosage. Pituitary Neoplasms / drug therapy. Pituitary Neoplasms / mortality. Prolactinoma / drug therapy. Prolactinoma / mortality

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  • (PMID = 19524180.001).
  • [ISSN] 1879-0828
  • [Journal-full-title] European journal of internal medicine
  • [ISO-abbreviation] Eur. J. Intern. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Dopamine Agonists
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59. Kars M, Dekkers OM, Pereira AM, Romijn JA: Update in prolactinomas. Neth J Med; 2010 Mar;68(3):104-12
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Update in prolactinomas.
  • Prolactinomas are a frequent cause of gonadal dysfunction and infertility, especially in women.
  • Dopamine agonists are first-line therapy and their efficacy in the treatment of prolactinomas is well established.
  • Current challenges related to the management of prolactinomas remain in the recurrence of the disease after withdrawal of dopamine agonists, the potential of increased risk of cardiac valvulopathy, which is observed in patients treated with high-dose cabergoline for Parkinson's disease, the effects of pregnancy, and impaired quality of life associated with pituitary adenomas in general, and prolactinomas in particular.
  • Although most prolactinomas are biochemically well controlled by pharmaceutical treatment, long-term follow-up is required.
  • [MeSH-major] Pituitary Neoplasms / diagnosis. Pituitary Neoplasms / therapy. Prolactinoma / diagnosis. Prolactinoma / therapy

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  • (PMID = 20308704.001).
  • [ISSN] 1872-9061
  • [Journal-full-title] The Netherlands journal of medicine
  • [ISO-abbreviation] Neth J Med
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 96
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60. Ozturk M, Chiu CY, Akdeniz N, Jenq SF, Chang SC, Hsa CY, Jap TS: Two novel mutations in the MEN1 gene in subjects with multiple endocrine neoplasia-1. J Endocrinol Invest; 2006 Jun;29(6):523-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Multiple endocrine neoplasia type 1 (MEN1) is characterized by parathyroid, enteropancreatic endocrine and pituitary adenomas as well as germline mutation of the MEN1 gene.
  • One family was of Turkish origin, and the index patient had primary hyperparathyroidism (PHPT) plus a prolactinoma; three relatives had PHPT only.
  • This patient presented with a complaint of epigastric pain and watery diarrhea over the past 3 months, and had undergone subtotal parathyroidectomy and enucleation of pancreatic islet cell tumor about 10 yr before.
  • There was also a prolactinoma.
  • [MeSH-minor] Adenoma / genetics. Adolescent. Adult. Aged. Amino Acid Sequence. Child. Child, Preschool. DNA Mutational Analysis. Female. Humans. Hyperparathyroidism, Primary / genetics. Male. Middle Aged. Parathyroid Neoplasms / genetics. Pituitary Neoplasms / genetics. Prolactinoma / genetics. Taiwan. Turkey

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  • (PMID = 16840830.001).
  • [ISSN] 0391-4097
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / MEN1 protein, human; 0 / Proto-Oncogene Proteins
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61. Colson A, Brooke AM, Walker D, Besser GM, Chew SL, Grossman AB, Jenkins PJ, Drake WM, Monson JP: Growth hormone deficiency and replacement in patients with treated Cushing's Disease, prolactinomas and non-functioning pituitary adenomas: effects on body composition, glucose metabolism, lipid status and bone mineral density. Horm Res; 2006;66(6):257-67
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Growth hormone deficiency and replacement in patients with treated Cushing's Disease, prolactinomas and non-functioning pituitary adenomas: effects on body composition, glucose metabolism, lipid status and bone mineral density.
  • BACKGROUND/AIMS: This study was designed to determine whether previous Cushing's disease (CD) or prolactinoma (PRL) could exert adverse effects additional to those of growth hormone (GH) deficiency as a consequence of variable degrees of prior hypogonadism or hypercatabolism.
  • We report the effects of 5 years GH treatment in 124 GH deficiency adults; 42 patients with non-functioning pituitary adenomas (NFPA), 43 with treated PRL and 39 with treated CD.
  • RESULTS: Mean body mass index remained unchanged in the PRL group and tended to increase in the NFPA group.
  • Baseline lumbar spine and hip BMD were lower in the PRL and CD groups than in the NFPA group, decreased over 1 year in all groups and subsequently increased by 2 years in NFPA with a subsequent increase in lumbar spine BMD in PRL and CD groups delayed to 3-5 years.
  • CONCLUSIONS: Baseline characteristics and response to GH replacement are qualitatively similar in NFPA, PRL and CD patients.
  • Because improvements in BMD occur later in PRL and CD patients, an extended trial of GH therapy may be indicated in those patients who were commenced on GH therapy as an additional treatment for reduced BMD.
  • [MeSH-major] Adenoma / physiopathology. Adenoma / therapy. Blood Glucose / metabolism. Body Composition / drug effects. Bone Density / drug effects. Human Growth Hormone / deficiency. Human Growth Hormone / therapeutic use. Lipid Metabolism / drug effects. Pituitary ACTH Hypersecretion / physiopathology. Pituitary ACTH Hypersecretion / therapy. Pituitary Neoplasms / physiopathology. Pituitary Neoplasms / therapy. Prolactinoma / physiopathology. Prolactinoma / therapy


62. Giacomini D, Haedo M, Gerez J, Druker J, Páez-Pereda M, Labeur M, Stalla GK, Arzt E: Differential gene expression in models of pituitary prolactin-producing tumoral cells. Horm Res; 2009 Apr;71 Suppl 2:88-94
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differential gene expression in models of pituitary prolactin-producing tumoral cells.
  • Although several genes and signalling pathways have been identified as important effectors in the development of pituitary tumours, our understanding of pituitary tumorigenesis remains incomplete and is the focus of much current research.
  • Use of the mRNA differential display technique in prolactinomas from D2-receptor knockout mice and in stable GH3 cell line clones with enhanced tumorigenicity in vivo has led to the identification of two genes that are involved in the pathogenic process--BMP-4 and RSUME.
  • Bone morphogenetic protein-4 (BMP-4) has been found to have a crucial role in prolactinoma development and also in signalling crosstalk with oestrogens.
  • RSUME (RWD-containing sumoylation enhancer) was identified from a transformed lactosomatotrophic cell line that had increased tumorigenic and angiogenic potential.
  • The differential expression and action of BMP-4 in prolactinomas and corticotrophinomas highlights the importance of studying a gene with contrasting actions in two cell lineages of the same organ in order to understand the pituitary transformation process.
  • Both BMP-4 and RSUME may be interesting targets for inhibiting steps involved in pituitary tumorigenesis.
  • [MeSH-major] Bone Morphogenetic Protein 4 / biosynthesis. Gene Expression Regulation, Neoplastic. Models, Biological. Neoplasm Proteins / biosynthesis. Prolactinoma / metabolism. Transcription Factors / biosynthesis
  • [MeSH-minor] Animals. Cell Hypoxia / genetics. Cell Line, Tumor. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / metabolism. Gene Expression Profiling. Humans. Mice. Mice, Knockout. Receptors, Dopamine D2 / genetics. Receptors, Dopamine D2 / metabolism. Signal Transduction / genetics

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  • [Copyright] Copyright 2009 S. Karger AG, Basel.
  • (PMID = 19407504.001).
  • [ISSN] 1423-0046
  • [Journal-full-title] Hormone research
  • [ISO-abbreviation] Horm. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / BMP4 protein, human; 0 / Bone Morphogenetic Protein 4; 0 / Neoplasm Proteins; 0 / RSUME protein, human; 0 / Receptors, Dopamine D2; 0 / Transcription Factors
  • [Number-of-references] 56
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63. De Martino I, Visone R, Wierinckx A, Palmieri D, Ferraro A, Cappabianca P, Chiappetta G, Forzati F, Lombardi G, Colao A, Trouillas J, Fedele M, Fusco A: HMGA proteins up-regulate CCNB2 gene in mouse and human pituitary adenomas. Cancer Res; 2009 Mar 1;69(5):1844-50
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HMGA proteins up-regulate CCNB2 gene in mouse and human pituitary adenomas.
  • We have recently reported that transgenic mice carrying the Hmga1 or Hmga2 genes under transcriptional control of the cytomegalovirus promoter develop pituitary adenomas secreting prolactin and growth hormone.
  • We have shown that the mechanism of the HMGA2-induced pituitary adenoma is based on the increased E2F1 activity.
  • The expression profile of mouse normal pituitary glands and adenomas induced in HMGA transgenic mice revealed an increased expression of the ccnb2 gene, coding for the cyclin B2 protein, in the neoplastic tissues compared with the normal pituitary gland.
  • Finally, we report an increased CCNB2 expression in human pituitary adenomas of different histotypes that is directly correlated with HMGA1 and HMGA2 expression.
  • Because cyclin B2 is involved in the regulation of the cell cycle, these results taken together indicate that HMGA-induced cyclin B2 overexpression gives an important contribution to experimental and human pituitary tumorigenesis.
  • [MeSH-major] Adenoma / genetics. Cyclin B / genetics. Gene Expression Regulation, Neoplastic. HMGA1a Protein / physiology. HMGA2 Protein / physiology. Pituitary Neoplasms / genetics


64. Botelho CH, Magalhães AV, Mello PA, Schmitt FC, Casulari LA: Expression of p53, Ki-67 and c-erb B2 in growth hormone-and/or prolactin-secreting pituitary adenomas. Arq Neuropsiquiatr; 2006 Mar;64(1):60-6
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  • [Title] Expression of p53, Ki-67 and c-erb B2 in growth hormone-and/or prolactin-secreting pituitary adenomas.
  • The subcellular events implicated on the formation and behavior of pituitary adenomas are not fully understood.
  • In this study we investigated the presence of p53, Ki-67 and c-erb B2 in 38 pituitary adenomas with immunohistochemical positivity for GH and prolactin (n=26; 68.4%), for prolactin (n=9; 23.7%) and for GH (n=3. 7.8%).
  • Our results demonstrated a high percentage of GH/prolactin-, prolactin- and GH-secreting tumors with immunohistochemical positivity for c-erb B2.
  • [MeSH-major] Growth Hormone / secretion. Ki-67 Antigen / analysis. Neoplasm Proteins / analysis. Pituitary Neoplasms / metabolism. Prolactinoma / metabolism. Receptor, ErbB-2 / analysis. Tumor Suppressor Protein p53 / analysis

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  • (PMID = 16622555.001).
  • [ISSN] 0004-282X
  • [Journal-full-title] Arquivos de neuro-psiquiatria
  • [ISO-abbreviation] Arq Neuropsiquiatr
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Neoplasm Proteins; 0 / Tumor Suppressor Protein p53; 9002-72-6 / Growth Hormone; EC 2.7.10.1 / Receptor, ErbB-2
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65. Basu A, Brabant G, Gnanalingham KK: More than a prolactinoma. Pituitary; 2010;13(1):87-8
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  • [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

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  • (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
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66. 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
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  • [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

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  • (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
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67. Ansarin H, Aziz-Jalali MH, Rasi A, Soltani-Arabshahi R: Clinical presentation and etiologic factors of hirsutism in premenopausal Iranian women. Arch Iran Med; 2007 Jan;10(1):7-13
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  • The disease may be associated with other clinical signs of hyperandrogenism.
  • METHODS: In a cross-sectional study, 790 consecutive premenopausal women referred to the dermatology Clinics of Hazrat-e Rasool and Firoozgar University Hospitals and three private dermatology clinics during 2001 - 2003 with the clinical diagnosis of hirsutism were studied.
  • Etiology of hirsutism was identified as polycystic ovary syndrome (62.53%), idiopathic (35.19%), congenital adrenal hyperplasia (0.38%), prolactinoma (0.13%), and undetermined (1.77%).
  • Eumenorrhea does not rule out endocrine abnormality and particularly polycystic ovary syndrome which is a common cause of hirsutism.

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  • (PMID = 17198446.001).
  • [ISSN] 1029-2977
  • [Journal-full-title] Archives of Iranian medicine
  • [ISO-abbreviation] Arch Iran Med
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] Iran
  • [Chemical-registry-number] 0 / Androgens
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68. Piccoli GB, Bermont F, Magnano A, Soragna G, Terzolo M: Prolactinoma in a diabetic dialysis patient with erectile dysfunction: a difficult differential diagnosis. Rev Diabet Stud; 2006;3(4):200-4
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  • [Title] Prolactinoma in a diabetic dialysis patient with erectile dysfunction: a difficult differential diagnosis.
  • Diabetes, diffuse vascular disease and pharmacological therapy are attendant causes of this condition, severely impairing the quality of life.
  • Nevertheless, a careful differential diagnosis is also warranted in well dialyzed patients to identify causes and corrigible patterns.
  • On examination, the penile echo-Doppler was normal, and suggested a cause other than dia-betic vascular disease.
  • Whilst the rising prolactine level (76.1 microg/l and 129 ng/ml) was still in the range commonly found in dialysis patients, a nuclear magnetic resonance examination was carried out and led to the identification of prolactinoma.
  • It underlines the importance of a non-minimalist approach to the problem of sexual disorders in renal replacement therapy (RRT) patients, at least when dialysis efficiency is high and onset is rapid.
  • It also suggests considering prolactinoma as an emerging diagnosis in the general population, which can be detected by the use of sensitive imaging techniques in the differential diagnosis of this condition.

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  • [Cites] J Am Soc Nephrol. 2002 Nov;13(11):2770-5 [12397048.001]
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  • (PMID = 17487344.001).
  • [ISSN] 1614-0575
  • [Journal-full-title] The review of diabetic studies : RDS
  • [ISO-abbreviation] Rev Diabet Stud
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Other-IDs] NLM/ PMC1828284
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69. McCormack AI, McDonald KL, Gill AJ, Clark SJ, Burt MG, Campbell KA, Braund WJ, Little NS, Cook RJ, Grossman AB, Robinson BG, Clifton-Bligh RJ: Low O6-methylguanine-DNA methyltransferase (MGMT) expression and response to temozolomide in aggressive pituitary tumours. Clin Endocrinol (Oxf); 2009 Aug;71(2):226-33
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  • [Title] Low O6-methylguanine-DNA methyltransferase (MGMT) expression and response to temozolomide in aggressive pituitary tumours.
  • CONTEXT: Recent case reports detail the successful use of temozolomide in the management of aggressive pituitary tumours.
  • OBJECTIVE: To study MGMT expression in pituitary tumours and consider whether MGMT expression is associated with response to temozolomide therapy in aggressive pituitary tumours.
  • PATIENTS: We report two patients with aggressive pituitary tumours treated with temozolomide, one who responded to temozolomide and the other who did not.
  • MGMT expression was assessed in a further 88 archived pituitary tumour samples.
  • RESULTS: Low MGMT expression and MGMT promoter methylation were found in the pituitary tumour of the patient who responded to temozolomide.
  • Prolactinomas were more likely to have low MGMT expression compared with other pituitary tumour subtypes (P < 0.001).
  • CONCLUSION: MGMT expression as assessed by immunohistochemistry may predict response to temozolomide therapy in patients with aggressive pituitary tumours.
  • MGMT promoter methylation is likely to explain low MGMT expression in some, but not all, pituitary tumours.
  • [MeSH-major] Dacarbazine / analogs & derivatives. Gene Expression / drug effects. O(6)-Methylguanine-DNA Methyltransferase / genetics. Pituitary Neoplasms / drug therapy


70. Bunck MC, Debono M, Giltay EJ, Verheijen AT, Diamant M, Gooren LJ: Autonomous prolactin secretion in two male-to-female transgender patients using conventional oestrogen dosages. BMJ Case Rep; 2009;2009
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  • [Title] Autonomous prolactin secretion in two male-to-female transgender patients using conventional oestrogen dosages.
  • Oestrogen-induced prolactinomas have been reported in male-to-female (MTF) transgender patients after excessive oestrogen self-administration.
  • Here, two prolactinoma cases after 14 years (case 1) and 30 years (case 2) of relatively low-dose oestrogen treatment are reported.
  • During the first year of oestrogen treatment the patient in case 1 showed a remarkable (7.2-fold) increase in serum prolactin concentration, returning to within the normal range for 13 years until the start of autonomous prolactin secretion.
  • It is hypothesised that this strong first-year prolactin response may be a sign of increased pituitary oestrogen sensitivity.
  • Therefore the patient's increase in prolactin concentration during the first 18 months was compared to 74 matched control patients from a database, and this increase was found to be significantly greater in the case patient.
  • It is suggested that in MTF patients an excessive first year increase in serum prolactin concentration may identify patients at risk for autonomous prolactin secretion later in life.

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  • [Cites] Verh K Acad Geneeskd Belg. 2001;63(6):561-73; discussion 574-6 [11813510.001]
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  • (PMID = 21829422.001).
  • [ISSN] 1757-790X
  • [Journal-full-title] BMJ case reports
  • [ISO-abbreviation] BMJ Case Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC3029513
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71. Li C, Sun Z, Gui S, Liu F, Zhang Y: Effects of fulvestrant, an estrogen receptor antagonist, on MMQ cells and its mechanism. Neuro Endocrinol Lett; 2009;30(2):268-74
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  • OBJECTIVES: Unlike the successful endocrine therapy of breast cancers and other estrogen-dependent diseases, little is known about the effect of anti-estrogen treatment on pituitary tumors.
  • Our objectives were to study the effect of fulvestrant, a new type anti-estrogen devoid of any agonistic activities, on prolactinoma cell line MMQ in vitro and its possible mechanisms.
  • DESIGN: In the experiment, the prolactin concentration, proliferation and apoptosis of the MMQ cell were measured to investigate the anti-tumor effect of the fulvestrant.
  • RESULTS: Fulvestrant significantly inhibited prolactin secretion (up to 85.5%), decreased proliferation (IC50 = 32.4 nmol/l), and promoted apoptosis of the MMQ cells.
  • Thus, fulvestrant has suppressive effects on prolactinoma cells and its anti-tumor mechanism appears to be related to the inhibition of ESR and the MAPK pathway.
  • [MeSH-major] Antineoplastic Agents, Hormonal / pharmacology. Estradiol / analogs & derivatives. Estrogen Antagonists / pharmacology. Prolactinoma / drug therapy. Prolactinoma / physiopathology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Survival / drug effects. MAP Kinase Kinase 4 / metabolism. MAP Kinase Signaling System / drug effects. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. Prolactin / secretion. RNA, Messenger / metabolism. Rats. Receptors, Estrogen / metabolism. p38 Mitogen-Activated Protein Kinases / metabolism

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  • (PMID = 19675520.001).
  • [ISSN] 0172-780X
  • [Journal-full-title] Neuro endocrinology letters
  • [ISO-abbreviation] Neuro Endocrinol. Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Sweden
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Estrogen Antagonists; 0 / RNA, Messenger; 0 / Receptors, Estrogen; 22X328QOC4 / fulvestrant; 4TI98Z838E / Estradiol; 9002-62-4 / Prolactin; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 2.7.12.2 / MAP Kinase Kinase 4
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72. Melmed S: Update in pituitary disease. J Clin Endocrinol Metab; 2008 Feb;93(2):331-8
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  • [Title] Update in pituitary disease.
  • The pituitary gland secretes vital trophic hormones that maintain homeostatic regulation of the metabolic milieu.
  • Not surprisingly, several thousand papers relevant to the pituitary gland were published this past year, including publication of important transforming advances in our understanding of the pathogenesis, diagnosis, and treatment of pituitary disorders.
  • High-quality articles were selected for their translational impact, scientific advances, enrichment of new knowledge, influence on how we understand pituitary disorders, transformation of therapeutic principles, and opening up new research vistas.
  • Using these selection criteria, highlighted papers within the following categorical topics were further selected for analysis and review: advances in understanding subcellular mechanisms subserving the pathogenesis of pituitary disorders including pituitary tumors and pituitary failure; new challenges facing the physician treating patients harboring prolactinomas with dopamine agonists; and the appearance of new publications reporting the efficacy of long-term prospective medical treatment of acromegaly that now provide more rigorous patient outcome information.
  • Selected papers categorized by these topics all serve to significantly impact how the endocrinologist views disease pathogenesis, diagnosis, and treatment outcomes of patients with pituitary disease in 2007.
  • The results of these publications have transformed our understanding of important principles underlying normal and abnormal pituitary function, as well as our approach to the management of pituitary disorders.
  • Notably, they open up new vistas for creative scholarship in unraveling the challenges of pituitary medicine.
  • [MeSH-major] Pituitary Diseases / pathology. Pituitary Diseases / therapy
  • [MeSH-minor] Acromegaly / pathology. Acromegaly / therapy. Female. Human Growth Hormone / deficiency. Humans. Male. Pituitary Neoplasms / genetics. Pituitary Neoplasms / pathology. Pituitary Neoplasms / therapy. Prolactinoma / pathology. Prolactinoma / therapy

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  • (PMID = 18258780.001).
  • [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; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 12629-01-5 / Human Growth Hormone
  • [Number-of-references] 42
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73. Drori-Herishanu L, Horvath A, Nesterova M, Patronas Y, Lodish M, Bimpaki E, Patronas N, Agarwal S, Salvatori R, Martari M, Mericq V, Stratakis CA: An Intronic mutation is associated with prolactinoma in a young boy, decreased penetrance in his large family, and variable effects on MEN1 mRNA and protein. Horm Metab Res; 2009 Aug;41(8):630-4
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  • [Title] An Intronic mutation is associated with prolactinoma in a young boy, decreased penetrance in his large family, and variable effects on MEN1 mRNA and protein.
  • Prolactinomas are rare tumors in prepubertal children.
  • A prolactinoma in a young child may be due to sequence variants in genes that are known to cause these tumors ( MEN1, PRKAR1A, AIP).
  • We conclude that a novel MEN1 variation was identified in a young boy with prolactinoma and six of his relatives who did not present with prolactinoma or other MEN1 related symptoms.
  • This novel MEN1 variation may be associated with low penetrance of the disease.
  • [MeSH-major] Introns. Mutation. Prolactinoma / genetics. Proto-Oncogene Proteins / genetics

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  • [Copyright] Copyright Georg Thieme Verlag KG Stuttgart. New York.
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  • (PMID = 19391077.001).
  • [ISSN] 1439-4286
  • [Journal-full-title] Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et métabolisme
  • [ISO-abbreviation] Horm. Metab. Res.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / ZIA HD000642-13
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / MEN1 protein, human; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger
  • [Other-IDs] NLM/ NIHMS305479; NLM/ PMC3124761
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74. Schlechte JA: Long-term management of prolactinomas. J Clin Endocrinol Metab; 2007 Aug;92(8):2861-5
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  • [Title] Long-term management of prolactinomas.
  • Prolactinomas are a frequent cause of gonadal dysfunction and infertility, especially in young women.
  • The regulation of prolactin secretion and the efficacy of dopamine agonists in the therapy of prolactinomas are well established.
  • The current challenges in management of prolactinomas are related to follow-up after successful therapy.
  • Issues and questions to be addressed in this approach to long-term management of prolactinomas include the frequency of radiographic monitoring, effect of pregnancy and menopause, safety of estrogen in women taking oral contraceptives, and the potential for discontinuation of dopamine agonist therapy.
  • [MeSH-major] Pituitary Neoplasms / therapy. Prolactinoma / therapy

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  • (PMID = 17682084.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contraceptives, Oral, Hormonal; 0 / Dopamine Agonists; 0 / Estrogens
  • [Number-of-references] 46
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75. Robinson SP, Howe FA, Griffiths JR, Ryan AJ, Waterton JC: Susceptibility contrast magnetic resonance imaging determination of fractional tumor blood volume: a noninvasive imaging biomarker of response to the vascular disrupting agent ZD6126. Int J Radiat Oncol Biol Phys; 2007 Nov 1;69(3):872-9
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  • METHODS AND MATERIALS: The transverse MRI relaxation rate R(2)( *) of rat GH3 prolactinomas was quantified prior to and following injection of 2.5 mgFe/kg feruglose, an ultrasmall superparamagnetic iron oxide intravascular contrast agent, and xi (%) was determined from the change in R(2)( *).
  • [MeSH-major] Blood Volume / drug effects. Contrast Media. Iron. Magnetic Resonance Imaging / methods. Organophosphorus Compounds / therapeutic use. Oxides. Prolactinoma / physiopathology
  • [MeSH-minor] Animals. Benzimidazoles / pharmacokinetics. Dextrans. Female. Ferrosoferric Oxide. Fluorescent Dyes / pharmacokinetics. Magnetite Nanoparticles. Pituitary Neoplasms. Rats

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  • (PMID = 17889267.001).
  • [ISSN] 0360-3016
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzimidazoles; 0 / Contrast Media; 0 / Fluorescent Dyes; 0 / Magnetite Nanoparticles; 0 / N-acetylcochinol-O-phosphate; 0 / Organophosphorus Compounds; 0 / Oxides; 0 / ferumoxtran-10; 23491-52-3 / HOE 33342; E1UOL152H7 / Iron; K3R6ZDH4DU / Dextrans; XM0M87F357 / Ferrosoferric Oxide
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76. Thodou E, Kontogeorgos G, Theodossiou D, Pateraki M: Mapping of somatostatin receptor types in GH or/and PRL producing pituitary adenomas. J Clin Pathol; 2006 Mar;59(3):274-9
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  • [Title] Mapping of somatostatin receptor types in GH or/and PRL producing pituitary adenomas.
  • BACKGROUND: Somatostatin is a tetradecapeptide exerting inhibitory action on endocrine and exocrine cell secretion and proliferation.
  • Using immunohistochemistry, the expression of SST(1), SST(2A), SST(2B), SST(3), SST(4), and SST(5) was studied in tissue microarrays (TMAs), using a series of 90 human pituitary adenomas producing growth hormone and/or prolactin, including 30 of each somatotroph, lactotroph, and mixed somatotroph/lactotroph adenoma type.
  • SST(5) and SST(2A) were the predominant receptors, showing strong expression in high frequency in all three adenoma types.
  • Strong expression of SST(1) was higher in lactotroph adenomas than in other tumour types.
  • [MeSH-major] Adenoma / chemistry. Biomarkers, Tumor / analysis. Pituitary Neoplasms / chemistry. Receptors, Somatostatin / analysis
  • [MeSH-minor] Case-Control Studies. Female. Growth Hormone / secretion. Humans. Immunohistochemistry / methods. Membrane Proteins / analysis. Prolactinoma / chemistry

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  • (PMID = 16505278.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Membrane Proteins; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 0 / somatostatin receptor 3; 0 / somatostatin receptor 5; 0 / somatostatin receptor subtype-4; 9002-72-6 / Growth Hormone
  • [Other-IDs] NLM/ PMC1860351
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77. Mathioudakis N, Salvatori R: Pituitary tumors. Curr Treat Options Neurol; 2009 Jul;11(4):287-96
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  • [Title] Pituitary tumors.
  • Pituitary adenomas are the most common intrasellar tumors.
  • With the exception of prolactinomas, first-line treatment is almost always surgical.
  • Prolactinomas are usually treated with dopamine agonists such as cabergoline or bromocriptine.
  • No effective medical therapy is available for adenomas that secrete adrenocorticotropic hormone, and occasionally bilateral adrenalectomy is required to resolve severe hypercortisolemia.
  • Radiation therapy (fractionated or radiosurgery) can be used for residual or recurrent pituitary tumors.
  • Asymptomatic, nonfunctioning pituitary adenomas may be followed without any intervention, but surgery is typically indicated if there are symptoms of mass effect on the optic chiasm or endocrine dysfunction.
  • In the hands of an experienced pituitary neurosurgeon, the prognosis for endocrinologic recovery and visual improvement is good.

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  • (PMID = 19523354.001).
  • [ISSN] 1092-8480
  • [Journal-full-title] Current treatment options in neurology
  • [ISO-abbreviation] Curr Treat Options Neurol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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78. Astaf'eva LI, Kadashev BA, Trunin IuIu, Rotin DL: [Development of secondary resistance to dopamine agonists in a patient with giant prolactinoma]. Zh Vopr Neirokhir Im N N Burdenko; 2010 Oct-Dec;(4):48-51; discussion 51-2
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Development of secondary resistance to dopamine agonists in a patient with giant prolactinoma].
  • Currently conservative treatment is therapy of choice in most patients with prolactinoma.
  • Alternative method of treatment in this situation is surgery, but in case of large invasive adenoma radical removal is often not possible.
  • In 1 case radiation therapy allowed effective control of tumor size and decrease of prolactin level.
  • [MeSH-major] Dopamine Agonists / administration & dosage. Drug Resistance, Neoplasm. Prolactinoma / therapy

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  • (PMID = 21374937.001).
  • [ISSN] 0042-8817
  • [Journal-full-title] Zhurnal voprosy neĭrokhirurgii imeni N. N. Burdenko
  • [ISO-abbreviation] Zh Vopr Neirokhir Im N N Burdenko
  • [Language] rus
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Dopamine Agonists; 0 / Receptors, Dopamine D2
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79. Daly AF, Rixhon M, Adam C, Dempegioti A, Tichomirowa MA, Beckers A: High prevalence of pituitary adenomas: a cross-sectional study in the province of Liege, Belgium. J Clin Endocrinol Metab; 2006 Dec;91(12):4769-75
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  • [Title] High prevalence of pituitary adenomas: a cross-sectional study in the province of Liege, Belgium.
  • CONTEXT: Prevalence data are important for assessing the burden of disease on the health care system; data on pituitary adenoma prevalence are very scarce.
  • OBJECTIVE: The objective of the study was to measure the prevalence of clinically relevant pituitary adenomas in a well-defined population.
  • DESIGN: This was a cross-sectional, intensive, case-finding study performed in three regions of the province of Liège, Belgium, to measure pituitary adenoma prevalence as of September 30, 2005.
  • Medical practitioners in these districts were recruited, and patients with pituitary adenomas under their care were identified.
  • RESULTS: Sixty-eight patients with clinically relevant pituitary adenomas were identified in a population of 71,972 individuals; the mean (+/- sd) prevalence was 94 +/- 19.3 cases per 100,000 population (95% confidence interval, 72.2 to 115.8).
  • The group was 67.6% female and had a mean age at diagnosis of 40.3 yr; 42.6% had macroadenomas and 55.9% underwent surgery.
  • Prolactinomas comprised 66% of the group, with the rest having nonsecreting tumors (14.7%), somatotropinomas (13.2%), or Cushing's disease (5.9%); 20.6% had hypopituitarism.
  • CONCLUSION: The prevalence of pituitary adenomas in the study population (one case in 1064 individuals) was more than 3.5-5 times that previously reported.
  • This increased prevalence may have important implications when prioritizing funding for research and treatment of pituitary adenomas.
  • [MeSH-major] Adenoma / epidemiology. Pituitary Neoplasms / epidemiology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Belgium / epidemiology. Child. Cross-Sectional Studies. Female. Growth Hormone-Secreting Pituitary Adenoma / epidemiology. Growth Hormone-Secreting Pituitary Adenoma / pathology. Growth Hormone-Secreting Pituitary Adenoma / therapy. Humans. Male. Middle Aged. Pituitary ACTH Hypersecretion / epidemiology. Pituitary ACTH Hypersecretion / pathology. Pituitary ACTH Hypersecretion / therapy. Prevalence. Prolactinoma / epidemiology. Prolactinoma / pathology. Prolactinoma / therapy


80. Cristina C, Díaz-Torga GS, Goya RG, Kakar SS, Perez-Millán MI, Passos VQ, Giannella-Neto D, Bronstein MD, Becu-Villalobos D: PTTG expression in different experimental and human prolactinomas in relation to dopaminergic control of lactotropes. Mol Cancer; 2007;6:4
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  • [Title] PTTG expression in different experimental and human prolactinomas in relation to dopaminergic control of lactotropes.
  • BACKGROUND: Pituitary tumor transforming gene (pttg) is a novel oncogene that is expressed at higher level in most of the tumors analyzed to date compared to normal tissues.
  • Nevertheless, its expression in prolactinomas and its relation with the pituitary dopamine receptor 2 (D2R) are not well defined.
  • We sought to determine the pituitary level of pttg in three different experimental models of prolactinomas with altered dopaminergic control of the pituitary: the dopaminergic D2R knockout female mouse, the estrogen-treated rat, and the senescent female rat.
  • These three models shared the characteristics of increased pituitary weight, hyperprolactinemia, lactotrope hyperplasia and reduced or absent dopaminergic action at the pituitary level.
  • In senescent rats no difference in pituitary PTTG protein expression was found when compared to young rats.
  • Therefore, in the three experimental models of prolactinomas, pituitary size was increased and there was hyperprolactinemia, but PTTG levels followed different patterns.Patients with macroprolactinomas were divided in those in which dopaminergic therapy normalized or failed to normalize prolactin levels (responsive and resistant, respectively).
  • When pituitary pttg mRNA level was analyzed in these macroprolactinomas, no differences were found.
  • We next analyzed estrogen action at the pituitary by measuring pituitary estrogen receptor alpha levels.
  • The D2R knockout female mice have low estrogen levels and in accordance, pituitary estrogen receptors were increased (P = 0.047).
  • Finally, in patients with dopamine resistant or responsive prolactinomas no significant differences in estrogen receptor alpha levels were found.
  • Therefore, pituitary PTTG was increased only if estrogen action was increased, which correlated with a decrease in pituitary estrogen receptor level.
  • CONCLUSION: We conclude that PTTG does not correlate with prolactin levels or tumor size in animal models of prolactinoma, and its pituitary content is not related to a decrease in dopaminergic control of the lactotrope, but may be influenced by estrogen action at the pituitary level.
  • Therefore it is increased only in prolactinomas generated by estrogen treatment, and not in prolactinomas arising from deficient dopamine control, or in dopamine resistant compared with dopamine responsive human prolactinomas.
  • These results are important in the search for reliable prognostic indicators for patients with pituitary adenomas which will make tumor-specific therapy possible, and help to elucidate the poorly understood phenomenon of pituitary tumorigenesis.
  • [MeSH-major] Dopamine / metabolism. Lactotrophs / metabolism. Neoplasm Proteins / metabolism. Pituitary Neoplasms / metabolism. Prolactinoma / metabolism
  • [MeSH-minor] Adult. Animals. Antineoplastic Agents, Hormonal / pharmacology. Drug Resistance, Neoplasm. Estrogen Receptor alpha / metabolism. Female. Humans. Male. Mice. Mice, Inbred C57BL. Mice, Knockout. Neoplasms, Hormone-Dependent / metabolism. Neoplasms, Hormone-Dependent / pathology. Rats. Rats, Sprague-Dawley. Receptors, Dopamine / genetics. Securin

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  • (PMID = 17222350.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Estrogen Receptor alpha; 0 / Neoplasm Proteins; 0 / Receptors, Dopamine; 0 / Securin; 0 / pituitary tumor-transforming protein 1, human; VTD58H1Z2X / Dopamine
  • [Other-IDs] NLM/ PMC1779802
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81. Lebrun JJ: Activin, TGF-beta and menin in pituitary tumorigenesis. Adv Exp Med Biol; 2009;668:69-78
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Activin, TGF-beta and menin in pituitary tumorigenesis.
  • Pituitary adenomas are common monoclonal neoplasms accounting for approximately one-fifth of primary intracranial tumors.
  • Prolactin-secreting pituitary adenomas (prolactinomas) are the most common form of pituitary tumors in humans.
  • They are associated with excessive release of the hormone prolactin and increased tumor growth, giving rise to severe endocrine disorders and serious clinical concerns for the patients.
  • Recent studies indicated that the activin/TGF-beta family of growth factors plays a prominent role in regulating pituitary tumor growth and prolactin secretion from anterior pituitary lactotrope cells.
  • Furthermore, these studies highlighted the tumor suppressor menin and the protein Smads as central regulators of these biological processes in the pituitary.
  • This chapter will review the role and intracellular molecular mechanisms of action by which activin, TGF-beta, Smads and menin act in concert to prevent pituitary tumor cell growth and control hormonal synthesis by the anterior pituitary.
  • [MeSH-major] Activins / metabolism. Adenoma / metabolism. Pituitary Neoplasms / metabolism. Proto-Oncogene Proteins / metabolism. Transforming Growth Factor beta / metabolism
  • [MeSH-minor] Gene Expression Regulation, Neoplastic. Humans. Prolactin / genetics. Prolactin / metabolism. Signal Transduction / physiology. Smad Proteins / metabolism

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  • (PMID = 20175454.001).
  • [ISSN] 0065-2598
  • [Journal-full-title] Advances in experimental medicine and biology
  • [ISO-abbreviation] Adv. Exp. Med. Biol.
  • [Language] eng
  • [Grant] Canada / Canadian Institutes of Health Research / / MOP-53141
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MEN1 protein, human; 0 / Proto-Oncogene Proteins; 0 / Smad Proteins; 0 / Transforming Growth Factor beta; 104625-48-1 / Activins; 9002-62-4 / Prolactin
  • [Number-of-references] 85
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82. Lee MR: The history of ergot of rye (Claviceps purpurea) III: 1940-80. J R Coll Physicians Edinb; 2010 Mar;40(1):77-80
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  • It is widely used for the suppression of lactation, the treatment of prolactinomas and the management of Parkinson's disease.
  • [MeSH-major] Bromocriptine / history. Claviceps / chemistry. Ergot Alkaloids / history. Lysergic Acid Diethylamide / history. Parkinson Disease / history. Prolactinoma / history. Receptors, Dopamine / history

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  • (PMID = 20503690.001).
  • [ISSN] 1478-2715
  • [Journal-full-title] The journal of the Royal College of Physicians of Edinburgh
  • [ISO-abbreviation] J R Coll Physicians Edinb
  • [Language] eng
  • [Publication-type] Biography; Historical Article; Journal Article; Portraits
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Ergot Alkaloids; 0 / Receptors, Dopamine; 25447-66-9 / Dihydroergocryptine; 3A64E3G5ZO / Bromocriptine; 8NA5SWF92O / Lysergic Acid Diethylamide
  • [Personal-name-as-subject] Hofmann A; Stoll A
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83. Xia R, Berger F, Piallat B, Benabid AL: Alteration of hormone and neurotransmitter production in cultured cells by high and low frequency electrical stimulation. Acta Neurochir (Wien); 2007 Jan;149(1):67-73; discussion 73
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  • In vitro cellular effects of high (HFS) and low (LFS) frequency electrical stimulation on prolactin secretion in GH3 cell lines (prolactinoma), as well as the catecholaminergic secretion on PC12 cells (pheochromocytoma) were investigated.
  • Cells were cultured in dishes with integrated electrodes to deliver stimulation at the same parameters as those used in clinical conditions to treat advanced forms of Parkinson's disease.
  • Prolactin production was measured in GH3 using a Radio-Immuno-Assay.
  • HFS for 24 hours reduced prolactin secretion by 40.3%, dopamine by 32.7%, epinephrine by 18.1% (non significant) and norepinephrine by 27.0%.
  • [MeSH-major] Catecholamines / metabolism. Electric Stimulation. Epithelial Cells / metabolism. Neurons / metabolism. Prolactin / metabolism
  • [MeSH-minor] Cell Culture Techniques. Cell Line, Tumor. Humans. Prolactinoma

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  • (PMID = 17171296.001).
  • [ISSN] 0001-6268
  • [Journal-full-title] Acta neurochirurgica
  • [ISO-abbreviation] Acta Neurochir (Wien)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Austria
  • [Chemical-registry-number] 0 / Catecholamines; 9002-62-4 / Prolactin
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84. Hána V, Seidl Z, Vanĕcková M, Diblík P, Weiss V, Masopust V, Krsek M, Marek J: [Randomly discovered enlargement in the region of sella turcica]. Vnitr Lek; 2007 Jul-Aug;53(7-8):816-20
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  • This is not surprising if we consider that autopsies show the presence of hypophysial adenomas of 10-15% of population on an average.
  • A number of tumours of diverse etiology occur in the hypothalamus-hypophysial region, but hypophysial adenomas are by far the most frequent among all (above 90 %).
  • The symptomatology can be linked with possible slight hormonal overproduction of hypophysial adenomas, a deficit of hypophysial hormones or local manifestations of expansion.
  • Depending on the type and extension of the tumour the options considered are pharmacotherapy (the treatment of choice in the case of prolactinomas), surgery, radiotherapy (today prevailingly using the gamma knife), and if no intervention is necessary, follow up with regular MRI examinations.
  • [MeSH-major] Pituitary Neoplasms / diagnosis. Sella Turcica

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  • (PMID = 17915425.001).
  • [ISSN] 0042-773X
  • [Journal-full-title] Vnitr̆ní lékar̆ství
  • [ISO-abbreviation] Vnitr Lek
  • [Language] cze
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Czech Republic
  • [Number-of-references] 7
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85. Zatelli MC, Minoia M, Filieri C, Tagliati F, Buratto M, Ambrosio MR, Lapparelli M, Scanarini M, Degli Uberti EC: Effect of everolimus on cell viability in nonfunctioning pituitary adenomas. J Clin Endocrinol Metab; 2010 Feb;95(2):968-76
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  • [Title] Effect of everolimus on cell viability in nonfunctioning pituitary adenomas.
  • CONTEXT: Pituitary adenomas can cause specific syndromes due to hormone excess and/or determine sellar mass symptoms.
  • Pituitary cell growth can sometimes be influenced by medical therapy, such as for somatotroph adenomas treated with somatostatin analogs or prolactinomas treated with dopaminergic drugs.
  • However, nonfunctioning pituitary adenomas (NFAs) are still orphans of medical therapy.
  • Cell viability and apoptosis were evaluated after 48 h, and vascular endothelial growth factor (VEGF) secretion was assessed after an 8-h incubation.
  • RESULTS: In 28 cultures (70%), Everolimus significantly reduced cell viability (by approximately 40%; P < 0.05 vs. control), promoted apoptosis (+30%; P < 0.05 vs. control), inhibited p70S6K activity (-20%), and blocked IGF-I proliferative and antiapoptotic effects.
  • CONCLUSIONS: Everolimus reduced NFA cell viability by inducing apoptosis, with a mechanism likely involving IGF-I signaling but not VEGF secretion, suggesting that it might represent a possible medical treatment of invasive/recurrent NFAs.
  • [MeSH-major] Adenoma / drug therapy. Immunosuppressive Agents / pharmacology. Pituitary Neoplasms / drug therapy. Sirolimus / analogs & derivatives
  • [MeSH-minor] Aged. Apoptosis / drug effects. Cell Line, Tumor. Cell Survival / drug effects. Ergolines / pharmacology. Everolimus. Female. Humans. Male. Middle Aged. Receptors, Somatostatin / physiology. Ribosomal Protein S6 Kinases, 70-kDa / metabolism. Somatostatin / analogs & derivatives. Somatostatin / pharmacology. Vascular Endothelial Growth Factor A / secretion

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  • (PMID = 19965918.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ergolines; 0 / Immunosuppressive Agents; 0 / Receptors, Somatostatin; 0 / Vascular Endothelial Growth Factor A; 0 / somatostatin receptor 2; 51110-01-1 / Somatostatin; 98H1T17066 / pasireotide; 9HW64Q8G6G / Everolimus; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa; LL60K9J05T / cabergoline; W36ZG6FT64 / Sirolimus
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86. Al-Zadjali NK, Turgut Tali E, Al Azzaz A: Giant prolactinoma mimicking bone tumor. Neuroradiol J; 2007 Apr 30;20(2):196-9
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  • [Title] Giant prolactinoma mimicking bone tumor.
  • Prolactinomas are the most common of the hormone-secreting pituitary tumours.
  • It is well known that clinical presentations of prolactinomas are quite different between genders (4,5).
  • The vast majority (95%) of prolactinomas in women are microadenomas which present with the clinical manifestations of hyperprolactinaemia.
  • In contrast, men with prolactinomas often present because of symptoms due to the size of the tumour rather than impotence, loss of libido or infertility (1,3).
  • Giant pituitary tumours (larger than 4 cm) are rare and most of them are nonfunctional.
  • Giant prolactinomas with massive extrasellar extension are also rare and their clinical management is sometimes problematic.

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  • (PMID = 24299644.001).
  • [ISSN] 1971-4009
  • [Journal-full-title] The neuroradiology journal
  • [ISO-abbreviation] Neuroradiol J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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87. Revill K, Dudley KJ, Clayton RN, McNicol AM, Farrell WE: Loss of neuronatin expression is associated with promoter hypermethylation in pituitary adenoma. Endocr Relat Cancer; 2009 Jun;16(2):537-48
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  • [Title] Loss of neuronatin expression is associated with promoter hypermethylation in pituitary adenoma.
  • The imprinted gene, neuronatin (NNAT), is one of the most abundant transcripts in the pituitary and is thought to be involved in the development and maturation of this gland.
  • In a recent whole-genome approach, exploiting a pituitary tumour cell line, we identified hypermethylation associated loss of NNAT.
  • In this report, we determined the expression pattern of NNAT in individual cell types of the normal gland and within each of the different pituitary adenoma subtypes.
  • Immunohistochemical (IHC) co-localization studies of normal pituitaries showed that each of the hormone secreting cells (GH, PRL, ACTH, FSH and TSH) expressed NNAT.
  • However, 33 out of 47 adenomas comprising, 11 somatotrophinomas, 10 prolactinomas, 12 corticotrophinomas and 14 non-functioning tumours, irrespective of subtype failed to express either NNAT transcript or protein as determined by quantitative real-time RT-PCR and IHC respectively.
  • In normal pituitaries and adenomas that expressed NNAT the promoter-associated CpG island showed characteristics of an imprinted gene where approximately 50% of molecules were densely methylated.
  • However, in the majority of adenomas that showed loss or significantly reduced expression of NNAT, relative to normal pituitaries, the gene-associated CpG island showed significantly increased methylation.
  • Collectively, these findings point to an important role for NNAT in the pituitary and perhaps tumour development in this gland.
  • [MeSH-major] DNA Methylation. Membrane Proteins / genetics. Nerve Tissue Proteins / genetics. Pituitary Gland / pathology. Pituitary Neoplasms / genetics. Promoter Regions, Genetic / genetics

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  • (PMID = 19218280.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Membrane Proteins; 0 / NNAT protein, human; 0 / Nerve Tissue Proteins; 0 / RNA, Messenger
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88. Elsässer Imboden PN, De Tribolet N, Lobrinus A, Gaillard RC, Portmann L, Pralong F, Gomez F: Apoplexy in pituitary macroadenoma: eight patients presenting in 12 months. Medicine (Baltimore); 2005 May;84(3):188-96
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  • [Title] Apoplexy in pituitary macroadenoma: eight patients presenting in 12 months.
  • Pituitary apoplexy is an ill-defined clinical entity.
  • Some authors include hypoxic pituitary infarction, even in the absence of tumor after hemorrhagic delivery, whereas others apply this term strictly to hemorrhage within a pituitary adenoma.
  • We conducted the present study to establish the prevalence, clinical characteristics, and outcome of pituitary apoplexy, defined as an endocrine crisis characterized by acute intense headache, with or without altered consciousness, rapid development of visual or motor ocular disorders, and pituitary failure, associated with a large pituitary adenoma.
  • We describe 8 consecutive patients (1 woman and 7 men, aged 29-66 yr) presenting over 12 months with pituitary apoplexy.
  • We examined our pituitary tumors database for cases of macroadenoma without apoplexy occurring during the same period.
  • In 6 patients (3 nonsecreting tumors, 1 free-alpha-subunit-secreting tumor, 1 growth hormone and prolactin-secreting tumor with acromegaly, and 1 prolactinoma), no pituitary disease was suspected before the acute event, representing 19% of newly diagnosed pituitary macroadenomas during the same period of time, a higher proportion than expected from our previously published series.
  • The 2 other patients had known pituitary macroadenomas, a nonsecreting tumor and a prolactinoma on dopamine agonist therapy.
  • Pituitary insufficiency at diagnosis included adrenal failure in 4 patients.
  • The newly diagnosed prolactinoma was treated with dopamine agonist.
  • Complete neuro-ophthalmic recovery was observed in all cases, but only 2 patients displayed normal pituitary function on follow-up.
  • These data show that early surgical decompression prevents persistent neuro-ophthalmic deficit, but does not prevent persistent pituitary insufficiency.
  • Our data confirm that apoplexy occurs most often as the inaugural manifestation of pituitary macroadenoma, and suggest a recent increase of cases of apoplexy in our area.
  • [MeSH-major] Adenoma / complications. Pituitary Apoplexy / etiology. Pituitary Neoplasms / complications

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  • (PMID = 15879908.001).
  • [ISSN] 0025-7974
  • [Journal-full-title] Medicine
  • [ISO-abbreviation] Medicine (Baltimore)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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89. Ciccarelli A, Daly AF, Beckers A: The epidemiology of prolactinomas. Pituitary; 2005;8(1):3-6
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  • [Title] The epidemiology of prolactinomas.
  • Prolactin-secreting tumors (prolactinomas), the most frequently occurring pituitary tumor, have a frequency that varies with age and sex.
  • In the pediatric-adolescent age group, prolactinomas have a prevalence of 100/million population, and account for less than 2% of all intracranial tumors.
  • Prolactinomas occur in approximately 30% of patients with multiple endocrine neoplasia type 1 and in this setting, they may be more aggressive than their sporadic counterparts.
  • Patients with Carney complex or McCune-Albright syndrome may exhibit hyperprolactinemia due to a pituitary tumor derived from somatomammotropic cells that secrete both growth hormone and prolactin.
  • Few familial cases of prolactinoma unrelated to MEN-1 are reported in literature.
  • [MeSH-major] Pituitary Neoplasms / epidemiology. Prolactinoma / epidemiology

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  • (PMID = 16411062.001).
  • [ISSN] 1386-341X
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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90. Rocque BG, Herold KA, Salamat MS, Shenker Y, Kuo JS: Symptomatic hyperprolactinemia from an ectopic pituitary adenoma located in the clivus. Endocr Pract; 2009 Mar;15(2):143-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Symptomatic hyperprolactinemia from an ectopic pituitary adenoma located in the clivus.
  • OBJECTIVE: To report a case of an ectopic pituitary adenoma in the clivus.
  • METHODS: The clinical, laboratory, and imaging findings of the case are reviewed, and the embryogenesis of the pituitary gland, the pathophysiologic features of this condition, the diagnosis, and the treatment options are discussed.
  • RESULTS: A 20-year-old man presented to a local physician because of a milky nipple discharge of 2 months' duration.
  • Serum prolactin, insulinlike growth factor-I, and alpha-fetoprotein were measured.
  • After the resected tissue was examined, the patient was diagnosed as having an ectopic prolactin-producing pituitary adenoma.
  • CONCLUSION: Ectopic prolactinoma in the clivus is an uncommon lesion.
  • Surgical resection was undertaken in our patient because of the uncertainty of the diagnosis and the aggressive natural history of more common tumors of the clivus, such as chordomas.
  • Although it is possible that a successful trial of dopaminergic therapy would have obviated surgical intervention, this approach would be associated with additional risks if the diagnosis were incorrect.
  • [MeSH-major] Cranial Fossa, Posterior / pathology. Hyperprolactinemia / diagnosis. Hyperprolactinemia / pathology. Pituitary Neoplasms / diagnosis. Pituitary Neoplasms / pathology

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  • (PMID = 19289326.001).
  • [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
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91. Casanueva FF, Molitch ME, Schlechte JA, Abs R, Bonert V, Bronstein MD, Brue T, Cappabianca P, Colao A, Fahlbusch R, Fideleff H, Hadani M, Kelly P, Kleinberg D, Laws E, Marek J, Scanlon M, Sobrinho LG, Wass JA, Giustina A: Guidelines of the Pituitary Society for the diagnosis and management of prolactinomas. Clin Endocrinol (Oxf); 2006 Aug;65(2):265-73
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  • [Title] Guidelines of the Pituitary Society for the diagnosis and management of prolactinomas.
  • In June 2005, an ad hoc Expert Committee formed by the Pituitary Society convened during the 9th International Pituitary Congress in San Diego, California.
  • Members of this committee consisted of invited international experts in the field, and included endocrinologists and neurosurgeons with recognized expertise in the management of prolactinomas.
  • Discussions were held that included all interested participants to the Congress and resulted in formulation of these guidelines, which represent the current recommendations on the diagnosis and management of prolactinomas based upon comprehensive analysis and synthesis of all available data.
  • [MeSH-major] Algorithms. Pituitary Neoplasms. Pregnancy Complications, Neoplastic. Prolactinoma
  • [MeSH-minor] Adenoma / diagnosis. Adenoma / therapy. Adult. Child. Dopamine Agonists / therapeutic use. Female. Follow-Up Studies. Humans. Hyperprolactinemia / diagnosis. Hyperprolactinemia / etiology. Hyperprolactinemia / therapy. Male. Pregnancy

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  • (PMID = 16886971.001).
  • [ISSN] 0300-0664
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article; Practice Guideline
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Dopamine Agonists
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92. Fanciulli G, Tomasi PA, Delitala G: Absence of an opioid stimulatory tone on growth hormone secretion in women with microprolactinoma. Endocr Res; 2008;33(3):104-10
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  • INTRODUCTION: Literature data suggest that prolactinoma is a tumor with a complex pathogenesis and that its growth is the result of changes at the pituitary and/or hypothalamic level.
  • Abnormal release of hypothalamic factors (including endogenous opioid peptides) may contribute to prolactinoma development.
  • An increased endogenous opioid tone (EOT) occurs in patients with prolactinoma, and seems to play an important role in pituitary secretion, as suggested by the ability of the opiate receptor antagonist naloxone to stimulate luteinizing hormone pulsatile secretion in these patients.
  • OBJECTIVE: To investigate the effect of the EOT on growth hormone (GH) secretion in women with prolactinoma.
  • DESIGN: Eleven women aged 30.4+/-6.7 years (range 20-41), with an established diagnosis of microprolactinoma, were studied.
  • CONCLUSION: Our data suggest that an opioid stimulatory tone on GH secretion in women with prolactinoma is absent.
  • [MeSH-major] Human Growth Hormone / secretion. Opioid Peptides / physiology. Prolactinoma / physiopathology

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  • (PMID = 19156568.001).
  • [ISSN] 1532-4206
  • [Journal-full-title] Endocrine research
  • [ISO-abbreviation] Endocr. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Narcotic Antagonists; 0 / Opioid Peptides; 12629-01-5 / Human Growth Hormone; 36B82AMQ7N / Naloxone; 9034-39-3 / Growth Hormone-Releasing Hormone
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93. Daly AF, Vanbellinghen JF, Khoo SK, Jaffrain-Rea ML, Naves LA, Guitelman MA, Murat A, Emy P, Gimenez-Roqueplo AP, Tamburrano G, Raverot G, Barlier A, De Herder W, Penfornis A, Ciccarelli E, Estour B, Lecomte P, Gatta B, Chabre O, Sabaté MI, Bertagna X, Garcia Basavilbaso N, Stalldecker G, Colao A, Ferolla P, Wémeau JL, Caron P, Sadoul JL, Oneto A, Archambeaud F, Calender A, Sinilnikova O, Montañana CF, Cavagnini F, Hana V, Solano A, Delettieres D, Luccio-Camelo DC, Basso A, Rohmer V, Brue T, Bours V, Teh BT, Beckers A: Aryl hydrocarbon receptor-interacting protein gene mutations in familial isolated pituitary adenomas: analysis in 73 families. J Clin Endocrinol Metab; 2007 May;92(5):1891-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aryl hydrocarbon receptor-interacting protein gene mutations in familial isolated pituitary adenomas: analysis in 73 families.
  • CONTEXT: An association between germline aryl hydrocarbon receptor-interacting protein (AIP) gene mutations and pituitary adenomas was recently shown.
  • OBJECTIVE: The objective of the study was to assess the frequency of AIP gene mutations in a large cohort of patients with familial isolated pituitary adenoma (FIPA).
  • RESULTS: Seventy-three FIPA families were identified, with 156 patients with pituitary adenomas; the FIPA cohort was evenly divided between families with homogeneous and heterogeneous tumor expression.
  • Somatotropinomas predominated among FIPA families with AIP mutations, but mixed GH/prolactin-secreting tumors, prolactinomas, and nonsecreting adenomas were also noted.
  • Approximately 85% of the FIPA cohort and 50% of those with familial somatotropinomas were negative for AIP mutations.
  • Although pituitary tumors occurring in association with AIP mutations are predominantly somatotropinomas, other tumor types are also seen.
  • Further study of the impact of AIP mutations on protein expression and activity is necessary to elucidate their role in pituitary tumorigenesis in FIPA.
  • [MeSH-major] Adenoma / genetics. Pituitary Neoplasms / genetics. Proteins / genetics
  • [MeSH-minor] Adult. Aged. Cohort Studies. Female. Gene Frequency. Germ-Line Mutation / genetics. Growth Hormone / metabolism. Humans. Immunohistochemistry. Intracellular Signaling Peptides and Proteins. Male. Middle Aged. Molecular Sequence Data. Mutation / physiology. Prolactinoma / genetics. Prolactinoma / metabolism. Prolactinoma / pathology


94. Ferone D, Pivonello R, Resmini E, Boschetti M, Rebora A, Albertelli M, Albanese V, Colao A, Culler MD, Minuto F: Preclinical and clinical experiences with the role of dopamine receptors in the treatment of pituitary adenomas. Eur J Endocrinol; 2007 Apr;156 Suppl 1:S37-43
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  • [Title] Preclinical and clinical experiences with the role of dopamine receptors in the treatment of pituitary adenomas.
  • Pituitary tumors can cause symptoms of mass effect and hormonal hypersecretion that can be reversed with surgical resection or debulking of the adenoma, radiotherapy, or medical treatment.
  • Medical treatment is the primary choice for prolactinomas because dopamine agonists are very effective in the treatment of these tumors, with rates of control (tumor size reduction and hormone suppression) as high as 80-90% for microprolactinomas and 60-75% for macroprolactinomas.
  • The function of dopamine receptors in other histotypes of pituitary adenoma is still debated.
  • However, new insights into receptor physiology and the introduction of new clinically available, as well as experimental, compounds have reopened a potential role of dopaminergic drugs in the medical treatment of pituitary tumors.
  • The differences between the effectiveness and the resistance to different dopaminergic agents, the new challenging results from clinical and experimental studies, as well as the future of dopamine agonists in the therapy of pituitary tumors are discussed.

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  • [ErratumIn] Eur J Endocrinol. 2007 Oct;157(4):543
  • (PMID = 17413187.001).
  • [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 / Dopamine Agonists; 0 / Receptors, Dopamine
  • [Number-of-references] 43
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95. Fernandez A, Karavitaki N, Wass JA: Prevalence of pituitary adenomas: a community-based, cross-sectional study in Banbury (Oxfordshire, UK). Clin Endocrinol (Oxf); 2010 Mar;72(3):377-82
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prevalence of pituitary adenomas: a community-based, cross-sectional study in Banbury (Oxfordshire, UK).
  • BACKGROUND: Pituitary adenomas (PAs) are associated with increased morbidity and mortality.
  • All cases of PAs were found following an exhaustive computer database search of agreed terms by the staff of each Practice and data on age, gender, presenting manifestations and their duration, imaging features at diagnosis, history of multiple endocrine neoplasia type 1 and family history of PA were collected.
  • RESULTS: A total of 63 patients with PA were identified amongst the study population of 81,149, with a prevalence of 77.6 PA cases/100,000 inhabitants (prolactinomas; PRLoma: 44.4, nonfunctioning PAs: 22.2, acromegaly; ACRO: 8.6, corticotroph adenoma: 1.2 and unknown functional status; UFS: 1.2/100,000 inhabitants).
  • The distribution of each PA subtype was for PRLoma 57%, nonfunctioning PAs 28%, ACRO 11%, corticotroph adenoma 2% and UFS 2%.
  • The median age at diagnosis and the duration of symptoms until diagnosis (in years) were for PRLoma 32.0 and 1.5, nonfunctioning PAs 51.5 and 0.8, ACRO 47 and 4.5 and corticotroph adenoma 57 and 7, respectively.
  • Five patients (7.9%) presented with classical pituitary apoplexy, with a prevalence of 6.2 cases/100,000 inhabitants.
  • [MeSH-major] Adenoma / epidemiology. Pituitary Neoplasms / epidemiology
  • [MeSH-minor] Adolescent. Adult. Aged. Cross-Sectional Studies. Delayed Diagnosis. England / epidemiology. Female. Humans. Male. Middle Aged. Prevalence. Young Adult

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  • [CommentIn] Clin Endocrinol (Oxf). 2010 Mar;72(3):290-1 [19832856.001]
  • (PMID = 19650784.001).
  • [ISSN] 1365-2265
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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96. Heidari Z, Hosseinpanah F, Shirazian N: Achievement of fertility in an infertile man with resistant macroprolactinoma using high-dose bromocriptine and a combination of human chorionic gonadotropin and an aromatase inhibitor. Endocr Pract; 2010 Jul-Aug;16(4):669-72
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Testosterone replacement or hCG therapy in this patient resulted in an increase in serum prolactin levels, which declined after discontinuation of this therapy.
  • The combination of high doses of bromocriptine, hCG, and an aromatase inhibitor facilitated near-normalization of serum prolactin levels, shrinkage of the macroprolactinoma, recovery of serum testosterone levels, sexual function, and sperm count, and achievement of fertility.
  • CONCLUSION: An aromatase inhibitor may facilitate successful testosterone replacement therapy in male patients with prolactinoma.
  • [MeSH-major] Aromatase Inhibitors / therapeutic use. Bromocriptine / therapeutic use. Chorionic Gonadotropin / therapeutic use. Dopamine Agonists / therapeutic use. Infertility, Male / drug therapy. Pituitary Neoplasms / physiopathology. Prolactinoma / physiopathology
  • [MeSH-minor] Adult. Drug Resistance, Neoplasm. Drug Therapy, Combination. Galactorrhea / etiology. Hormone Replacement Therapy. Humans. Male. Testosterone / blood. Testosterone / deficiency. Tumor Burden / drug effects

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  • Hazardous Substances Data Bank. TESTOSTERONE .
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  • (PMID = 20439242.001).
  • [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 / Aromatase Inhibitors; 0 / Chorionic Gonadotropin; 0 / Dopamine Agonists; 3A64E3G5ZO / Bromocriptine; 3XMK78S47O / Testosterone
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97. Leontiou CA, Gueorguiev M, van der Spuy J, Quinton R, Lolli F, Hassan S, Chahal HS, Igreja SC, Jordan S, Rowe J, Stolbrink M, Christian HC, Wray J, Bishop-Bailey D, Berney DM, Wass JA, Popovic V, Ribeiro-Oliveira A Jr, Gadelha MR, Monson JP, Akker SA, Davis JR, Clayton RN, Yoshimoto K, Iwata T, Matsuno A, Eguchi K, Musat M, Flanagan D, Peters G, Bolger GB, Chapple JP, Frohman LA, Grossman AB, Korbonits M: The role of the aryl hydrocarbon receptor-interacting protein gene in familial and sporadic pituitary adenomas. J Clin Endocrinol Metab; 2008 Jun;93(6):2390-401
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The role of the aryl hydrocarbon receptor-interacting protein gene in familial and sporadic pituitary adenomas.
  • CONTEXT: Mutations have been identified in the aryl hydrocarbon receptor-interacting protein (AIP) gene in familial isolated pituitary adenomas (FIPA).
  • OBJECTIVE: AIP sequence changes and expression were studied in FIPA and sporadic adenomas.
  • The function of normal and mutated AIP molecules was studied on cell proliferation and protein-protein interaction.
  • Cellular and ultrastructural AIP localization was determined in pituitary cells.
  • PATIENTS: Twenty-six FIPA kindreds and 85 sporadic pituitary adenoma patients were included in the study.
  • Overexpression of wild-type AIP in TIG3 and HEK293 human fibroblast and GH3 pituitary cell lines dramatically reduced cell proliferation, whereas mutant AIP lost this ability.
  • In normal pituitary, AIP colocalizes exclusively with GH and prolactin, and it is found in association with the secretory vesicle, as shown by double-immunofluorescence and electron microscopy staining.
  • In sporadic pituitary adenomas, however, AIP is expressed in all tumor types.
  • In addition, whereas AIP is expressed in the secretory vesicle in GH-secreting tumors, similar to normal GH-secreting cells, in lactotroph, corticotroph, and nonfunctioning adenomas, it is localized to the cytoplasm and not in the secretory vesicles.
  • CONCLUSIONS: Our functional evaluation of AIP mutations is consistent with a tumor-suppressor role for AIP and its involvement in familial acromegaly.
  • The abnormal expression and subcellular localization of AIP in sporadic pituitary adenomas indicate deranged regulation of this protein during tumorigenesis.
  • [MeSH-major] Adenoma / genetics. Pituitary Neoplasms / genetics. Proteins / physiology
  • [MeSH-minor] Acromegaly / genetics. Acromegaly / metabolism. Adolescent. Adult. Aged. Cell Proliferation. Child. Cyclic Nucleotide Phosphodiesterases, Type 4 / metabolism. Female. Gene Expression Regulation, Neoplastic. Genetic Testing. Human Growth Hormone / secretion. Humans. Intracellular Signaling Peptides and Proteins. Male. Middle Aged. Protein Binding. Transfection. Tumor Cells, Cultured


98. Halperin Rabinovich I, Obiols Alfonso G, Soto Moreno A, Torres Vela E, Tortosa Henzi F, Català Bauset M, Gilsanz Peral A, Girbés Borràs J, Moreno Esteban B, Picó Alfonso A, Del Pozo Picó C, Zugasti Murillo A, Lucas Morante T, Páramo Fernández C, Varela da Sousa C, Villabona Artero C: Clinical practice guideline for hypotalamic-pituitary disturbances in pregnancy and the postpartum period. Endocrinol Nutr; 2008 Jan;55(1):29-43
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical practice guideline for hypotalamic-pituitary disturbances in pregnancy and the postpartum period.
  • Major anatomical and histological changes are produced in the pituitary, with an increase of up to 40% in the size of the gland.
  • There are wide variations in the function of the hypothalamus-pituitary-thyroid axis that effect iodine balance, the overall activity of the gland, as well as transport of thyroid hormones in plasma and peripheral metabolism of thyroid hormones.
  • Given the effects of hypothyroidism on fetal development, both the diagnosis and appropriate therapeutic management of thyroid hypofunction are essential.
  • The most important modification to the hypothalamus-pituitary-adrenal axis during pregnancy is the rise in serum cortisol levels due to an increase in cortisol-binding proteins.
  • Although Cushing's syndrome during pregnancy is infrequent, both diagnosis and treatment of this disorder are especially difficult.
  • However, postpartum pituitary necrosis (Sheehan's syndrome) is a well-known complication that occurs after delivery and, together with lymphocytic hypophysitis, constitutes the most frequent cause of adrenal insufficiency.
  • The management of prolactinoma during pregnancy requires suppression of dopaminergic agonists and their reintroduction if there is tumoral growth.

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  • [Copyright] Copyright © 2008 Sociedad Española de Endocrinología y Nutrición. Published by Elsevier Espana. All rights reserved.
  • (PMID = 22967849.001).
  • [ISSN] 1575-0922
  • [Journal-full-title] Endocrinología y nutrición : órgano de la Sociedad Española de Endocrinología y Nutrición
  • [ISO-abbreviation] Endocrinol Nutr
  • [Language] eng; spa
  • [Publication-type] Journal Article
  • [Publication-country] Spain
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99. Harding B, Lemos MC, Reed AA, Walls GV, Jeyabalan J, Bowl MR, Tateossian H, Sullivan N, Hough T, Fraser WD, Ansorge O, Cheeseman MT, Thakker RV: Multiple endocrine neoplasia type 1 knockout mice develop parathyroid, pancreatic, pituitary and adrenal tumours with hypercalcaemia, hypophosphataemia and hypercorticosteronaemia. Endocr Relat Cancer; 2009 Dec;16(4):1313-27
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  • [Title] Multiple endocrine neoplasia type 1 knockout mice develop parathyroid, pancreatic, pituitary and adrenal tumours with hypercalcaemia, hypophosphataemia and hypercorticosteronaemia.
  • Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant disorder characterized in man by parathyroid, pancreatic, pituitary and adrenal tumours.
  • Men1(+/-) mice developed, by 9 months of age, parathyroid hyperplasia, pancreatic tumours which were mostly insulinomas, by 12 months of age, pituitary tumours which were mostly prolactinomas, and by 15 months parathyroid adenomas and adrenal cortical tumours.
  • Pancreatic and pituitary tumours expressed chromogranin A (CgA), somatostatin receptor type 2 and vascular endothelial growth factor-A.
  • [MeSH-major] Adrenal Gland Neoplasms / etiology. Corticosterone / blood. Hypercalcemia / etiology. Hypophosphatemia / etiology. Pancreatic Neoplasms / etiology. Parathyroid Neoplasms / etiology. Pituitary Neoplasms / etiology. Proto-Oncogene Proteins / physiology


100. 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
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  • [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

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  • [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
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