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1. Bakhtiar Y, Arita K, Hirano H, Habu M, Fujio S, Kitajima S, Tanimoto A: Prolactin-producing pituitary adenoma with abundant spherical amyloid deposition masquerading as extensive calcification. Neurol Med Chir (Tokyo); 2010;50(11):1023-6
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  • [Title] Prolactin-producing pituitary adenoma with abundant spherical amyloid deposition masquerading as extensive calcification.
  • A 53-year-old male presented with a case of prolactin-producing pituitary adenoma with abundant spherical amyloid depositions masquerading as extensive calcification and manifesting as visual disturbance.
  • Magnetic resonance imaging revealed a heterogeneously enhanced large pituitary tumor reaching lateral ventricle.
  • Blood prolactin level was elevated to 5971 ng/ml.
  • Immunohistochemically, the tumor was strongly positive for prolactin.
  • [MeSH-major] Amyloid / metabolism. Calcinosis / pathology. Pituitary Neoplasms / pathology. Plaque, Amyloid / pathology. Prolactin / secretion. Prolactinoma / pathology
  • [MeSH-minor] Diagnosis, Differential. Humans. Male. Middle Aged

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  • (PMID = 21123991.001).
  • [ISSN] 1349-8029
  • [Journal-full-title] Neurologia medico-chirurgica
  • [ISO-abbreviation] Neurol. Med. Chir. (Tokyo)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Amyloid; 9002-62-4 / Prolactin
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2. Sikoski P, Trybus J, Cline JM, Muhammad FS, Eckhoff A, Tan J, Lockard M, Jolley T, Britt S, Kock ND: Cystic mammary adenocarcinoma associated with a prolactin-secreting pituitary adenoma in a New Zealand white rabbit (Oryctolagus cuniculus). Comp Med; 2008 Jun;58(3):297-300
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  • [Title] Cystic mammary adenocarcinoma associated with a prolactin-secreting pituitary adenoma in a New Zealand white rabbit (Oryctolagus cuniculus).
  • Pituitary adenoma in a rabbitA 44-mo-old, female, nulliparous New Zealand White Rabbit (Oryctolagus cuniculus) presented with bilaterally diffusely enlarged mammary glands with enlarged, discolored teats that exuded brown, mucoid discharge.
  • Computed tomography and serum prolactin levels supported the diagnosis of mammary gland dysplasia, possibly due to a prolactin-secreting pituitary adenoma.
  • Histologic evaluation confirmed the presence of a pituitary adenoma, mammary hyperplasia, dysplasia, and cystic mammary adenocarcinoma.
  • Immunohistochemical staining confirmed the presence of abundant prolactin secreting cells in the pituitary adenoma.
  • This is the second report of hyperprolactinemia with mammary dysplasia in rabbits, and the first report of cystic mammary adenocarcinoma associated with a prolactin-secreting pituitary adenoma in a rabbit.
  • [MeSH-major] Adenocarcinoma / pathology. Adenoma / secretion. Mammary Neoplasms, Experimental / pathology. Prolactin / secretion

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  • [Cites] Comp Med. 2003 Aug;53(4):424-32 [14524419.001]
  • [Cites] Acta Endocrinol (Copenh). 1976 Aug;82(4):746-52 [181935.001]
  • [Cites] Breast Cancer. 2007;14(3):302-6 [17690509.001]
  • [Cites] Lab Anim Sci. 1994 Apr;44(2):114-20 [8028271.001]
  • [Cites] Cancer. 1982 Jul 1;50(1):125-9 [7200826.001]
  • (PMID = 18589874.001).
  • [ISSN] 1532-0820
  • [Journal-full-title] Comparative medicine
  • [ISO-abbreviation] Comp. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 9002-62-4 / Prolactin
  • [Other-IDs] NLM/ PMC2704120
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3. Ahtiainen P, Sharp V, Rulli SB, Rivero-Müller A, Mamaeva V, Röyttä M, Huhtaniemi I: Enhanced LH action in transgenic female mice expressing hCGbeta-subunit induces pituitary prolactinomas; the role of high progesterone levels. Endocr Relat Cancer; 2010 Sep;17(3):611-21
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  • [Title] Enhanced LH action in transgenic female mice expressing hCGbeta-subunit induces pituitary prolactinomas; the role of high progesterone levels.
  • The etiology of pituitary adenomas remains largely unknown, with the exception of involvement of estrogens in the formation of prolactinomas.
  • We have examined the molecular pathogenesis of prolactin-producing pituitary adenomas in transgenic female mice expressing the human choriongonadotropin (hCG) beta-subunit.
  • Curiously, despite normal estrogen levels, large prolactinomas developed in these mice, and we provide here several lines of evidence that the elevated P(4) levels are involved in the growth of these estrogen-dependent tumors.
  • Evidence for direct growth-promoting effect of P(4) was obtained from cultures of primary mouse pituitary cells and rat somatomammotroph GH3 cells.
  • If extrapolated to humans, and given the importance of endogenous P(4) and synthetic progestins in female reproductive functions and their pharmacotherapy, it is relevant to revisit the potential role of these hormones in the origin and growth of prolactinomas.

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  • [Cites] J Clin Endocrinol Metab. 2000 Jan;85(1):168-74 [10634382.001]
  • [Cites] Endocr Relat Cancer. 2009 Mar;16(1):113-22 [18852162.001]
  • [Cites] J Mammary Gland Biol Neoplasia. 1998 Jan;3(1):63-72 [10819505.001]
  • [Cites] J Neuroendocrinol. 2001 Mar;13(3):302-9 [11207946.001]
  • [Cites] Endocrinology. 2001 Oct;142(10):4479-85 [11564713.001]
  • [Cites] J Clin Invest. 2002 Jan;109(2):277-83 [11805140.001]
  • [Cites] Endocrinology. 2002 Oct;143(10):4084-95 [12239120.001]
  • [Cites] J Biol Chem. 2002 Sep 27;277(39):35819-25 [12121979.001]
  • [Cites] Endocrinology. 2002 Dec;143(12):4536-43 [12446580.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Feb 4;100(3):1034-9 [12552124.001]
  • [Cites] Front Horm Res. 2004;32:34-62 [15281339.001]
  • [Cites] Mol Cell Biol. 2004 Aug;24(16):7260-74 [15282324.001]
  • [Cites] Science. 1966 Oct 21;154(3747):402-3 [4288164.001]
  • [Cites] Endocrinology. 1970 Mar;86(3):503-5 [5410438.001]
  • [Cites] J Endocrinol. 1973 Feb;56(2):309-14 [4703244.001]
  • [Cites] Endocrinology. 1976 Dec;99(6):1482-9 [826392.001]
  • [Cites] J Biol Chem. 1982 Mar 10;257(5):2133-6 [7061411.001]
  • [Cites] Adv Exp Med Biol. 1981;138:151-63 [7342713.001]
  • [Cites] Arch Pathol Lab Med. 1983 Sep;107(9):488-91 [6309114.001]
  • [Cites] Cancer Res. 1985 Mar;45(3):1015-9 [2982481.001]
  • [Cites] J Endocrinol. 1989 Jun;121(3):409-17 [2547009.001]
  • [Cites] Endocrinology. 1991 Jul;129(1):270-6 [1711463.001]
  • [Cites] Nature. 1992 Sep 24;359(6393):295-300 [1406933.001]
  • [Cites] Cancer Res. 1993 Apr 1;53(7):1546-9 [8453621.001]
  • [Cites] Acta Endocrinol (Copenh). 1993 Jul;129 Suppl 1:1-5 [8396832.001]
  • [Cites] Hum Reprod. 1994 Jun;9 Suppl 1:63-8 [7962471.001]
  • [Cites] J Cell Sci Suppl. 1994;18:89-96 [7883799.001]
  • [Cites] Cancer Res. 1995 Nov 1;55(21):4892-8 [7585526.001]
  • [Cites] J Biol Chem. 1996 Aug 23;271(34):20608-16 [8702807.001]
  • [Cites] J Endocrinol. 1996 Nov;151(2):175-84 [8958777.001]
  • [Cites] Endocrinology. 1998 Apr;139(4):1602-9 [9528940.001]
  • [Cites] EMBO J. 1998 Apr 1;17(7):2008-18 [9524123.001]
  • [Cites] Nat Genet. 1998 Apr;18(4):360-4 [9537419.001]
  • [Cites] Genes Dev. 1998 Sep 15;12(18):2899-911 [9744866.001]
  • [Cites] Endocrinology. 2005 Nov;146(11):4917-25 [16123159.001]
  • [Cites] Oncogene. 2005 Nov 10;24(49):7301-9 [16007123.001]
  • [Cites] Cancer Cell. 2006 Jun;9(6):459-71 [16766265.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Dec;91(12):4769-75 [16968795.001]
  • [Cites] Cell Cycle. 2008 Jan 1;7(1):71-80 [18196959.001]
  • [Cites] Horm Metab Res. 2008 Apr;40(4):245-50 [18548383.001]
  • [Cites] Eur J Endocrinol. 2008 Sep;159(3):197-202 [18567667.001]
  • [Cites] J Reprod Med. 1999 Dec;44(12 Suppl):1121-6 [10649822.001]
  • (PMID = 20453081.001).
  • [ISSN] 1479-6821
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] ENG
  • [Grant] United Kingdom / Wellcome Trust / / 063552; United Kingdom / Wellcome Trust / / 082101
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Chorionic Gonadotropin, beta Subunit, Human; 4G7DS2Q64Y / Progesterone; 9002-62-4 / Prolactin; 9002-67-9 / Luteinizing Hormone; EC 2.7.11.22 / Cyclin-Dependent Kinase 4
  • [Other-IDs] NLM/ PMC2881531
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4. 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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  • [Cites] Mol Endocrinol. 1999 Sep;13(9):1522-34 [10478843.001]
  • [Cites] Endocrinology. 2005 Jul;146(7):2952-62 [15817666.001]
  • [Cites] Endocrinology. 2006 Oct;147(10):4781-91 [16809444.001]
  • [Cites] Front Horm Res. 2006;35:50-63 [16809922.001]
  • [Cites] Endocrinology. 1999 Nov;140(11):5348-55 [10537166.001]
  • [Cites] Nat Med. 1999 Nov;5(11):1317-21 [10546001.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Feb;86(2):867-74 [11158059.001]
  • [Cites] Brain Pathol. 2001 Jul;11(3):356-70 [11414477.001]
  • [Cites] J Clin Invest. 2002 Jan;109(2):277-83 [11805140.001]
  • [Cites] Endocrinology. 2002 Apr;143(4):1270-9 [11897683.001]
  • [Cites] Exp Biol Med (Maywood). 2002 Jul;227(7):492-9 [12094014.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Sep;87(9):4238-44 [12213878.001]
  • [Cites] Histol Histopathol. 2003 Jan;18(1):245-51 [12507303.001]
  • [Cites] Clin Endocrinol (Oxf). 2003 Feb;58(2):141-50 [12580928.001]
  • [Cites] Eur J Endocrinol. 2003 Feb;148(2):203-11 [12590639.001]
  • [Cites] J Comp Neurol. 2003 Apr 14;458(4):319-25 [12619067.001]
  • [Cites] Mol Cancer. 2004 Jul 8;3:18 [15242522.001]
  • [Cites] Front Horm Res. 2004;32:175-85 [15281346.001]
  • [Cites] J Natl Cancer Inst. 1978 Sep;61(3):753-63 [278852.001]
  • [Cites] Mol Endocrinol. 2005 Sep;19(9):2371-9 [15919720.001]
  • [Cites] Curr Gene Ther. 2006 Feb;6(1):125-9 [16475950.001]
  • [Cites] Endocrinology. 1981 Feb;108(2):440-4 [7449733.001]
  • [Cites] Endocrinology. 1981 Mar;108(3):903-7 [7460850.001]
  • [Cites] Science. 1982 Nov 12;218(4573):684-6 [7134966.001]
  • [Cites] Mech Ageing Dev. 1990 Oct;56(1):77-88 [2259256.001]
  • [Cites] Proc Soc Exp Biol Med. 1991 Feb;196(2):218-21 [1846677.001]
  • [Cites] Mol Endocrinol. 1993 Jul;7(7):879-88 [8413312.001]
  • [Cites] J Steroid Biochem Mol Biol. 1994 Mar;48(4):325-36 [8142311.001]
  • [Cites] Mol Endocrinol. 1997 Apr;11(4):433-41 [9092795.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Jun;82(6):1675-81 [9177361.001]
  • [Cites] Carcinogenesis. 1997 Jun;18(6):1155-61 [9214597.001]
  • [Cites] Neuron. 1997 Jul;19(1):103-13 [9247267.001]
  • [Cites] Neuron. 1997 Jul;19(1):115-26 [9247268.001]
  • [Cites] Am J Physiol. 1998 Mar;274(3 Pt 1):E534-40 [9530138.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Feb;84(2):761-7 [10022450.001]
  • [Cites] Science. 1999 Jul 16;285(5426):418-22 [10411507.001]
  • (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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5. Filopanti M, Lania AG, Spada A: Pharmacogenetics of D2 dopamine receptor gene in prolactin-secreting pituitary adenomas. Expert Opin Drug Metab Toxicol; 2010 Jan;6(1):43-53
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  • [Title] Pharmacogenetics of D2 dopamine receptor gene in prolactin-secreting pituitary adenomas.
  • IMPORTANCE OF THE FIELD: Dopamine-agonists are the treatment of choice of prolactin-secreting pituitary adenomas (PRL-omas).
  • AREAS COVERED IN THIS REVIEW: PRL-omas are well-differentiated endocrine tumors expressing DRD2.
  • The dopamine-agonist cabergoline (CB), normalizes prolactin and reduces tumor size in about 80 - 90% of patients.
  • One study carried out in patients with PRL-omas found a correlation between NcoI and TaqIA and resistance to CB.
  • WHAT THE READER WILL GAIN: This review deals with the connection between DRD2 polymorphisms and PRL-oma treatment and suggests hypotheses for further studies.
  • Further studies, including pituitary and hypothalamus in vivo determination of DRD2 binding according to DRD2 genotypes, investigation of possible post-receptorial mechanisms involved, as well as population studies in collaboration with psychiatrists and neurologists, are needed.
  • [MeSH-major] Dopamine Agonists / pharmacokinetics. Dopamine Agonists / therapeutic use. Prolactinoma / drug therapy. Prolactinoma / genetics. Receptors, Dopamine D2 / drug effects. Receptors, Dopamine D2 / genetics

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  • (PMID = 19929252.001).
  • [ISSN] 1744-7607
  • [Journal-full-title] Expert opinion on drug metabolism & toxicology
  • [ISO-abbreviation] Expert Opin Drug Metab Toxicol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Dopamine Agonists; 0 / Receptors, Dopamine D2
  • [Number-of-references] 67
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6. 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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7. Tanaka S, Link MJ, Brown PD, Stafford SL, Young WF Jr, Pollock BE: Gamma knife radiosurgery for patients with prolactin-secreting pituitary adenomas. World Neurosurg; 2010 Jul;74(1):147-52
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  • [Title] Gamma knife radiosurgery for patients with prolactin-secreting pituitary adenomas.
  • OBJECTIVE: To evaluate the efficacy of stereotactic radiosurgery (SRS) for patients with prolactin (PRL)-secreting pituitary adenomas that were refractory to medical management.
  • The median serum PRL concentration before SRS was 88.4 ng/mL (range, 25-943).
  • Serum PRL concentration was significantly lower (median, 28.4 ng/mL) (P = 0.006) at last follow-up, but the 4-year actuarial rate of biochemical remission off medications was only 17%.
  • Overall, four patients (18%) had biochemical remission off medications and clinical improvement, three patients (14%) had normal serum PRL concentrations and clinical improvement on dopamine agonist therapy, seven patients (32%) had improved symptoms off medications but continued to have elevated serum PRL levels, and eight patients (36%) continued to be symptomatic with elevated PRL levels either on (n = 3) or off (n = 5) dopamine agonist therapy.
  • The incidence of new anterior pituitary deficits was 42% at 4 years.
  • CONCLUSIONS: SRS was effective in controlling tumor growth for patients with PRL-secreting pituitary adenomas, and the majority of patients were clinically improved.
  • [MeSH-major] Pituitary Neoplasms / surgery. Prolactinoma / surgery. Radiosurgery
  • [MeSH-minor] Actuarial Analysis. Adult. Aged. Dopamine Agonists / therapeutic use. Female. Follow-Up Studies. Humans. Hypopituitarism / blood. Male. Middle Aged. Postoperative Complications / blood. Prolactin / blood. Retrospective Studies. Treatment Outcome. Young Adult

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • [CommentIn] World Neurosurg. 2010 Jul;74(1):103-4 [21299992.001]
  • (PMID = 21300006.001).
  • [ISSN] 1878-8769
  • [Journal-full-title] World neurosurgery
  • [ISO-abbreviation] World Neurosurg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dopamine Agonists; 9002-62-4 / Prolactin
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8. Ma ZM, Qiu B, Hou YH, Liu YS: [Gamma knife treatment for pituitary prolactinomas]. Zhong Nan Da Xue Xue Bao Yi Xue Ban; 2006 Oct;31(5):714-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Gamma knife treatment for pituitary prolactinomas].
  • OBJECTIVE: To evaluate the outcome of gamma knife for prolactinomas.
  • CONCLUSION: Gamma knife radiosurgery can be used as a primary treatment for selected prolactinomas,especially for pituitary microadenomas.
  • [MeSH-major] Hypophysectomy / methods. Pituitary Neoplasms / surgery. Prolactinoma / surgery. Radiosurgery / instrumentation

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  • (PMID = 17062937.001).
  • [ISSN] 1672-7347
  • [Journal-full-title] Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences
  • [ISO-abbreviation] Zhong Nan Da Xue Xue Bao Yi Xue Ban
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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9. 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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10. 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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11. Filopanti M, Barbieri AM, Angioni AR, Colao A, Gasco V, Grottoli S, Peri A, Baglioni S, Fustini MF, Pigliaru F, Monte PD, Borretta G, Ambrosi B, Jaffrain-Rea ML, Gasperi M, Brogioni S, Cannavò S, Mantovani G, Beck-Peccoz P, Lania A, Spada A: Dopamine D2 receptor gene polymorphisms and response to cabergoline therapy in patients with prolactin-secreting pituitary adenomas. Pharmacogenomics J; 2008 Oct;8(5):357-63
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  • [Title] Dopamine D2 receptor gene polymorphisms and response to cabergoline therapy in patients with prolactin-secreting pituitary adenomas.
  • Dopamine-agonist cabergoline (CB) reduces prolactin (PRL) secretion and tumor size in 80% of patients with prolactin-secreting adenomas (PRL-omas) by binding type 2 dopamine receptor (DRD2).
  • To assess the association of DRD2 with sensitivity to CB, TaqI-A1/A2, TaqI-B1/B2, HphI-G/T and NcoI-C/T genotypes were determined in a cross-sectional retrospective study, including 203 patients with PRL-oma.
  • Conversely, NcoI-T allele frequency was higher in resistant rather than responsive patients, considering both PRL normalization (56.6 vs 45.3%, P=0.038) and tumor shrinkage (70.4 vs 41.4%, P=0.006).
  • Finally, [TaqI A1-/TaqI B1-/HphI T-/NcoI T-] haplotype was found in 34.5% of patients normalizing PRL with < or =3 mg/week of CB vs 11.3% of resistants (P=0.021).
  • [MeSH-major] Adenoma / drug therapy. Dopamine Agonists / therapeutic use. Ergolines / therapeutic use. Pituitary Neoplasms / drug therapy. Polymorphism, Genetic. Prolactin / secretion. Receptors, Dopamine D2 / genetics

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  • (PMID = 18332900.001).
  • [ISSN] 1473-1150
  • [Journal-full-title] The pharmacogenomics journal
  • [ISO-abbreviation] Pharmacogenomics J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dopamine Agonists; 0 / Ergolines; 0 / Receptors, Dopamine D2; 9002-62-4 / Prolactin; LL60K9J05T / cabergoline
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12. Kontogeorgos G, Horvath E, Kovacs K, Coire C, Lloyd RV, Scheithauer BW, Smyth HS: Morphologic changes of prolactin-producing pituitary adenomas after short treatment with dopamine agonists. Acta Neuropathol; 2006 Jan;111(1):46-52
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  • [Title] Morphologic changes of prolactin-producing pituitary adenomas after short treatment with dopamine agonists.
  • Treatment of patients with prolactin (PRL)-producing pituitary adenomas with dopamine agonists has proved successful for most cases.
  • Dopamine agonists inhibit PRL secretion, suppress cell proliferation, and may induce apoptosis to adenoma cells.
  • Dopamine agonists induce striking morphologic changes in the majority of treated PRL-producing adenomas.
  • To date, these morphologic effects have been primarily described only after long-term treatment.
  • The purpose of this report is to describe the morphologic changes seen in PRL-producing adenomas after short-term dopamine agonist treatment.
  • We present two cases of PRL-producing macroadenomas, both from male patients who received treatment with dopamine agonists, the first for 5 and the second for 8 days.
  • In contrast to long-term treatment, no striking reduction of PRL immunoreactivity was noted.
  • In addition to typical apoptotic cells, numerous "dark" cells representing another common form of cell death were also noted.
  • [MeSH-major] Dopamine Agonists / therapeutic use. Pituitary Neoplasms / drug therapy. Pituitary Neoplasms / pathology. Prolactinoma / drug therapy. Prolactinoma / pathology
  • [MeSH-minor] Adult. Apoptosis / drug effects. Cell Proliferation / drug effects. DNA, Neoplasm / analysis. DNA, Neoplasm / genetics. Dose-Response Relationship, Drug. Fibrosis. Humans. Immunohistochemistry. Male. Middle Aged. Prolactin / analysis. Time Factors

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  • (PMID = 16328513.001).
  • [ISSN] 0001-6322
  • [Journal-full-title] Acta neuropathologica
  • [ISO-abbreviation] Acta Neuropathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Dopamine Agonists; 9002-62-4 / Prolactin
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13. Uccella S, Tibiletti MG, Bernasconi B, Finzi G, Oldrini R, Capella C: Aneuploidy, centrosome alteration and securin overexpression as features of pituitary somatotroph and lactotroph adenomas. Anal Quant Cytol Histol; 2005 Oct;27(5):241-52

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

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  • (PMID = 16447816.001).
  • [ISSN] 0884-6812
  • [Journal-full-title] Analytical and quantitative cytology and histology
  • [ISO-abbreviation] Anal. Quant. Cytol. Histol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Securin; 0 / pituitary tumor-transforming protein 1, human
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14. 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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15. Mucha SA, Meleń-Mucha G, Godlewski A, Stepień H: Inhibition of estrogen-induced pituitary tumor growth and angiogenesis in Fischer 344 rats by the matrix metalloproteinase inhibitor batimastat. Virchows Arch; 2007 Mar;450(3):335-41
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  • [Title] Inhibition of estrogen-induced pituitary tumor growth and angiogenesis in Fischer 344 rats by the matrix metalloproteinase inhibitor batimastat.
  • The development of estrogen-induced pituitary prolactinoma in Fischer 344 (F344) rats is associated with enhanced neovascularization.
  • Based on the significance of matrix metalloproteinases (MMPs) for tumor growth and angiogenesis, we have studied the effect of batimastat (BB-94), a synthetic MMPs inhibitor (MMPI) on the progression of prolactin-secreting pituitary adenoma in rats.
  • Pituitary tumors were induced in male F344 rats by s.c. implantation of Silastic tubes containing diethylstilbestrol (DES).
  • The effects of chronic treatment with BB-94 (30 mg/kg b.w.) on pituitary weight, cell proliferation, apoptosis and vascular density were evaluated.
  • We have stated that chronic treatment with batimastat caused a significant reduction in the pituitary weight.
  • Batimastat has been found to decrease cell proliferation evaluated by a number of PCNA-positive stained cell nuclei.
  • A marked increase in the apoptotic index within the pituitary was observed in the study group.
  • The results of our study provide evidence for an inhibitory effect of batimastat, a synthetic MMPI, on the growth and angiogenesis in an experimental model of human prolactinoma.
  • The ability of BB-94 to suppress established pituitary tumor growth suggests a possible application of MMPIs in the treatment of pituitary adenomas.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Neovascularization, Pathologic / prevention & control. Phenylalanine / analogs & derivatives. Pituitary Gland, Anterior / blood supply. Pituitary Neoplasms / drug therapy. Prolactinoma / drug therapy. Protease Inhibitors / therapeutic use. Thiophenes / therapeutic use
  • [MeSH-minor] Animals. Cell Proliferation / drug effects. Diethylstilbestrol / toxicity. Drug Screening Assays, Antitumor. Drug Therapy, Combination. Estrogens / toxicity. Image Processing, Computer-Assisted. Male. Metalloendopeptidases / antagonists & inhibitors. Organ Size / drug effects. Proliferating Cell Nuclear Antigen / metabolism. Rats. Rats, Inbred F344

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  • (PMID = 17235567.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Estrogens; 0 / Proliferating Cell Nuclear Antigen; 0 / Protease Inhibitors; 0 / Thiophenes; 47E5O17Y3R / Phenylalanine; 731DCA35BT / Diethylstilbestrol; BK349F52C9 / batimastat; EC 3.4.24.- / Metalloendopeptidases
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16. Jamjoom BA, Sharab MA, Nasser TA, Jamjoom AB: Pseudotumor cerebri and prolactin secreting pituitary adenoma. Association or coincidence? Neurosciences (Riyadh); 2010 Jul;15(3):200-3
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  • [Title] Pseudotumor cerebri and prolactin secreting pituitary adenoma. Association or coincidence?
  • The occurrence of pseudotumor cerebri (PTC) and hyperprolactinemia related to a prolactinoma are extremely rare, and the link between these pathologies has not been examined adequately in the post-MRI era.
  • We report a patient with a small intrasellar prolactinoma who also developed PTC.
  • However 9 months later, her PTC symptoms recurred despite a normal serum prolactin level and a mild reduction of the pituitary tumor size on MRI.
  • We conclude that the findings in our patient do not support an association between PTC and hyperprolactinemia or prolactinoma.
  • However, the case supports the need for clinicians to consider the diagnosis of PTC when patients with small pituitary lesions exhibit raised intracranial pressure features.
  • [MeSH-major] Pituitary Neoplasms / complications. Prolactinoma / complications. Pseudotumor Cerebri / complications

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  • (PMID = 20831031.001).
  • [ISSN] 1319-6138
  • [Journal-full-title] Neurosciences (Riyadh, Saudi Arabia)
  • [ISO-abbreviation] Neurosciences (Riyadh)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Saudi Arabia
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17. Shetty R, Babu RB, Suresh M, Samprathi AB, Shetty BK: Neuro-ophthalmic disorders presenting as a diagnostic surprise during pre-LASIK evaluation. J Cataract Refract Surg; 2007 Sep;33(9):1653-6
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  • On examination, prolactinoma of the pituitary gland was seen in one patient and multiple sclerosis was diagnosed in the other patient.
  • [MeSH-major] Keratomileusis, Laser In Situ. Multiple Sclerosis / diagnosis. Optic Nerve Diseases / diagnosis. Pituitary Neoplasms / diagnosis. Prolactinoma / diagnosis. Vision Disorders / diagnosis

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  • (PMID = 17720088.001).
  • [ISSN] 0886-3350
  • [Journal-full-title] Journal of cataract and refractive surgery
  • [ISO-abbreviation] J Cataract Refract Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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18. Balci H, Akgun-Dar K, Gazioglu N, Kapucu A, Bolayirli M, Oz B: The relationship between prolactin (PRL), leptin, nitric oxide (NO), and cytokines in patients with hyperprolactinemia. Pituitary; 2009;12(3):170-6
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  • [Title] The relationship between prolactin (PRL), leptin, nitric oxide (NO), and cytokines in patients with hyperprolactinemia.
  • The study consists of 16 consecutive patients with high prolactin (PRL) levels (group I) and a control group of 11 normoprolactinemic patients (group II).
  • Pituitary tumor tissues of patients in groups I and II were analyzed for immunohistochemical (IHC) expression of prolactin and leptin.
  • There is a strong correlation between PRL and leptin concentrations in group I.
  • IHC staining showed that there was strong immunoreactivity for leptin protein in PRL-secreting pituitary adenomas.
  • Double immunostaining of adenoma tissues with PRL and leptin showed that the adenoma cells expressed both.
  • These findings together are suggestive that leptin co-secretion from a prolactinoma may be the cause of increased serum leptin concentration, independently from the peripheral action of prolactin.
  • [MeSH-major] Hyperprolactinemia / blood. Interleukin-6 / blood. Leptin / blood. Nitric Oxide / blood. Prolactin / blood. Tumor Necrosis Factor-alpha / blood
  • [MeSH-minor] Adult. Female. Humans. Immunohistochemistry. Male. Middle Aged. Pituitary Neoplasms / metabolism

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  • (PMID = 18752070.001).
  • [ISSN] 1573-7403
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukin-6; 0 / Leptin; 0 / Tumor Necrosis Factor-alpha; 31C4KY9ESH / Nitric Oxide; 9002-62-4 / Prolactin
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19. Wiesner TD, Trantakis C, Meixensberger J, Koch CA, Zimmer C, Paschke R: [Structure of an interdisciplinary pituitary outpatient care unit at the University Hospital of Leipzig and results for treatment of prolactin and growth hormone secreting pituitary tumors]. Med Klin (Munich); 2005 Apr 15;100(4):173-9
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  • [Title] [Structure of an interdisciplinary pituitary outpatient care unit at the University Hospital of Leipzig and results for treatment of prolactin and growth hormone secreting pituitary tumors].
  • BACKGROUND: Treatment of patients with pituitary adenomas is complex and involves several medical specialties.
  • At the Medical Center of the University of Leipzig, Germany, an interdisciplinary pituitary outpatient care unit has been established for 6 years.
  • METHODS: The interdisciplinary collaboration and the outcome of patients with growth hormone-(GH-) and prolactin-secreting pituitary adenomas are described.
  • Moreover, therapeutic strategies for patients with hormonally active pituitary adenomas are presented and discussed.
  • RESULTS: In patients suffering from GH-producing adenomas, a remission could be achieved in 80% (microadenomas) and 40% (macroadenomas) of the cases, respectively.
  • Furthermore, prolactinomas decreased in size during treatment in at least 75% of all cases depending on the initial size of the lesion which is also comparable to data from other groups.
  • CONCLUSION: Taken together, an interdisciplinary approach improves outcome and quality of care of patients with hormonally active pituitary adenomas.
  • [MeSH-major] Adenoma / therapy. Pituitary Neoplasms / therapy. Prolactinoma / therapy
  • [MeSH-minor] Acromegaly / drug therapy. Acromegaly / surgery. Acromegaly / therapy. Adult. Age Factors. Combined Modality Therapy. Dopamine Agonists / therapeutic use. Female. Follow-Up Studies. Germany. Growth Hormone / blood. Growth Hormone / secretion. Hospital Units. Humans. Interdisciplinary Communication. Male. Middle Aged. Outpatients. Patient Care Team. Prolactin / blood. Prolactin / secretion. Sex Factors. Time Factors

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  • (PMID = 15834525.001).
  • [ISSN] 0723-5003
  • [Journal-full-title] Medizinische Klinik (Munich, Germany : 1983)
  • [ISO-abbreviation] Med. Klin. (Munich)
  • [Language] ger
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Dopamine Agonists; 9002-62-4 / Prolactin; 9002-72-6 / Growth Hormone
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20. Chatfield J, Zhang L, Ramey J, Bowsher T, Loskutoff N, O'Neill K: Resolution of a hyperprolactinemia in a western lowland gorilla (Gorilla gorilla gorilla). J Zoo Wildl Med; 2006 Dec;37(4):565-6
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  • [Title] Resolution of a hyperprolactinemia in a western lowland gorilla (Gorilla gorilla gorilla).
  • Prolactin-secreting pituitary adenomas are one of the most common causes of infertility in women.
  • Prolactin plays an important role in lactation and is involved in producing some of the normal mammalian breeding and maternal behaviors.
  • Elevated serum prolactin concentrations can adversely affect the reproductive cycle in females by inhibiting the normal lutenizing hormone surge that stimulates ovulation.
  • An MRI confirmed a pituitary mass and treatment was initiated with cabergoline.
  • Following 8 mo of treatment, mass size decreased and serum prolactin was within normal limits.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Ape Diseases / drug therapy. Ergolines / therapeutic use. Gorilla gorilla. Pituitary Neoplasms / veterinary. Prolactinoma / veterinary

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  • (PMID = 17315448.001).
  • [ISSN] 1042-7260
  • [Journal-full-title] Journal of zoo and wildlife medicine : official publication of the American Association of Zoo Veterinarians
  • [ISO-abbreviation] J. Zoo Wildl. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Ergolines; LL60K9J05T / cabergoline
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21. Pierantoni GM, Finelli P, Valtorta E, Giardino D, Rodeschini O, Esposito F, Losa M, Fusco A, Larizza L: High-mobility group A2 gene expression is frequently induced in non-functioning pituitary adenomas (NFPAs), even in the absence of chromosome 12 polysomy. Endocr Relat Cancer; 2005 Dec;12(4):867-74
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  • [Title] High-mobility group A2 gene expression is frequently induced in non-functioning pituitary adenomas (NFPAs), even in the absence of chromosome 12 polysomy.
  • By previous fluorescence in situ hybridization (FISH) and reverse transcriptase PCR analyses on human prolactin-secreting pituitary adenomas we detected rearrangement of the HMGA2 gene and amplification of its native region associated with activated expression.
  • These data indicated a role for the HMGA2 gene in the development of human pituitary prolactinomas, since they are consistent with the appearance of prolactin/growth hormone adenomas in transgenic mice overexpressing the HMGA2 gene.
  • To assess a more general role for HMGA2 in pituitary oncogenesis, we investigated HMGA2 amplification and expression in a panel of non-functioning pituitary adenomas (NFPAs) which account for 25% of all pituitary adenomas.
  • We provide evidence that out of 18 NFPA tumors tested, 12 expressed HMGA2, but, different from prolactinomas, only in two cases the upregulation of the gene could be associated with amplification and/or rearrangement of the HMGA2 locus.
  • A role for chromosome 12 polysomy to promote structural instability of HMGA2 is confirmed, but the mechanism via trisomy is less prevalent in the frequently diploid NFPAs than in the usually hyperdiploid prolactinomas.
  • Micro-rearrangements of HMGA2 gene not detectable by FISH analysis and/or sequence alterations could contribute to upregulation of HMGA2 gene in pituitary adenomas of the NFPA subtype.
  • [MeSH-major] Adenoma / genetics. Chromosomes, Human, Pair 12 / genetics. Gene Amplification. HMGA2 Protein / genetics. Pituitary Neoplasms / genetics

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  • (PMID = 16322327.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HMGA2 Protein
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22. Corona G, Mannucci E, Jannini EA, Lotti F, Ricca V, Monami M, Boddi V, Bandini E, Balercia G, Forti G, Maggi M: Hypoprolactinemia: a new clinical syndrome in patients with sexual dysfunction. J Sex Med; 2009 May;6(5):1457-66
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • INTRODUCTION: The physiological role of prolactin (PRL) in male sexual behavior is poorly understood.
  • Conversely, the association between PRL pathological elevation in both reproductive and sexual behavior is well defined.
  • AIM: The aim of the present study is to assess the correlates of normal PRL (PRL < 735 mU/L or 35 ng/mL), in male subjects consulting for sexual dysfunction.
  • MAIN OUTCOME MEASURES: Several hormonal (testosterone, thyroid stimulation hormone, and PRL) and biochemical parameters (glycemia and lipid profile) were studied, along with penile Doppler ultrasound (PDU) and SIEDY items.
  • RESULTS: After adjustment for confounders anxiety symptoms decreased across PRL quartiles (I: <113 mU/L or 5 ng/mL; II: 113-156 mU/L or 5.1-7 ng/mL; III: 157-229 mU/L or 7.1-11 ng/mL; IV: 229-734 mU/L or 11.1-34.9 ng/mL).
  • Patients in the lowest PRL quartile showed a higher risk of metabolic syndrome (MetS; odds ratio [OR] = 1.74 [1.01-2.99], P < 0.05), arteriogenic ED (peak systolic velocity at PDU < 35 cm/sec; OR = 1.43 [1.01-2.03], P < 0.05), and premature ejaculation (PE; OR = 1.38 [1.02-1.85]; P < 0.05).
  • Conversely, comparing subjects with PRL-secreting pituitary adenomas (N = 13) with matched controls, no significant difference was observed, except for a higher prevalence of hypoactive sexual desire in hyperprolactinemia.
  • CONCLUSIONS: Our findings demonstrate that, in subjects consulting for sexual dysfunction, PRL in the lowest quartile levels are associated with MetS and arteriogenic ED, as well as with PE and anxiety symptoms.
  • [MeSH-major] Hyperprolactinemia / complications. Pituitary Neoplasms / complications. Prolactin / deficiency. Prolactinoma / complications. Sexual Dysfunction, Physiological / blood. Sexual Dysfunction, Physiological / etiology


23. Mittelbronn M, Psaras T, Capper D, Meyermann R, Honegger J: ACTH- and prolactin-producing pituitary gland microadenoma with biphasic features of atypia and intermediate filament expression. Neuro Endocrinol Lett; 2006 Feb-Apr;27(1-2):89-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ACTH- and prolactin-producing pituitary gland microadenoma with biphasic features of atypia and intermediate filament expression.
  • Herein, we report the case of a 28-year old woman clinically presenting with unclear weight gain over the last years.
  • Endocrinological examinations led to the diagnosis of Cushing's disease.
  • Histological and immunohistochemical investigations revealed a pituitary gland adenoma showing a biphasic tumor growth pattern with two morphologically different tumor areas producing ACTH and prolactin respectively.
  • Co-expression of ACTH and prolactin is exceedingly rare in pituitary adenoma.
  • To our surprise, both tumor areas exhibited features of atypia consisting in elevated MIB-1 proliferation index in the ACTH-producing portion as well as p53 expression selectively in the prolactin-producing tumor parts.
  • To our knowledge, this is the first case of an ACTH- and prolactin-producing pituitary gland adenoma exhibiting biphasic features of atypia.
  • [MeSH-major] Adenoma / metabolism. Adrenocorticotropic Hormone / biosynthesis. Intermediate Filament Proteins / biosynthesis. Pituitary Neoplasms / metabolism. Prolactin / biosynthesis
  • [MeSH-minor] Adult. Cell Proliferation. Female. Humans. Immunohistochemistry. Ki-67 Antigen / metabolism. Pituitary Hormones / chemistry. Pituitary Hormones / metabolism. Tumor Suppressor Protein p53 / biosynthesis

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  • (PMID = 16648816.001).
  • [ISSN] 0172-780X
  • [Journal-full-title] Neuro endocrinology letters
  • [ISO-abbreviation] Neuro Endocrinol. Lett.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Sweden
  • [Chemical-registry-number] 0 / Intermediate Filament Proteins; 0 / Ki-67 Antigen; 0 / Pituitary Hormones; 0 / Tumor Suppressor Protein p53; 9002-60-2 / Adrenocorticotropic Hormone; 9002-62-4 / Prolactin
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24. Zylberberg D, Naliato EC, Sarmet A, Sato E, Costa FS, Violante AH: [IGF-1 plasma levels evaluation in prolactinoma]. Arq Neuropsiquiatr; 2006 Sep;64(3B):849-54
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [IGF-1 plasma levels evaluation in prolactinoma].
  • [Transliterated title] Avaliação plasmática de IGF-1 no prolactinoma.
  • Prolactinomas are the most frequent pituitary tumors and may co-secrete GH (growth hormone).
  • IGF-1 (insulin-like growth factor-1) is the main responsible for GH actions and a parameter for the diagnosis of acromegaly.
  • With the objective of identifying through a IGF-1 levels analysis, in the initial evaluation of prolactinoma patients, the existence of mixed tumors [GH and prolactin (PRL)], we studied 7 men and 27 women, aged between 19 and 72 years, confronting them with the results of basal and glucose stimulated (glucose tolerance test--GTT) GH levels, indicated when GH >0.4 ng/mL or IGF-1 levels were elevated.
  • However, we suggest that, they should be submitted to IGF-1 evaluation, due to the risk of GH co-secretion in prolactinomas.
  • Special attention should be paid to those who present a significant decrease of PRL levels without concomitant tumor size reduction.
  • [MeSH-major] Biomarkers, Tumor / blood. Insulin-Like Growth Factor I / analysis. Pituitary Neoplasms / blood. Prolactinoma / blood

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  • (PMID = 17057896.001).
  • [ISSN] 0004-282X
  • [Journal-full-title] Arquivos de neuro-psiquiatria
  • [ISO-abbreviation] Arq Neuropsiquiatr
  • [Language] por
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 67763-96-6 / Insulin-Like Growth Factor I
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25. Okawara M, Yamaguchi H, Hayashi S, Matsumoto Y, Inoue Y, Okawara S: [A case of ruptured internal carotid artery aneurysm mimicking pituitary apoplexy]. No Shinkei Geka; 2007 Dec;35(12):1169-74
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  • [Title] [A case of ruptured internal carotid artery aneurysm mimicking pituitary apoplexy].
  • Nineteen years before, she had undergone a transsphenoidal surgery for a prolactin producing pituitary adenoma at our hospital without intraoperative arterial bleeding.
  • MRI revealed a pituitary tumor with intratumoral hemorrhage, intraventricular hemorrhage and subdural hemorrhage.
  • Her medical history and radiological findings suggested the rupture of a de novo aneurysm causing a hemorrhage into a pituitary adenoma mimicking pituitary apoplexy.
  • Because of rapid improvement of visual acuity, administration of terguride was chosen for shrinking the pituitary adenoma.
  • If a pituitary adenoma is present, the possibility of a coincidental aneurysm should always be considered.
  • This association should be kept in mind when evaluating any case of pituitary apoplexy.
  • [MeSH-major] Carotid Artery Diseases / diagnosis. Carotid Artery, Internal. Intracranial Aneurysm / diagnosis. Pituitary Apoplexy / diagnosis
  • [MeSH-minor] Cerebral Hemorrhage / etiology. Diagnosis, Differential. Embolization, Therapeutic. Female. Humans. Lisuride / analogs & derivatives. Lisuride / therapeutic use. Middle Aged. Pituitary Neoplasms / complications. Pituitary Neoplasms / drug therapy. Rupture, Spontaneous

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  • (PMID = 18080517.001).
  • [ISSN] 0301-2603
  • [Journal-full-title] No shinkei geka. Neurological surgery
  • [ISO-abbreviation] No Shinkei Geka
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 21OJT43Q88 / dironyl; E0QN3D755O / Lisuride
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26. Ciccarelli A, Guerra E, De Rosa M, Milone F, Zarrilli S, Lombardi G, Colao A: PRL secreting adenomas in male patients. Pituitary; 2005;8(1):39-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] PRL secreting adenomas in male patients.
  • Prolactinomas are the most frequent pituitary tumors and their frequency varies with age and sex, occurring most frequently in females between 20-50 yr-old.
  • Prolactin (PRL) plays a role in the process of spermatogenesis, and normal serum PRL levels are required for normal testicular function.
  • Cabergoline treatments is able to induce normalization of PRL levels and a reduction of tumor mass in the majority of patients and consequently restoring the normal semen quality and ameliorating the quality of life of men with pituitary PRL-secreting adenoma.
  • [MeSH-major] Pituitary Neoplasms / physiopathology. Prolactin / secretion. Prolactinoma / physiopathology

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  • (PMID = 16411067.001).
  • [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 / Dopamine Agonists; 0 / Ergolines; 9002-62-4 / Prolactin; LL60K9J05T / cabergoline
  • [Number-of-references] 20
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27. Astaf'eva LI, Kadashev BA, Kalinin PL, Kutin MA, Faĭzullaev RB, Sidneva IuG, Tenedieva VD, Tropinskaia OF: [Selection of management tactics in treatment of giant prolactin-secreting pituitary adenomas]. Zh Vopr Neirokhir Im N N Burdenko; 2009 Apr-Jun;(2):23-8; discussion 28-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Selection of management tactics in treatment of giant prolactin-secreting pituitary adenomas].
  • Surgical treatment of giant pituitary adenomas is one of the most complicated problems of modern neurosurgery.
  • Advances in modern pharmacology allowed to approach the alternative way of management of giant prolactinomas (GP).
  • Assessment of neurological status, visual functions, hypopituitary disorders and prolactin level was performed.
  • [MeSH-major] Dopamine Agonists / therapeutic use. Ergolines / therapeutic use. Pituitary Neoplasms / drug therapy. Pituitary Neoplasms / surgery. Prolactin / secretion. Prolactinoma / drug therapy. Prolactinoma / surgery

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  • (PMID = 19569545.001).
  • [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] Clinical Trial; English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Dopamine Agonists; 0 / Ergolines; 9002-62-4 / Prolactin; LL60K9J05T / cabergoline
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28. da Costa LB, Riva-Cambrin J, Tandon A, Tymianski M: Pituitary adenoma associated with intraventricular meningioma: case report. Skull Base; 2007 Sep;17(5):347-51
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pituitary adenoma associated with intraventricular meningioma: case report.
  • Although rare, the association of intracranial meningiomas and pituitary adenomas has been reported.
  • We report a patient who harbored a prolactin-secreting pituitary adenoma and a fourth ventricle meningioma who was treated with surgical resection of the latter and medical treatment for the former.

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  • [Cites] Neurol India. 2000 Mar;48(1):72-4 [10751818.001]
  • [Cites] Arq Neuropsiquiatr. 1998 Jun;56(2):193-9 [9698727.001]
  • [Cites] Clin Neurol Neurosurg. 1992;94(2):181-4 [1324820.001]
  • [Cites] Climacteric. 2003 Dec;6(4):285-92 [15006250.001]
  • [Cites] Neurol Med Chir (Tokyo). 1988 Jan;28(1):86-90 [2455250.001]
  • [Cites] Neurol Med Chir (Tokyo). 1988 Oct;28(10):996-1000 [2462692.001]
  • [Cites] Br J Neurosurg. 1989;3(1):59-69 [2675917.001]
  • [Cites] Acta Neurochir (Wien). 1986;83(3-4):83-91 [3492867.001]
  • [Cites] Neurosurgery. 1986 Aug;19(2):267-70 [3748357.001]
  • [Cites] J Comput Assist Tomogr. 1977 Oct;1(4):517-20 [615235.001]
  • [Cites] Neurosurgery. 1981 Jan;8(1):20-5 [6259551.001]
  • [Cites] Neurochirurgia (Stuttg). 1982 Mar;25(2):68-72 [6287323.001]
  • [Cites] J Endocrinol. 1995 Apr;145(1):155-61 [7798021.001]
  • [Cites] Eur Neurol. 1993;33(6):416-22 [8307062.001]
  • [Cites] J Endocrinol. 1997 Jun;153(3):365-71 [9203990.001]
  • [Cites] Cancer Detect Prev. 2000;24(2):163-8 [10917137.001]
  • (PMID = 18330434.001).
  • [ISSN] 1531-5010
  • [Journal-full-title] Skull base : official journal of North American Skull Base Society ... [et al.]
  • [ISO-abbreviation] Skull Base
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2095121
  • [Keywords] NOTNLM ; Intraventricular tumor / meningioma / pituitary tumor / prolactinoma
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29. Fedele M, De Martino I, Pivonello R, Ciarmiello A, Del Basso De Caro ML, Visone R, Palmieri D, Pierantoni GM, Arra C, Schmid HA, Hofland L, Lombardi G, Colao A, Fusco A: SOM230, a new somatostatin analogue, is highly effective in the therapy of growth hormone/prolactin-secreting pituitary adenomas. Clin Cancer Res; 2007 May 1;13(9):2738-44
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] SOM230, a new somatostatin analogue, is highly effective in the therapy of growth hormone/prolactin-secreting pituitary adenomas.
  • PURPOSE: We have previously shown that transgenic mice ubiquitously overexpressing the HMGA2 gene develop growth hormone/prolactin-secreting pituitary adenomas.
  • This animal model has been used to evaluate the therapeutic efficacy of SOM230, a somatostatin analogue with high affinity for the somatostatin receptor subtypes 1, 2, 3, and 5, on the growth of the pituitary adenomas.
  • The development of the tumor before and after therapy was monitored by magnetic resonance imaging of the pituitary region and evaluation of the serum prolactin levels.
  • CONCLUSIONS: These results clearly support the efficacy of the SOM230 treatment in human pituitary adenomas secreting prolactin based on the dramatic tumor shrinkage and fall in prolactin levels.
  • [MeSH-major] Growth Hormone-Secreting Pituitary Adenoma / drug therapy. Pituitary Neoplasms / drug therapy. Somatostatin / analogs & derivatives
  • [MeSH-minor] Animals. Cell Proliferation / drug effects. Female. HMGA2 Protein / genetics. Mice. Mice, Transgenic. Treatment Outcome

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  • (PMID = 17473207.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HMGA2 Protein; 51110-01-1 / Somatostatin; 98H1T17066 / pasireotide
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30. Coiré CI, Smyth HS, Rosso D, Horvath E, Kovacs K: A double pituitary adenoma presenting as a prolactin-secreting tumor with partial response to medical therapy. Case report. Endocr Pathol; 2010 Jun;21(2):135-8

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

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  • (PMID = 20058099.001).
  • [ISSN] 1559-0097
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Ergolines; LL60K9J05T / cabergoline
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31. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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  • [Cites] J Clin Endocrinol Metab. 1987 Dec;65(6):1127-34 [2824549.001]
  • [Cites] Front Horm Res. 2004;32:235-52 [15281350.001]
  • [Cites] J Clin Endocrinol Metab. 1994 Feb;78(2):398-403 [8106629.001]
  • [Cites] Cancer Res. 1994 Jul 1;54(13):3455-9 [8012966.001]
  • [Cites] J Clin Endocrinol Metab. 1994 Sep;79(3):724-9 [7521350.001]
  • [Cites] Life Sci. 1995;56(5):333-42 [7530798.001]
  • [Cites] J Clin Endocrinol Metab. 1995 Apr;80(4):1386-92 [7714115.001]
  • [Cites] Endocr Rev. 1995 Aug;16(4):427-42 [8521788.001]
  • [Cites] J Neuroendocrinol. 1996 Aug;8(8):605-10 [8866248.001]
  • [Cites] J Clin Invest. 1997 Feb 15;99(4):789-98 [9045884.001]
  • [Cites] Int J Cancer. 1997 Mar 4;70(5):530-7 [9052751.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Sep;82(9):3011-8 [9284735.001]
  • [Cites] J Endocrinol Invest. 1997 Jun;20(6):348-67 [9294784.001]
  • [Cites] J Clin Invest. 1997 Nov 1;100(9):2386-92 [9410919.001]
  • [Cites] Nat Med. 1998 Jul;4(7):844-7 [9662379.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Jul;83(7):2417-20 [9661621.001]
  • [Cites] Am J Pathol. 1998 Jul;153(1):233-45 [9665484.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Aug;83(8):2997-3000 [9709982.001]
  • [Cites] Clin Cancer Res. 1998 Sep;4(9):2047-52 [9748118.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Feb;84(2):775-80 [10022452.001]
  • [Cites] Front Neuroendocrinol. 1999 Jul;20(3):157-98 [10433861.001]
  • [Cites] Clin Cancer Res. 1999 Aug;5(8):1966-75 [10473073.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Sep;84(9):3268-76 [10487698.001]
  • [Cites] Virchows Arch. 2001 Dec;439(6):787-97 [11787852.001]
  • [Cites] Virchows Arch. 2002 May;440(5):461-75 [12021920.001]
  • [Cites] Surg Today. 2002;32(8):690-4 [12181718.001]
  • [Cites] Endocr Rev. 2003 Feb;24(1):28-47 [12588807.001]
  • [Cites] Endocr Rev. 2003 Aug;24(4):389-427 [12920149.001]
  • [Cites] Clin Cancer Res. 1999 Nov;5(11):3483-7 [10589762.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Feb;85(2):781-92 [10690891.001]
  • [Cites] J Biol Chem. 2000 Mar 17;275(11):7862-9 [10713101.001]
  • [Cites] Diagn Mol Pathol. 2000 Mar;9(1):47-57 [10718213.001]
  • [Cites] Lab Invest. 2000 Dec;80(12):1943-9 [11140706.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Jan;86(1):140-5 [11231991.001]
  • [Cites] Eur J Clin Invest. 2001 Mar;31(3):208-14 [11264647.001]
  • [Cites] Clin Endocrinol (Oxf). 2001 May;54(5):641-9 [11380495.001]
  • [Cites] J Natl Cancer Inst. 2001 Aug 1;93(15):1141-6 [11481385.001]
  • [Cites] Gut. 2002 Jan;50(1):52-60 [11772967.001]
  • [Cites] N Engl J Med. 1983 Dec 15;309(24):1495-501 [6139753.001]
  • [Cites] Clin Endocrinol (Oxf). 1986 Aug;25(2):201-12 [2878748.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Apr;89(4):1577-85 [15070915.001]
  • [Cites] Neuroendocrinology. 2004 Mar;79(3):142-8 [15103227.001]
  • [Cites] Cancer Res. 1990 Sep 15;50(18):5969-77 [2168286.001]
  • (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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32. Elsässer Imboden PN, Gomez F: [Medical treatment of prolactinoma. Quo usque tandem..]. Rev Med Suisse; 2005 Feb 9;1(6):440-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Medical treatment of prolactinoma. Quo usque tandem..].
  • [Transliterated title] Traitement médical du prolactinome. Quo usque tandem...
  • Dopamine agonists are the first choice therapy for prolactinoma.
  • They decrease tumor secretion and volume, restore the gonadotropic axis, preserve the remaining pituitary functions, and correct the ophthalmologic symptoms.
  • [MeSH-major] Dopamine Agonists / therapeutic use. Pituitary Neoplasms / drug therapy. Prolactinoma / drug therapy

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  • (PMID = 15786649.001).
  • [ISSN] 1660-9379
  • [Journal-full-title] Revue médicale suisse
  • [ISO-abbreviation] Rev Med Suisse
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Dopamine Agonists
  • [Number-of-references] 23
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33. Chahal HS, Chapple JP, Frohman LA, Grossman AB, Korbonits M: Clinical, genetic and molecular characterization of patients with familial isolated pituitary adenomas (FIPA). Trends Endocrinol Metab; 2010 Jul;21(7):419-27
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical, genetic and molecular characterization of patients with familial isolated pituitary adenomas (FIPA).
  • Familial pituitary adenomas can occur in MEN1 and Carney complex, as well as in the recently characterized familial isolated pituitary adenoma (FIPA) syndrome.
  • FIPA is an autosomal dominant disease with incomplete penetrance, characterized by early-onset disease, often aggressive tumor growth and a predominance of somatotroph and lactotroph adenomas.
  • [MeSH-major] Pituitary Neoplasms / genetics. Pituitary Neoplasms / pathology

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  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20570174.001).
  • [ISSN] 1879-3061
  • [Journal-full-title] Trends in endocrinology and metabolism: TEM
  • [ISO-abbreviation] Trends Endocrinol. Metab.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0701307
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / aryl hydrocarbon receptor-interacting protein
  • [Number-of-references] 92
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34. Vera-Lastra O, Jara LJ, Medina G, Rojas JL, Veláquez F, Ariza R, Normandía A, Fuentes M: Functional hyperprolactinemia and hypophyseal microadenoma in systemic sclerosis. J Rheumatol; 2006 Jun;33(6):1108-12
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  • However, the association with pituitary adenoma and the status of hypothalamic dopaminergic tone using metoclopramide (MTC) test has not been studied.
  • We investigated the prevalence of prolactin (PRL)-secreting pituitary adenoma and evaluated production of PRL by dynamic testing with MTC in SSc.
  • Serum PRL concentrations were determined by radioimmunoassay in all subjects, and PRL response was measured 30, 60, 90, and 120 min after injection of 10 mg of MTC.
  • RESULTS: The mean basal serum PRL levels before and after stimulation with MTC in SSc patients versus controls were: basal 18.2 +/- 5.4 versus 8.7 +/- 1.6 ng/ml, p = NS; 30 min: 175.0 +/- 5.4 versus 61.0 +/- 42 ng/ml, p < 0.001; 60 min: 160 +/- 64 versus 52 +/- 30 ng/ml, p < 0.001; 90 min: 125 +/- 57 versus 42 +/- 21.0 ng/ml, p < 0.05; 120 min: 108.0 +/- 57 versus 30.0 +/- 10 ng/ml, p < 0.005.
  • PRL may have a role in the pathogenesis of SSc.
  • [MeSH-major] Adenoma / blood. Hyperprolactinemia / blood. Pituitary Neoplasms / blood. Scleroderma, Diffuse / blood. Scleroderma, Limited / blood


35. 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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36. 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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37. Bussade I, Naliato EC, Mendonça LM, Violante AH, Farias ML: [Decreased bone mineral density in pre-menopause women with prolactinoma]. Arq Bras Endocrinol Metabol; 2007 Dec;51(9):1522-7
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  • [Title] [Decreased bone mineral density in pre-menopause women with prolactinoma].
  • [Transliterated title] Redução da densidade mineral óssea em mulheres na menacme com prolactinoma.
  • Bone mineral density (BMD) was measured by dual-energy RX absorptiometry in 24 patients with prolactinoma (15 macro and 9 micro adenomas; age range = 18 to 49 years).
  • No difference was found in densitometric parameters for the comparison between macro and microprolactinoma, or those with normal prolactin versus hyperprolactinemia.
  • CONCLUSIONS: Decreased bone mineral density was detected in 20.83% of our young patients with prolactinoma.
  • The great involvement of trabecular bone skeletal regions, such as vertebrae, suggests the participation of hypogonadism in the pathogenesis of bone disease.
  • Irrespective of prolactin levels, return to normal menses seems the best index of good control.
  • [MeSH-major] Bone Density / physiology. Hyperprolactinemia / physiopathology. Osteoporosis / physiopathology. Pituitary Neoplasms / physiopathology. Premenopause / physiology. Prolactinoma / physiopathology

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  • (PMID = 18209896.001).
  • [ISSN] 0004-2730
  • [Journal-full-title] Arquivos brasileiros de endocrinologia e metabologia
  • [ISO-abbreviation] Arq Bras Endocrinol Metabol
  • [Language] por
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Brazil
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38. Nociti V, Frisullo G, Tartaglione T, Patanella AK, Iorio R, Tonali PA, Batocchi AP: Multiple sclerosis attacks triggered by hyperprolactinemia. J Neurooncol; 2010 Jul;98(3):407-9
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  • Multiple sclerosis (MS) is a T-cell autoimmune disease of the central nervous system (CNS).
  • Predominance of women in autoimmune diseases suggests that sex hormones may play a role in disease susceptibility.
  • A possible role for prolactin, a neuroendocrine peptide with powerful immunomodulatory properties, is suggested in MS.
  • We describe the case of a 32-year-old man affected by relapsing-remitting MS who experienced the first MS clinical event during the development of a prolactin-secreting adenoma and the only two MS relapses during adenoma recurrence.
  • Prolactin may have facilitated the inflammatory process and triggered MS clinical attacks, suggesting a role of prolactin in immunomodulation and therefore in autoimmune disease course.

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  • (PMID = 19957009.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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39. Fedele M, Palmieri D, Fusco A: HMGA2: A pituitary tumour subtype-specific oncogene? Mol Cell Endocrinol; 2010 Sep 15;326(1-2):19-24
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  • [Title] HMGA2: A pituitary tumour subtype-specific oncogene?
  • The high mobility group AT-hook (HMGA) proteins, a family of DNA architectural factors, are highly expressed during embryogenesis and play a crucial role in several different biological processes, as well as in tumorigenesis of a wide range of tissues, including pituitary.
  • Indeed, HMGA2 has been found rearranged and amplified in human prolactinomas, and transgenic mice overexpressing either Hmga1 or Hmga2 develop pituitary adenomas secreting prolactin and growth hormone.
  • Here, we overview HMGA proteins in human tumours, focusing on pituitary adenomas and the mechanisms by which the HMGA proteins are involved in their onset and development.
  • Different HMGA-dependent potential drives of pituitary oncogenesis are discussed as future research directions in the field.
  • [MeSH-major] Adenoma / etiology. HMGA2 Protein / physiology. Oncogene Proteins / physiology. Pituitary Neoplasms / etiology

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  • [Copyright] 2010 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 20347930.001).
  • [ISSN] 1872-8057
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / HMGA1c Protein; 0 / HMGA2 Protein; 0 / Oncogene Proteins; 124543-08-4 / HMGA1b Protein; 124544-67-8 / HMGA1a Protein
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40. Jaffe CA: Clinically non-functioning pituitary adenoma. Pituitary; 2006;9(4):317-21
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  • [Title] Clinically non-functioning pituitary adenoma.
  • Non-functioning pituitary tumors are relatively common.
  • A large number of these tumors are incidentally found pituitary microadenomas (<1 cm) and are usually of no clinical importance.
  • Visual field defects are present in roughly 70% of patients with non-functioning macroadenoma at the time of diagnosis and the majority of these patients have at least growth deficiency and hypogonadism.
  • By immunocytochemistry, the large majority of these tumors are glycoprotein producing and less commonly they are non-functioning somatotroph, lactotroph or corticotoph adenomas.
  • Surgery improves visual defects in the majority of patients and a lesser number will recover pituitary function.
  • In the past, pituitary radiation was commonly administered following pituitary surgery; however the need for routine radiation has recently been reevaluated.
  • Close follow-up with surveillance pituitary scans should be performed after surgery and radiation therapy reserved for patients having significant tumor recurrence.
  • [MeSH-major] Adenoma / diagnosis. Adenoma / therapy. Pituitary Neoplasms / diagnosis. Pituitary Neoplasms / therapy

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  • (PMID = 17082898.001).
  • [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 / Antineoplastic Agents, Hormonal; 0 / Biomarkers
  • [Number-of-references] 17
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41. Spinks JJ, Ryan FJ: Cabergoline resistance in pediatric prolactinomas. J Pediatr Hematol Oncol; 2009 May;31(5):377-9
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  • [Title] Cabergoline resistance in pediatric prolactinomas.
  • We report 3 cases of cabergoline resistance in adolescents with prolactinomas.
  • There are few reports on the management and outcome of dopamine agonist resistance in prolactinomas in the pediatric population, and our case series highlights the need for further research.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Drug Resistance, Neoplasm. Ergolines / administration & dosage. Pituitary Neoplasms / drug therapy. Prolactinoma / drug therapy

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  • (PMID = 19415025.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Ergolines; LL60K9J05T / cabergoline
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42. Bangash MH, Clarke DB, Holness RO: Brain & chiasmal herniations into sella after medical treatment of prolactinoma. Can J Neurol Sci; 2006 May;33(2):240-2
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  • [Title] Brain & chiasmal herniations into sella after medical treatment of prolactinoma.
  • BACKGROUND: Dopamine agonists are widely used in the treatment of pituitary prolactinomas.
  • We report a case of inferior mesial frontal lobe (gyrus rectus) and chiasmal herniations into an enlarged sella following successful medical treatment of a pituitary macroadenoma.
  • Endocrine evaluation revealed an elevated prolactin level.
  • Serum prolactin levels normalized (5.16 ng/ml).
  • CONCLUSIONS: We report a case where successful medical treatment of a large pituitary prolactinoma has resulted in inferior frontal lobe and chiasmal herniatons into an enlarged sella.
  • [MeSH-major] Encephalocele / etiology. Neurosurgical Procedures / adverse effects. Pituitary Neoplasms / surgery. Postoperative Complications / etiology. Prolactinoma / surgery. Sella Turcica / pathology
  • [MeSH-minor] Aged. Bromocriptine / therapeutic use. Frontal Lobe / injuries. Frontal Lobe / pathology. Hemianopsia / diagnosis. Hemianopsia / etiology. Hemianopsia / physiopathology. Hormone Antagonists / therapeutic use. Humans. Magnetic Resonance Imaging. Male. Optic Chiasm / injuries. Optic Chiasm / pathology. Prolactin / antagonists & inhibitors. Prolactin / blood

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  • (PMID = 16736739.001).
  • [ISSN] 0317-1671
  • [Journal-full-title] The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques
  • [ISO-abbreviation] Can J Neurol Sci
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Hormone Antagonists; 3A64E3G5ZO / Bromocriptine; 9002-62-4 / Prolactin
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43. Stepień H, Lawnicka H, Mucha S, Wagrowska-Danilewicz M, Stepień B, Siejka A, Komorowski J: Inhibitory effect of thalidomide on the growth, secretory function and angiogenesis of estrogen-induced prolactinoma in Fischer 344 rats. Life Sci; 2006 Sep 27;79(18):1741-8
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  • [Title] Inhibitory effect of thalidomide on the growth, secretory function and angiogenesis of estrogen-induced prolactinoma in Fischer 344 rats.
  • The process of angiogenesis has been found to be essential for the development of estrogen-induced pituitary prolactinoma in Fischer 344 rats.
  • Thalidomide [(alpha-(N-phthalimido)-glutarimide] is known to be a potent immunomodulatory drug with antiangiogenic properties, but its effect on lactotroph cell secretory function and pituitary prolactinoma formation has not been described yet.
  • The purpose of this study was to examine the effects of thalidomide on secretion of prolactin (PRL) and vascular endothelial growth factor (VEGF), cell proliferation, apoptosis and angiogenesis within the anterior pituitary gland in long-term diethylstilboestrol (DES)-treated male F344 rats in vivo and in vitro.
  • It was found that DES sharply increased serum PRL and VEGF levels.
  • On the other hand, simultaneous treatment of F344 rats with thalidomide for the last 15 days of the experiment attenuated the stimulatory effect of DES on PRL and VEGF secretion.
  • It also diminished prolactin cell proliferation evaluated as the number of proliferating cell nuclear antigen (PCNA)-positive stained cell nuclei and increased the number of apoptotic bodies determined by the terminal deoxynucleotidyl-mediated dUTP nick-end labeling (TUNEL) method in sections of the DES-induced pituitary prolactinoma.
  • The density of pituitary microvessels evaluated by microscopic counting of CD-31-positive blood vessels was also diminished by the tested drug.
  • In addition, thalidomide (10(-4) to 10(-6) M) inhibited cell proliferation, prolactin and VEGF secretion from rat pituitary prolactinoma cells cultured in vitro.
  • In conclusion, our results provide strong evidence for the antiprolactin and antitumor activity of thalidomide in experimentally DES-induced pituitary adenoma.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Neovascularization, Pathologic / drug therapy. Pituitary Neoplasms / drug therapy. Prolactin / metabolism. Prolactinoma / drug therapy. Thalidomide / therapeutic use
  • [MeSH-minor] Animals. Antigens, CD31 / analysis. Apoptosis. Cell Nucleus / chemistry. Cell Proliferation / drug effects. Diethylstilbestrol / toxicity. Estrogens / toxicity. Pituitary Gland / chemistry. Pituitary Gland / pathology. Proliferating Cell Nuclear Antigen / analysis. Rats. Rats, Inbred F344. Vascular Endothelial Growth Factor A

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  • (PMID = 16846617.001).
  • [ISSN] 0024-3205
  • [Journal-full-title] Life sciences
  • [ISO-abbreviation] Life Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antigens, CD31; 0 / Estrogens; 0 / Proliferating Cell Nuclear Antigen; 0 / Vascular Endothelial Growth Factor A; 4Z8R6ORS6L / Thalidomide; 731DCA35BT / Diethylstilbestrol; 9002-62-4 / Prolactin
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44. Hong JW, Lee MK, Kim SH, Lee EJ: Discrimination of prolactinoma from hyperprolactinemic non-functioning adenoma. Endocrine; 2010 Feb;37(1):140-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Discrimination of prolactinoma from hyperprolactinemic non-functioning adenoma.
  • The objective of this study was to evaluate characteristics that discriminate prolactinoma from non-functioning pituitary macroadenoma with hyperprolactinemia.
  • We included 117 patients with hyperprolactinemic pituitary macroadenomas.
  • Patients were divided into three groups according to treatment outcomes and pathologic results: (A) prolactinoma that responded to dopamine agonist (DA) treatment (PRDA);.
  • (B) prolactinoma requiring surgical treatment (PRS); and (C) non-functioning pituitary adenoma with hyperprolactinemia (NFPAH).
  • Old age, low serum prolactin levels, and extrasellar extension were associated with NFPAH.
  • Most patients with NFPAH had serum prolactin levels less than 100 ng/ml.
  • In conclusion, old age, extrasellar tumor extension with relatively low prolactin levels, visual defect, and GH deficiency were considered suggestive of non-functioning pituitary adenoma rather than prolactinoma in hyperprolactinemic pituitary macroadenoma.
  • [MeSH-major] Adenoma / blood. Adenoma / diagnosis. Hyperprolactinemia / etiology. Pituitary Neoplasms / blood. Pituitary Neoplasms / diagnosis. Prolactinoma / diagnosis
  • [MeSH-minor] Adult. Aging. Amenorrhea. Decision Trees. Diagnosis, Differential. Dopamine Agonists / therapeutic use. Female. Galactorrhea. Humans. Immunohistochemistry. Male. Middle Aged. Prolactin / blood. Retrospective Studies. Sella Turcica. Treatment Outcome. Young Adult

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  • (PMID = 20963563.001).
  • [ISSN] 1559-0100
  • [Journal-full-title] Endocrine
  • [ISO-abbreviation] Endocrine
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dopamine Agonists; 9002-62-4 / Prolactin
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45. Schäffler A: [Treatment of pituitary gland hyperfunction: from acromegaly to prolactinoma]. Internist (Berl); 2006 Dec;47(12):1215-6, 1218-20, 1222
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Treatment of pituitary gland hyperfunction: from acromegaly to prolactinoma].
  • [Transliterated title] Therapie der Hypophysenüberfunktion: Von der Akromegalie zum Prolaktinom.
  • Evidence based drug therapy is currently available for the treatment of prolactinomas and growth hormone secreting adenomas (acromegaly).
  • [MeSH-major] Acromegaly / therapy. Adenoma / therapy. Hyperpituitarism / therapy. Pituitary Neoplasms / therapy. Prolactinoma / therapy

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  • (PMID = 17033781.001).
  • [ISSN] 0020-9554
  • [Journal-full-title] Der Internist
  • [ISO-abbreviation] Internist (Berl)
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Dopamine Antagonists; 0 / Receptors, Somatotropin; 51110-01-1 / Somatostatin
  • [Number-of-references] 42
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46. Naliato EC, Farias ML, Violante AH: [Prolactinomas and bone mineral density in men]. Arq Bras Endocrinol Metabol; 2005 Apr;49(2):183-95
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Prolactinomas and bone mineral density in men].
  • [Transliterated title] Prolactinomas e densidade mineral óssea em homens.
  • In this paper, we analyze aspects related to bone loss in men with hyperprolactinemia due to prolactinomas: prevalence, clinical relevance, physiopathology, diagnosis and the consequences of the treatment of hyperprolactinemia and hypogonadism on bone mineral density.
  • [MeSH-major] Bone Density. Hyperprolactinemia / complications. Osteoporosis / etiology. Pituitary Neoplasms / complications. Prolactinoma / complications

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  • (PMID = 16184246.001).
  • [ISSN] 0004-2730
  • [Journal-full-title] Arquivos brasileiros de endocrinologia e metabologia
  • [ISO-abbreviation] Arq Bras Endocrinol Metabol
  • [Language] por
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Brazil
  • [Number-of-references] 83
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47. Kars M, Dekkers OM, Pereira AM, Romijn JA: Update in prolactinomas. Neth J Med; 2010 Mar;68(3):104-12
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  • [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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48. Kararizou E, Stamboulis E, Markou I, Alevizaki M, Gkiatas K: Amyotrophic lateral sclerosis and prolactinoma. Funct Neurol; 2007 Jan-Apr;22(1):39-41
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  • [Title] Amyotrophic lateral sclerosis and prolactinoma.
  • Investigations revealed the co-existence of a pituitary adenoma of the prolactinoma type.
  • The possible relation between endocrinological disturbances and this neurological disease is discussed.
  • [MeSH-major] Amyotrophic Lateral Sclerosis / complications. Pituitary Neoplasms / complications. Prolactinoma / complications

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  • (PMID = 17509242.001).
  • [ISSN] 0393-5264
  • [Journal-full-title] Functional neurology
  • [ISO-abbreviation] Funct. Neurol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Hormone Antagonists; 3A64E3G5ZO / Bromocriptine
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49. Dinc C, Bikmaz K, Iplikcioglu AC, Kosdere S, Latifaci I: Cystic giant prolactinoma in childhood. J Clin Neurosci; 2008 Jan;15(1):76-9
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  • [Title] Cystic giant prolactinoma in childhood.
  • In childhood and adolescence, pituitary adenomas are rare and half are prolactinomas.
  • However, cystic giant prolactinoma in prepuberty is extremely rare.
  • In this report, we present a 10-year-old boy with a cystic giant prolactinoma who was treated with two-stage surgery as the tumor was dumbbell shaped.
  • To our knowledge, this is the second reported case of a cystic giant prolactinoma in a prepubertal child.
  • [MeSH-major] Cysts. Pituitary Neoplasms. Prolactinoma
  • [MeSH-minor] Child. Humans. Magnetic Resonance Imaging. Male. Prolactin / secretion. Tomography, X-Ray Computed

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  • (PMID = 18042387.001).
  • [ISSN] 0967-5868
  • [Journal-full-title] Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
  • [ISO-abbreviation] J Clin Neurosci
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Scotland
  • [Chemical-registry-number] 9002-62-4 / Prolactin
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50. 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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51. Colao A, Galderisi M, Di Sarno A, Pardo M, Gaccione M, D'Andrea M, Guerra E, Pivonello R, Lerro G, Lombardi G: Increased prevalence of tricuspid regurgitation in patients with prolactinomas chronically treated with cabergoline. J Clin Endocrinol Metab; 2008 Oct;93(10):3777-84
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  • [Title] Increased prevalence of tricuspid regurgitation in patients with prolactinomas chronically treated with cabergoline.
  • BACKGROUND: Cabergoline, a dopamine receptor-2 agonist used to treat prolactinomas, was associated with increased risk of cardiac valve disease in Parkinson's disease.
  • OBJECTIVE: Our objective was to evaluate prevalence of cardiac valve regurgitation in cabergoline-treated patients with prolactinomas.
  • PATIENTS: Fifty treated patients (44 women and six men) and 50 sex- and age-matched control subjects participated; 20 de novo patients were also studied.
  • RESULTS: In de novo patients, treated patients, and controls, the prevalence of mild regurgitation of mitral (35, 22, and 12%, P = 0.085), aortic (0, 4, and 2%, P = 0.59), tricuspid (55, 30, and 42%, P = 0.13) or pulmonic (20, 12, and 6%, P = 0.22) valves was similar.
  • Conversely, the prevalence of moderate tricuspid regurgitation was higher in the treated patients (54%) than in de novo patients (0%) and controls (18%, P < 0.0001).
  • CONCLUSION: Moderate tricuspid regurgitation is more frequent in patients taking cabergoline (at higher cumulative doses) than in de novo patients and control subjects, but the clinical significance of this finding has not been established.
  • [MeSH-major] Ergolines / administration & dosage. Ergolines / adverse effects. Pituitary Neoplasms / drug therapy. Prolactinoma / drug therapy. Tricuspid Valve Insufficiency / chemically induced. Tricuspid Valve Insufficiency / epidemiology
  • [MeSH-minor] Adult. Antineoplastic Agents / administration & dosage. Antineoplastic Agents / adverse effects. Case-Control Studies. Chronic Disease. Dose-Response Relationship, Drug. Female. Humans. Male. Middle Aged. Prevalence. Time Factors

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  • (PMID = 18682513.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00460616
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Ergolines; LL60K9J05T / cabergoline
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52. 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


53. 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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54. Santos Andrade EH, Pan PM, da Silva PF, Gadelha A: New insights in the management of antipsychotics in the treatment of schizophrenia in a patient with prolactinoma: a case report and review of the literature. Case Rep Med; 2010;2010:573252

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] New insights in the management of antipsychotics in the treatment of schizophrenia in a patient with prolactinoma: a case report and review of the literature.
  • Prolactinomas are the commonest pituitary adenomas and the major pathological cause of hyperprolactinaemia.
  • Symptomatic prolactinomas are treated mainly by dopamine agonists; surgery and radiotherapy are options for nonresponders.
  • We report a case of a 39-year-old schizophrenic male patient that was diagnosed with a macroprolactinoma 8 years after his first psychotic episode.
  • The association of Schizophrenia and prolactinoma represents a clinical challenge once the treatment of one disease can exacerbate the symptoms of the other.

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  • (PMID = 21076684.001).
  • [ISSN] 1687-9635
  • [Journal-full-title] Case reports in medicine
  • [ISO-abbreviation] Case Rep Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2977938
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55. Fideleff HL, Boquete HR, Suárez MG, Azaretzky M: Prolactinoma in children and adolescents. Horm Res; 2009;72(4):197-205
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prolactinoma in children and adolescents.
  • The evolution of prolactinomas in children and adolescents continues to be controversial.
  • The larger prevalence of macroadenomas in males is consistent with findings in adults and would not be related to a later diagnosis.
  • In patients with asymptomatic hyperprolactinemia, the presence of altered proportions of PRL isoforms should be evaluated.
  • The diagnosis of prolactinoma requires both radiographic evidence of pituitary adenoma and laboratory analysis documenting the presence of sustained hyperprolactinemia.
  • [MeSH-major] Pituitary Neoplasms. Prolactinoma

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  • (PMID = 19786791.001).
  • [ISSN] 1423-0046
  • [Journal-full-title] Hormone research
  • [ISO-abbreviation] Horm. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Number-of-references] 40
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56. Semple P, Fieggen G, Parkes J, Levitt N: Giant prolactinomas in adolescence: an uncommon cause of blindness. Childs Nerv Syst; 2007 Feb;23(2):213-7
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  • [Title] Giant prolactinomas in adolescence: an uncommon cause of blindness.
  • INTRODUCTION: Prolactinomas in childhood and adolescence are rare.
  • However, in male patients in particular they may become extremely large and invasive, resulting in visual impairment without necessarily producing endocrine symptoms.
  • Prolactin levels in both patients were markedly elevated, and a diagnosis of prolactinoma was made.
  • Bromocriptine treatment was started resulting in lowered prolactin levels, improved vision and tumour shrinkage on imaging.
  • CONCLUSION: A male child or adolescent presenting with diminished vision and found to have suprasellar or anterior skull base tumour should have their prolactin levels checked to rule out a prolactinoma, which can be successfully managed with medical therapy.
  • [MeSH-major] Blindness / etiology. Pituitary Neoplasms / complications. Prolactinoma / complications

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  • (PMID = 16983572.001).
  • [ISSN] 0256-7040
  • [Journal-full-title] Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery
  • [ISO-abbreviation] Childs Nerv Syst
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
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57. Goodin GS, McCarville MB, Thibodeau SN, Skapek SX, Khoury JD, Spunt SL: Prolactinoma as the first manifestation of Gardner's syndrome. Pediatr Blood Cancer; 2008 Feb;50(2):409-12
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prolactinoma as the first manifestation of Gardner's syndrome.
  • Familial adenomatous polyposis (FAP) is an inherited condition causing numerous adenomatous colorectal polyps and a markedly elevated risk of colon cancer.
  • We describe a pediatric patient who initially presented with prolactinoma and later was found to have Gardner's syndrome.
  • Our case illustrates the association between prolactinoma and FAP, which may represent a rare subtype of Gardner's and BTP syndromes.
  • [MeSH-major] Gardner Syndrome / genetics. Prolactinoma / genetics

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 16862550.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 23099; United States / NCI NIH HHS / CA / P30 CA 21765
  • [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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58. Camihort GA, Hereñú CB, Luna GC, Rodríguez SS, Bracamonte MI, Goya RG, Cónsole GM: Morphological changes induced by insulin-like growth factor-I gene therapy in pituitary cell populations in experimental prolactinomas. Cells Tissues Organs; 2010;191(4):316-25

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

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  • [Cites] Lab Invest. 1992 May;66(5):639-45 [1573857.001]
  • [Cites] Endocrinology. 1992 Feb;130(2):882-94 [1310281.001]
  • [Cites] Endocrinology. 1993 Jan;132(1):23-9 [7678216.001]
  • [Cites] J Clin Endocrinol Metab. 1993 Oct;77(4):1059-66 [7691862.001]
  • [Cites] Oncogene. 1994 Apr;9(4):1021-7 [8134105.001]
  • [Cites] Peptides. 1994;15(3):547-82 [7937331.001]
  • [Cites] Endocr Rev. 1997 Apr;18(2):206-28 [9101137.001]
  • [Cites] Eur J Endocrinol. 1998 Mar;138(3):309-15 [9539306.001]
  • [Cites] Physiol Res. 1998;47(2):125-31 [9706996.001]
  • [Cites] Ann Intern Med. 1998 Sep 15;129(6):472-83 [9735086.001]
  • [Cites] Endocrinology. 1999 Mar;140(3):1183-91 [10067842.001]
  • [Cites] Endocrinology. 1999 Sep;140(9):3881-9 [10465256.001]
  • [Cites] Exp Biol Med (Maywood). 2005 Dec;230(11):800-7 [16339744.001]
  • [Cites] Gene Ther. 2007 Feb;14(3):237-45 [16988717.001]
  • [Cites] Eur J Neurosci. 2007 Jan;25(1):191-200 [17241280.001]
  • [Cites] Endocrinology. 2007 Jul;148(7):3131-9 [17412817.001]
  • [Cites] Mol Cancer. 2008;7:13 [18218140.001]
  • [Cites] Curr Med Chem. 2008;15(29):3095-112 [19075656.001]
  • [Cites] Cells Tissues Organs. 2009;190(1):20-6 [18957836.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Mar;85(3):1296-305 [10720079.001]
  • [Cites] Biol Reprod. 2000 Sep;63(3):865-71 [10952933.001]
  • [Cites] Cells Tissues Organs. 2001;169(1):64-72 [11340263.001]
  • [Cites] Eur J Endocrinol. 2001 Oct;145(4):497-503 [11581010.001]
  • [Cites] Endocr Rev. 2001 Oct;22(5):631-56 [11588145.001]
  • [Cites] Neuropsychopharmacology. 2001 Dec;25(6):881-91 [11750181.001]
  • [Cites] Steroids. 2002 Jun;67(7):573-9 [11996929.001]
  • [Cites] Neuroendocrinology. 2002 May;75(5):316-25 [12006785.001]
  • [Cites] Endocrinology. 2002 Jul;143(7):2750-8 [12072410.001]
  • [Cites] Reprod Biol. 2003 Mar;3(1):7-28 [14666141.001]
  • [Cites] Am J Physiol. 1977 Sep;233(3):E235-9 [410310.001]
  • [Cites] Science. 1982 Nov 12;218(4573):684-6 [7134966.001]
  • [Cites] JAMA. 1983 Apr 22-29;249(16):2204-7 [6834618.001]
  • [Cites] Am J Pathol. 1983 Nov;113(2):198-206 [6638150.001]
  • [Cites] Proc Natl Acad Sci U S A. 1984 Feb;81(3):935-9 [6583688.001]
  • [Cites] Endocr Rev. 1989 Feb;10(1):68-91 [2666112.001]
  • [Cites] Endocrinology. 1992 Dec;131(6):2588-94 [1280202.001]
  • (PMID = 19923782.001).
  • [ISSN] 1422-6421
  • [Journal-full-title] Cells, tissues, organs
  • [ISO-abbreviation] Cells Tissues Organs (Print)
  • [Language] eng
  • [Grant] United States / NIA NIH HHS / AG / R01 AG029798
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 67763-96-6 / Insulin-Like Growth Factor I
  • [Other-IDs] NLM/ PMC3696382
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59. Hnasko TS, Hnasko RM, Sotak BN, Kapur RP, Palmiter RD: Genetic disruption of dopamine production results in pituitary adenomas and severe prolactinemia. Neuroendocrinology; 2007;86(1):48-57
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  • [Title] Genetic disruption of dopamine production results in pituitary adenomas and severe prolactinemia.
  • BACKGROUND: Dopamine release from tuberoinfundibular dopamine neurons into the median eminence activates dopamine-D2 receptors in the pituitary gland where it inhibits lactotroph function.
  • Because these animals require daily treatment with 3,4-L-dihydroxyphenylalanine (L-dopa) to survive, it has not been possible to examine the consequences of chronic loss of dopamine on pituitary physiology.
  • RESULTS: We find that mice chronically lacking tuberoinfundibular dopamine secrete large amounts of prolactin due to the development of severely enlarged pituitaries composed principally of hyperplastic hypertrophic lactotrophs and multifocal prolactinomas.
  • CONCLUSION: Our observations are consistent with the hypothesis that hypothalamic dopamine is a critical inhibitor of lactotroph proliferation and suggest additional roles for dopamine in the regulation of pituitary function.
  • [MeSH-major] Adenoma / genetics. Dopamine / deficiency. Dopamine / genetics. Pituitary Neoplasms / genetics. Prolactin / blood

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  • [Copyright] (c) 2007 S. Karger AG, Basel.
  • (PMID = 17622754.001).
  • [ISSN] 1423-0194
  • [Journal-full-title] Neuroendocrinology
  • [ISO-abbreviation] Neuroendocrinology
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / T32 GM07270
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 9002-62-4 / Prolactin; VTD58H1Z2X / Dopamine
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60. 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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61. Jan M, Dufour H, Brue T, Jaquet P: Prolactinoma surgery. Ann Endocrinol (Paris); 2007 Jun;68(2-3):118-9
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  • [Title] Prolactinoma surgery.
  • Surgery is generally used as second-line treatment in prolactinomas.
  • In highly trained hands, selective adenomectomy results in normalization of prolactin levels in 75-90% of cases with little morbidity and no mortality.
  • A transsphenoidal or, less frequently, a transfrontal surgical approach is necessary in patients resistant to or intolerant of medical treatment, and also in rare cases such as pituitary apoplexy or cerebrospinal fluid rhinorrhea.
  • [MeSH-major] Pituitary Neoplasms / surgery. Prolactinoma / surgery
  • [MeSH-minor] Dopamine Agonists / therapeutic use. Drug Resistance. Humans. Hyperprolactinemia / drug therapy. Hyperprolactinemia / etiology. Pituitary Apoplexy / etiology. Skull Base Neoplasms / pathology

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  • (PMID = 17512893.001).
  • [ISSN] 0003-4266
  • [Journal-full-title] Annales d'endocrinologie
  • [ISO-abbreviation] Ann. Endocrinol. (Paris)
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Dopamine Agonists
  • [Number-of-references] 12
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62. 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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63. Mukdsi JH, De Paul AL, Gutiérrez S, Roth FD, Aoki A, Torres AI: Subcellular localisation of VEGF in different pituitary cells. Changes of its expression in oestrogen induced prolactinomas. J Mol Histol; 2005 Oct;36(8-9):447-54
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Subcellular localisation of VEGF in different pituitary cells. Changes of its expression in oestrogen induced prolactinomas.
  • Vascular endothelial growth factor (VEGF) is an important angiogenic factor in the pituitary gland.
  • The objective of this study was to unveil the VEGF subcellular localisation in different pituitary cell types and to evaluate changes in its expression at different time intervals after oestrogen stimulation.
  • Oestrogen treatment increased the number of VEGF immunopositive cells and its expression detected differentially by western blot in both nucleus and cytoplasm of pituitary cells when compared to the control.
  • In lactotrophs, the predominant cell of the tumour, VEGF was immunodetected in RER, Golgi complex, and vesicular organelles, supporting further the association with an auto-paracrine effect exerted by VEGF.
  • The presence of VEGF in the nucleus may probably be associated with a translocation to this cell compartment.
  • In the course of prolactinoma development, the oestrogen stimulated VEGF expression in tumoural cells, promoting a vascular adaptation which contributes to growth and progression of the tumour.
  • [MeSH-major] Estrogens / pharmacology. Lactotrophs / metabolism. Pituitary Neoplasms / metabolism. Prolactinoma / metabolism. Vascular Endothelial Growth Factor A / metabolism
  • [MeSH-minor] Animals. Blotting, Western. Cell Extracts. Cell Nucleus / drug effects. Cytoplasm / metabolism. Immunohistochemistry. Male. Protein Transport / drug effects. Rats. Rats, Wistar. Subcellular Fractions / drug effects. Subcellular Fractions / metabolism

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  • (PMID = 16733790.001).
  • [ISSN] 1567-2379
  • [Journal-full-title] Journal of molecular histology
  • [ISO-abbreviation] J. Mol. Histol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cell Extracts; 0 / Estrogens; 0 / Vascular Endothelial Growth Factor A
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64. Gillam MP, Molitch ME, Lombardi G, Colao A: Advances in the treatment of prolactinomas. Endocr Rev; 2006 Aug;27(5):485-534
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  • [Title] Advances in the treatment of prolactinomas.
  • Prolactinomas account for approximately 40% of all pituitary adenomas and are an important cause of hypogonadism and infertility.
  • The ultimate goal of therapy for prolactinomas is restoration or achievement of eugonadism through the normalization of hyperprolactinemia and control of tumor mass.
  • Complicated situations, such as those encountered in resistance to dopamine agonists, pregnancy, and giant or malignant prolactinomas, may require multimodal therapy involving surgery, radiotherapy, or both.
  • Progress in elucidating the mechanisms underlying the pathogenesis of prolactinomas may enable future development of novel molecular therapies for treatment-resistant cases.
  • This review provides a critical analysis of the efficacy and safety of the various modes of therapy available for the treatment of patients with prolactinomas with an emphasis on challenging situations, a discussion of the data regarding withdrawal of medical therapy, and a foreshadowing of novel approaches to therapy that may become available in the future.
  • [MeSH-major] Pituitary Neoplasms / therapy. Prolactinoma / therapy

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  • (PMID = 16705142.001).
  • [ISSN] 0163-769X
  • [Journal-full-title] Endocrine reviews
  • [ISO-abbreviation] Endocr. Rev.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / K08 DK066044
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contraceptives, Oral, Hormonal; 0 / Dopamine Agonists
  • [Number-of-references] 626
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65. Pouratian N, Sheehan J, Jagannathan J, Laws ER Jr, Steiner L, Vance ML: Gamma knife radiosurgery for medically and surgically refractory prolactinomas. Neurosurgery; 2006 Aug;59(2):255-66; discussion 255-66
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  • [Title] Gamma knife radiosurgery for medically and surgically refractory prolactinomas.
  • OBJECTIVE: Experience with gamma knife radiosurgery (GKRS) for prolactinomas is limited because of the efficacy of medical and surgical intervention.
  • We characterize the efficacy of GKRS for medically and surgically refractory prolactinomas.
  • METHODS: We reviewed our series of patients with prolactinomas who were treated with GKRS after failing medical and surgical intervention who had at least 1 year of follow-up.
  • Twenty-six percent of patients achieved a normal serum prolactin (remission) with an average time of 24.5 months.
  • Remission was significantly associated with being off of a dopamine agonist at the time of GKRS and a tumor volume less than 3.0 cm3 (P < 0.05 for both).
  • Complications included new pituitary hormone deficiencies in 28% of patients and cranial nerve palsy in two patients (7%).
  • However, because the GKRS treated tumors were refractory to other therapies and because complication rates were low, GKRS should be part of the armamentarium for treating refractory prolactinomas.
  • [MeSH-major] Pituitary Gland / pathology. Pituitary Gland / surgery. Pituitary Neoplasms / surgery. Prolactinoma / surgery. Radiosurgery / standards. Radiosurgery / statistics & numerical data
  • [MeSH-minor] Adolescent. Adult. Aged. Dopamine Agonists / therapeutic use. Female. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Neurosurgical Procedures / statistics & numerical data. Patient Selection. Postoperative Complications / etiology. Postoperative Complications / physiopathology. Prolactin / blood. Prolactin / secretion. Radiation Dosage. Remission Induction / methods. Retrospective Studies. Treatment Failure. Treatment Outcome

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  • (PMID = 16883166.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dopamine Agonists; 9002-62-4 / Prolactin
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66. Wu ZB, Su ZP, Wu JS, Zheng WM, Zhuge QC, Zhong M: Five years follow-up of invasive prolactinomas with special reference to the control of cavernous sinus invasion. Pituitary; 2008;11(1):63-70
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  • [Title] Five years follow-up of invasive prolactinomas with special reference to the control of cavernous sinus invasion.
  • BACKGROUND: Few data are presently available on the effective control of cavernous sinus (CS) invasion of invasive prolactinomas.
  • The aim of this retrospective study, through a mean period of 5 years follow up, is to observe the tumor shrinkage of CS invasive prolactinomas, as well as PRL normalization with bromocriptine therapy.
  • METHODS: 68 patients met the criteria of invasive prolactinomas (Grade III or IV in the classification scheme of Knosp and colleagues; serum PRL level greater than 200 ng/ml).
  • The other 35 patients received microsurgery as the primary treatment, after which two patients had normal PRL without taking bromocriptine and other 33 patients received bromocriptine treatment after microsurgery.
  • Of those 14 patients, seven still had elevated PRL levels; five had optic chiasmal herniation by different degrees (P < 0.05).
  • There were 49 patients with normal PRL levels (72%); five patients with PRL levels more than 200 ng/ml.
  • After the treatment, 14 patients with tumor volume disappearance on MR images and PRL normalization therefore withdrew from bromocriptine therapy.
  • During a subsequent one-and-a-half-year follow-up, tumor recurrence and PRL increase were not found in those 14 patients.
  • Twenty-seven patients maintained normal PRL levels with low-dose bromocriptine, of which 20 patients had their tumor disappear while seven patients had CS residual tumor.
  • CONCLUSIONS: About three-fourths of prolactinomas with CS invasion can be effectively controlled not only with regard to tumor volume disappearance but also in serum PRL normalization.
  • Residual tumor in the CS areas with PRL normalization and no pressure symptoms can be treated with low-dose of bromocriptine so as to achieve long-term tumor volume control and endocrine control.
  • [MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Bromocriptine / therapeutic use. Cavernous Sinus / drug effects. Dopamine Agonists / therapeutic use. Pituitary Neoplasms / drug therapy. Prolactinoma / drug therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Chemotherapy, Adjuvant. Empty Sella Syndrome / pathology. Female. Follow-Up Studies. Hernia / drug therapy. Hernia / pathology. Humans. Magnetic Resonance Imaging. Male. Microsurgery. Middle Aged. Neoplasm Invasiveness. Neoplasm Staging. Optic Chiasm / drug effects. Optic Chiasm / pathology. Prolactin / blood. Prolactin / secretion. Radiotherapy, Adjuvant. Retrospective Studies. Time Factors. Treatment Outcome. Young Adult

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  • (PMID = 17917811.001).
  • [ISSN] 1573-7403
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Dopamine Agonists; 3A64E3G5ZO / Bromocriptine; 9002-62-4 / Prolactin
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67. Altenberger T, Bilban M, Auer M, Knosp E, Wolfsberger S, Gartner W, Mineva I, Zielinski C, Wagner L, Luger A: Identification of DLK1 variants in pituitary- and neuroendocrine tumors. Biochem Biophys Res Commun; 2006 Feb 17;340(3):995-1005
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  • [Title] Identification of DLK1 variants in pituitary- and neuroendocrine tumors.
  • In a gene chip analysis of common pituitary tumor types, one of the genes with the most impressive tissue-specific expression regulation was delta-like 1 (DLK1), which was strongly expressed in GH-secreting (GH-S) pituitary tumors.
  • In addition to pituitary adenomas, various endocrine tumors were subjected to real-time-quantitative PCR revealing high expression of DLK1 in normal pituitary tissue, in GH-S-, in one prolactin-secreting pituitary adenoma and in pheochromocytomas.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Membrane Proteins / biosynthesis. Membrane Proteins / chemistry. Neuroendocrine Tumors / metabolism. Pituitary Neoplasms / metabolism. Repressor Proteins / biosynthesis. Repressor Proteins / chemistry

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  • (PMID = 16403460.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Codon, Terminator; 0 / DLK1 protein, human; 0 / DNA, Complementary; 0 / Intercellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / RNA, Messenger; 0 / Recombinant Proteins; 0 / Repressor Proteins; 9007-49-2 / DNA
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68. 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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  • [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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69. von Puttkamer J, Karges B, Wudy S, Wabitsch M: McCune-Albright syndrome with male premature pubarche of unusual origin. Horm Res; 2008;69(5):312-6
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  • Apart from fibrous dysplasia of the forehead and a growth hormone- and prolactin-producing pituitary adenoma, the boy presented with premature pubarche at the age of 6 years and 11 months.
  • This increased production might be due to an activating mutation of a hormone receptor in the zona reticularis of his adrenal glands leading to an increase in sulfotransferase activity and excessive DHEAS production.
  • [MeSH-major] Fibrous Dysplasia, Polyostotic / complications. Fibrous Dysplasia, Polyostotic / diagnosis. Puberty, Precocious / etiology
  • [MeSH-minor] Adenoma / complications. Adolescent. Follow-Up Studies. Humans. Male. Pituitary Neoplasms / complications

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  • [Copyright] (c) 2007 S. Karger AG, Basel
  • (PMID = 18259112.001).
  • [ISSN] 1423-0046
  • [Journal-full-title] Hormone research
  • [ISO-abbreviation] Horm. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
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70. Magri F, Villa C, Locatelli D, Scagnelli P, Lagonigro MS, Morbini P, Castellano M, Gabellieri E, Rotondi M, Solcia E, Daly AF, Chiovato L: Prevalence of double pituitary adenomas in a surgical series: Clinical, histological and genetic features. J Endocrinol Invest; 2010 May;33(5):325-31
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  • [Title] Prevalence of double pituitary adenomas in a surgical series: Clinical, histological and genetic features.
  • BACKGROUND: The term double pituitary adenomas (DPA) is usually referred to those rare lesions showing two distinct cellular components.
  • Genetic background may sustain the proliferation of more than one cell at the same time but no information is available on the presence of aip mutations in these patients.
  • The contribution of pituitary transcription factor immunostains in DPA was also evaluated.
  • RESULTS: One-hundred-seventeen patients out of 144 had a pituitary adenoma.
  • DPA was found in 3 (2.6%) out of 117 patients with pituitary adenoma.
  • The coexistence of somatotroph-lactotroph and silent mammosomatotroph histotype in 1 case and the coexistence of sparsely granulated lactotroph and null cell adenomas in the remaining two cases were first identified.
  • [MeSH-major] Adenoma / epidemiology. Pituitary Neoplasms / epidemiology
  • [MeSH-minor] Adult. Carrier Proteins / biosynthesis. Carrier Proteins / genetics. DNA Mutational Analysis. DNA, Neoplasm / genetics. Humans. Immunohistochemistry. Lactotrophs / pathology. Magnetic Resonance Imaging. Male. Middle Aged. Prolactinoma / genetics. Prolactinoma / pathology. Prolactinoma / surgery. Proto-Oncogene Proteins / genetics. Reverse Transcriptase Polymerase Chain Reaction. Transcription Factors / genetics. Treatment Outcome

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  • (PMID = 19955848.001).
  • [ISSN] 1720-8386
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / DNA, Neoplasm; 0 / MAGI2 protein, human; 0 / MEN1 protein, human; 0 / Proto-Oncogene Proteins; 0 / Transcription Factors
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71. Yavasoglu I, Kucuk M, Coskun A, Guney E, Kadikoylu G, Bolaman Z: Polycystic ovary syndrome and prolactinoma association. Intern Med; 2009;48(8):611-3
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  • [Title] Polycystic ovary syndrome and prolactinoma association.
  • Hyperprolactinemia is the most common pituitary hormone hypersecretion syndrome in both men and women.
  • Here, we present a patient with irregular menses, obesity, hirsutism and infertility, and hyperprolactinemia who was diagnosed as PCOS and prolactinoma and admitted to our clinic.
  • Prolactinoma and PCOS association is a rare condition.
  • Her laboratory results were as follows: prolactin was 74 ng/mL (normal range:1.8-20.3 ng/mL).
  • Pituitary MRI showed 6x8 mm microadenoma at left half.
  • After six months of bromocriptine treatment her prolactin level was normal and no adenoma was detected in pituitary MRI.
  • PCOS and prolactinoma association should be taken into account in PCOS cases with mild hyperprolactinoma.
  • [MeSH-major] Bromocriptine / therapeutic use. Pituitary Neoplasms / complications. Polycystic Ovary Syndrome / complications. Prolactinoma / complications

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  • (PMID = 19367058.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Hormone Antagonists; 3A64E3G5ZO / Bromocriptine
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72. Erem C, Kocak M, Nuhoglu I, Yılmaz M, Ucuncu O: Blood coagulation, fibrinolysis and lipid profile in patients with prolactinoma. Clin Endocrinol (Oxf); 2010 Oct;73(4):502-7
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  • [Title] Blood coagulation, fibrinolysis and lipid profile in patients with prolactinoma.
  • OBJECTIVE: Although the strong association between hyperprolactinaemia and platelet aggregation is well recognized, there are no studies on changes in coagulation and fibrinolytic status in patients with prolactinoma.
  • Therefore, the main purpose of this study was to evaluate the markers of endogenous coagulation/fibrinolysis, including TFPI and TAFI, and to investigate the relationships between prolactin (PRL) and these haemostatic parameters and serum lipid profile in patients with prolactinoma.
  • RESEARCH METHODS AND PROCEDURES: Twenty-two patients with untreated, newly diagnosed prolactinoma and 20 age-matched healthy controls were included in the study.
  • The relationships between serum PRL and these haemostatic parameters were evaluated.
  • RESULTS: Compared with the control subjects, total cholesterol, low density lipoprotein cholesterol, apolipoprotein B, platelet count, fibrinogen, AT-III, PAI-1 and PAI-1/t-PA ratio were significantly increased in patients with prolactinoma (P < 0.0001, P < 0.001, P < 0.05, P < 0.05, P < 0.0001, P < 0.05, P < 0.0001 and P < 0.0001, respectively), whereas TFPI levels were significantly decreased (P < 0.01).
  • Plasma TAFI Ag levels were not significantly different in patients with prolactinoma compared with the controls.
  • In patients with prolactinoma, serum PRL was positively correlated with plasma FVII levels and apo B (r: 0.679, P < 0.05; r: 0.548, P < 0.05, respectively).
  • CONCLUSION: We found some important differences in the haemostatic parameters between the patients with prolactinoma and healthy controls.
  • Increased platelet count, fibrinogen, PAI-1 and decreased TFPI in patients with prolactinoma may represent a potential hypercoagulable and hypofibrinolytic state, which might augment the risk for atherosclerotic and atherothrombotic complications.
  • Thus, disturbances of the haemostatic system and dyslipidaemia may lead to the excess mortality in patients with prolactinoma.
  • [MeSH-major] Blood Coagulation. Fibrinolysis. Lipids / blood. Prolactinoma / blood

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  • [Copyright] © 2010 Blackwell Publishing Ltd.
  • (PMID = 20039901.001).
  • [ISSN] 1365-2265
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Lipids; 0 / Lipoproteins; 0 / Plasminogen Activator Inhibitor 1; 0 / lipoprotein-associated coagulation inhibitor; EC 3.4.17.20 / Carboxypeptidase B2
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73. Krysiak R, Okopień B, Marek B, Szkróbka W: [Prolactinoma]. Przegl Lek; 2009;66(4):198-205
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  • [Title] [Prolactinoma].
  • [Transliterated title] Gruczolak przysadki wydzielajacy prolaktyne.
  • Prolactin-secreting tumours (prolactinomas) are benign neoplasms constituting about 40 percent of all pituitary tumours.
  • The clinical symptoms of prolactinomas are menstrual dysfunction and galactorrhea in women and loss of libido and potency in men.
  • Differential diagnosis of the disease should include the intake of various drugs, hypothyroidism, renal failure, liver cirrhosis, compression of the pituitary stalk by other pathologies, idiopathic hyperprolactinemia and other types of pituitary adenomas.
  • The authors review the diagnosis and management of prolactinomas, including progress made in recent years.
  • [MeSH-major] Pituitary Neoplasms / diagnosis. Pituitary Neoplasms / therapy. Prolactinoma / diagnosis. Prolactinoma / therapy
  • [MeSH-minor] Adult. Age Distribution. Causality. Dopamine Agonists / therapeutic use. Female. Humans. Iatrogenic Disease / epidemiology. Male. Pregnancy. Pregnancy Complications, Neoplastic / diagnosis. Pregnancy Complications, Neoplastic / epidemiology. Pregnancy Complications, Neoplastic / therapy. Prevalence. Sex Distribution. Young Adult

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  • (PMID = 19708510.001).
  • [ISSN] 0033-2240
  • [Journal-full-title] Przegla̧d lekarski
  • [ISO-abbreviation] Prz. Lek.
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Dopamine Agonists
  • [Number-of-references] 53
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74. Agha A, Carpenter R, Bhattacharya S, Edmonson SJ, Carlsen E, Monson JP: Parathyroid carcinoma in multiple endocrine neoplasia type 1 (MEN1) syndrome: two case reports of an unrecognised entity. J Endocrinol Invest; 2007 Feb;30(2):145-9
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  • Remarkably, she also reported primary amenorrhea and was found to have an invasive pituitary lactotroph adenoma, which was treated with cabergoline and external beam radiotherapy.
  • Magnetic resonance imaging (MRI) of the pancreas revealed a small lesion characteristic of an islet-cell tumor, which was clinically and biochemically non-functioning.
  • Pituitary MRI was normal.
  • [MeSH-major] Carcinoma / diagnosis. Multiple Endocrine Neoplasia Type 1 / diagnosis. Parathyroid Neoplasms / diagnosis
  • [MeSH-minor] Adult. Aged. Diagnosis, Differential. Female. Humans. Male. Syndrome


75. Chattopadhyay A, Bhansali A, Masoodi SR: Long-term efficacy of bromocriptine in macroprolactinomas and giant prolactinomas in men. Pituitary; 2005;8(2):147-54
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  • [Title] Long-term efficacy of bromocriptine in macroprolactinomas and giant prolactinomas in men.
  • We prospectively analyzed presentations and long-term therapeutic responses to bromocriptine (BRC) in 29 newly diagnosed men with macroprolactinomas including 14 patients with 'giant prolactinoma'.
  • Clinical symptoms, prolactin (PRL) levels and tumor size on MRI were measured before BRC and sequentially thereafter.
  • Pretreatment PRL ranged between 124 and 29200 ng/mL (1698 +/- 857.1) and tumor volume was between 2.81 and 132 cm(3) (21.1 +/- 24.3).
  • Baseline PRL levels did not correlated with tumor volume (r = 0.45, P > 0.05).
  • Significant decrease (P = 0.0003) in PRL, at least 96% of the pretreatment value from 1698 +/- 857.1 ng/mL to 42.4 +/- 30.6 ng/mL occurred in 26 patients.
  • Persistent normalization of PRL levels (< 16 ng/mL) for at least 6 months was achieved in 12 patients (40.8%).
  • Trans-sphenoidal / trans-frontal pituitary surgery was performed in 9 patients (31%) for various reasons: pituitary apoplexy in 1, CSF rhinorrhea in 2, increasing prolactin in spite of BRC therapy in 3, and intolerant /resistant to BRC in 3 patients.
  • These data suggest that, in male macro- and giant prolactinomas, dopamine agonists represent the first-line therapy effective in reducing PRL, restoration of libido and potency, improvement of VFD and determining tumor shrinkage.
  • [MeSH-major] Bromocriptine / therapeutic use. Pituitary Neoplasms / drug therapy. Prolactinoma / drug therapy
  • [MeSH-minor] Adolescent. Adult. Dopamine Agonists / therapeutic use. Humans. Male. Middle Aged. Pituitary Function Tests. Prolactin / blood. Prospective Studies. Visual Fields / drug effects

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  • (PMID = 16379032.001).
  • [ISSN] 1386-341X
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dopamine Agonists; 3A64E3G5ZO / Bromocriptine; 9002-62-4 / Prolactin
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76. Huang C, Ezzat S, Asa SL, Hamilton J: Dopaminergic resistant prolactinomas in the peripubertal population. J Pediatr Endocrinol Metab; 2006 Jul;19(7):951-3
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  • [Title] Dopaminergic resistant prolactinomas in the peripubertal population.
  • We report two children with macroadenomas and hyperprolactinemia resistant to medical therapy using dopamine agonists, who experienced secondary pituitary dysfunction.
  • [MeSH-major] Adenoma / drug therapy. Dopamine Agonists / therapeutic use. Drug Resistance. Hyperprolactinemia / drug therapy. Pituitary Neoplasms / drug therapy. Puberty / physiology

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  • (PMID = 16995577.001).
  • [ISSN] 0334-018X
  • [Journal-full-title] Journal of pediatric endocrinology & metabolism : JPEM
  • [ISO-abbreviation] J. Pediatr. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Dopamine Agonists
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77. 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

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  • (PMID = 16404500.001).
  • [ISSN] 0770-3198
  • [Journal-full-title] Clinical rheumatology
  • [ISO-abbreviation] Clin. Rheumatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Belgium
  • [Chemical-registry-number] 9002-62-4 / Prolactin
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78. Guitelman M: Long-term follow-up of prolactinomas: should dopamine agonist treatment be life-long? Front Horm Res; 2006;35:88-101
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  • [Title] Long-term follow-up of prolactinomas: should dopamine agonist treatment be life-long?
  • In our data, 16% of patients with prolactinomas remained normoprolactinemic after DA withdrawal.
  • The length of treatment recommended is 1-3 years, during which DA may be tapered off, and serum PRL levels should be monitored.
  • Tumor disappearance on MRI and the levels of PRL under the lower dose of DA will be determinant for DA withdrawal.
  • Factors influencing prolactinomas outcome are analyzed in the discussion.
  • [MeSH-major] Dopamine Agonists / therapeutic use. Pituitary Neoplasms / drug therapy. Prolactinoma / drug therapy
  • [MeSH-minor] Adenoma / drug therapy. Adenoma / surgery. Adolescent. Adult. Algorithms. Female. Follow-Up Studies. Humans. Long-Term Care. Male. Middle Aged. Neoplasm Recurrence, Local. Prolactin / blood. Retrospective Studies. Time Factors. Withholding Treatment

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  • (PMID = 16809925.001).
  • [ISSN] 0301-3073
  • [Journal-full-title] Frontiers of hormone research
  • [ISO-abbreviation] Front Horm Res
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Dopamine Agonists; 9002-62-4 / Prolactin
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79. López-Arbolay O, Morales-Sabina O, González-González JL, Valdés-Lorenzo N: [Transsphenoidal approach to prolactinomas]. Neurocirugia (Astur); 2006 Jun;17(3):226-31
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  • [Title] [Transsphenoidal approach to prolactinomas].
  • [Transliterated title] Cirugia transeptoesfenoidal en adenomas hipofisarios productores de prolactina.
  • INTRODUCTION: Transeptal transsphenoidal surgery for pituitary tumors is a well established surgical technique.
  • In particular the use of medical treatment in patient with prolactinomas has induced the control of hiperprolactinemia and the shrinkage of the tumor in the great majority of the patients, for that reason the treatment of the prolactinomas is controversial.
  • OBJECTIVE: We evaluate the results of transsphenoidal microsurgical treatment of prolactin secreting adenomas at our Unit.
  • METHODS: We made a retrospective analysis of 63 patients operated on via transsphenoidal microsurgical technique for prolactin secreting adenomas between 1996 and 2003.
  • Prolactin levels were reduced to non tumoral values in 90.6% of microadenomas (29 cases) and in 67.7% of macroadenomas (21 cases).
  • CONCLUSIONS: Transsphenoidal adenomectomy is a safe treatment option for patients with prolactin secreting adenomas with surgical indication.
  • [MeSH-major] Hyperprolactinemia / surgery. Neurosurgical Procedures / methods. Pituitary Neoplasms / surgery. Prolactinoma / surgery. Sphenoid Bone / surgery

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  • (PMID = 16855780.001).
  • [ISSN] 1130-1473
  • [Journal-full-title] Neurocirugía (Asturias, Spain)
  • [ISO-abbreviation] Neurocirugia (Astur)
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Spain
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80. Rosário PW, Purisch S: Biochemical acromegaly in patients with prolactinoma during treatment with dopaminergic agonists. Arq Bras Endocrinol Metabol; 2010 Aug;54(6):546-9
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  • [Title] Biochemical acromegaly in patients with prolactinoma during treatment with dopaminergic agonists.
  • OBJECTIVE: To evaluate the frequency of subclinical acromegaly (in the absence of clinical phenotype but biochemically uncontrolled) in patients with prolactinoma during treatment with dopaminergic agonists.
  • RESULTS: Initially, the laboratory diagnosis of acromegaly was unequivocal (elevated IGF-1 for gender and age with nadir GH > 1 μg/L) in two patients, and likely (elevated IGF-1 with nadir GH > cut-off but < 1 μg/L) in another patient.
  • In two other patients, this diagnosis was possible (normal IGF-1 with nadir GH > 1 μg/L).
  • Repetition of the tests 6 months after withdrawal of the dopaminergic agonist confirmed the diagnosis of subclinical acromegaly (elevated IGF-1 for gender and age with nadir GH > 1 μg/L) in these 5 patients.
  • CONCLUSION: In patients with prolactinomas, acromegaly should be investigated not only in cases with a clinical phenotype.
  • [MeSH-major] Acromegaly / diagnosis. Dopamine Agonists / therapeutic use. Pituitary Neoplasms / drug therapy. Prolactinoma / drug therapy

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  • (PMID = 20857059.001).
  • [ISSN] 1677-9487
  • [Journal-full-title] Arquivos brasileiros de endocrinologia e metabologia
  • [ISO-abbreviation] Arq Bras Endocrinol Metabol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Dopamine Agonists; 12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I
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81. Wu ZB, Li CZ, Zong XY, Su ZP, Zeng YJ, Zhang YZ: Correlation of alternative splicing of the D2 dopamine receptor mRNA and estrogen receptor mRNA in the prolactinomas and gonadotrope tumors. J Neurooncol; 2009 Aug;94(1):135-9
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  • [Title] Correlation of alternative splicing of the D2 dopamine receptor mRNA and estrogen receptor mRNA in the prolactinomas and gonadotrope tumors.
  • OBJECTIVE: Estradiol (E2) acts to modulate the ratio of two dopamine D2 receptor isoforms (D2L/D2S) by the nuclear estrogen receptor (ER) and to reduce dopamine's inhibitory action on PRL secretion.
  • Here we demonstrate the correlation between the expression of ER mRNA and D2R mRNA isoforms in pituitary neoplasms cells.
  • METHODS: Twenty-four human pituitary adenomas (14 prolactinomas and 10 gonadotrope tumors) were examined for the expression of both ER mRNA and D2R mRNA by means of semi-quantitative RT-PCR analysis.
  • RESULTS: No significant difference was found in ERbeta mRNA expression levels between prolactinomas and gonadotrope tumors (P = 0.871), but there was a significant difference in the expression of ERalpha mRNA (P = 0.003).
  • The significant difference was found between the two pituitary adenomas types in both levels of D2S and D2L mRNA expression (P = 0.036 and 0.007 respectively).
  • Furthermore, both levels of expression in prolactinomas were significantly higher than that in gonadotrope tumors.
  • CONCLUSION: This study for the first time shows a good correlation between expression of ER and D2R isoforms in prolactinomas and gonadotrope tumors.
  • Reducing the amount of the ERalpha in neoplasm cells can alter the ratio of D2L/D2S, which may increase the drug sensitivity of pituitary adenomas.
  • [MeSH-major] Alternative Splicing / genetics. Pituitary Neoplasms / genetics. Prolactinoma / genetics. RNA, Messenger / metabolism. Receptors, Dopamine D2 / genetics. Receptors, Estrogen / genetics

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  • (PMID = 19252821.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / Receptors, Dopamine D2; 0 / Receptors, Estrogen
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82. Jezková J, Hána V, Krsek M, Weiss V, Vladyka V, Liscák R, Vymazal J, Pecen L, Marek J: Use of the Leksell gamma knife in the treatment of prolactinoma patients. Clin Endocrinol (Oxf); 2009 May;70(5):732-41
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  • [Title] Use of the Leksell gamma knife in the treatment of prolactinoma patients.
  • OBJECTIVE: Pharmacological treatment with dopaminergic agonists (DA) is the treatment of choice for prolactinomas.
  • We describe our 12-year experience in treating prolactinomas with the Leksell gamma knife (LGK).
  • DESIGN: We followed 35 prolactinoma patients (25.7% microprolactinomas, 74.3% macroprolactinomas) treated with LGK irradiation.
  • Pituitary function was monitored regularly at 6-month intervals.
  • The median time to prolactin normalization after discontinuation of DA was 96 months.
  • After LGK irradiation, the prolactinoma stopped growing or decreased in size in all but one patient (97.1%).
  • The size of the adenoma decreased even in those patients in whom it was not changed by previous DA treatment.
  • [MeSH-major] Pituitary Neoplasms / surgery. Prolactinoma / surgery. Radiosurgery / instrumentation
  • [MeSH-minor] Adolescent. Adult. Aged. Dopamine Agonists / therapeutic use. Female. Follow-Up Studies. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Pregnancy. Prolactin / blood. Treatment Outcome. Young Adult

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  • (PMID = 18710463.001).
  • [ISSN] 1365-2265
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Dopamine Agonists; 9002-62-4 / Prolactin
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83. Gürlek A, Karavitaki N, Ansorge O, Wass JA: What are the markers of aggressiveness in prolactinomas? Changes in cell biology, extracellular matrix components, angiogenesis and genetics. Eur J Endocrinol; 2007 Feb;156(2):143-53
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  • [Title] What are the markers of aggressiveness in prolactinomas? Changes in cell biology, extracellular matrix components, angiogenesis and genetics.
  • Prolactinoma is the most common pituitary tumour in adults.
  • Some may even progress to pituitary carcinoma with craniospinal or systemic metastases.
  • Invasive prolactinomas may be associated with a high Ki-67/MIB-1 labelling index indicating increased cell proliferation, although this is not a universal finding.
  • The AA polymorphism in the cyclin adenine (A)/guanine (G) gene is more frequently detected in invasive prolactinomas.
  • Increased expression of the polysialylated neural cell adhesion molecule (NCAM) and reduced expression of the E-cadherin/catenin complex implies a contribution of altered cell-to-cell adhesion and cellular migration.
  • The induction of fibroblast growth factor and vascular endothelial growth factor via oestrogen-induced overexpression of novel genes (PTTG, hst and Edpm5) enhance cell growth, proliferation and angiogenesis contributing to invasiveness in prolactinomas.
  • Of the described mechanisms, only reduced E-cadherin/catenin expression and overexpression of hst gene seem to be relatively specific markers for prolactinoma invasiveness compared with other pituitary adenomas.
  • Further research is needed to clarify the molecular mechanisms behind the aggressive course of some prolactinomas to predict those with a potentially poor clinical outcome, and to devise treatments that will eventually enable the cure of these challenging tumours.

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  • (PMID = 17287403.001).
  • [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 / Biomarkers, Tumor
  • [Number-of-references] 108
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84. Biller BM, Colao A, Petersenn S, Bonert VS, Boscaro M: Prolactinomas, Cushing's disease and acromegaly: debating the role of medical therapy for secretory pituitary adenomas. BMC Endocr Disord; 2010;10:10

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

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  • [Cites] J Clin Endocrinol Metab. 2005 Jul;90(7):4081-6 [15886256.001]
  • [Cites] Eur J Endocrinol. 2005 Jul;153(1):135-41 [15994755.001]
  • [Cites] Clin Endocrinol (Oxf). 2005 Aug;63(2):168-75 [16060910.001]
  • [Cites] Clin Endocrinol (Oxf). 2005 Aug;63(2):176-84 [16060911.001]
  • [Cites] Eur J Endocrinol. 2005 Sep;153(3):R7-R10 [16131595.001]
  • [Cites] Horm Res. 2005;64(3):140-3 [16192738.001]
  • [Cites] Clin Endocrinol (Oxf). 2005 Nov;63(5):549-59 [16268808.001]
  • [Cites] Eur J Endocrinol. 2005 Dec;153(6):737-40 [16322377.001]
  • [Cites] Horm Metab Res. 2005 Dec;37(12):722-8 [16372224.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Apr;91(4):1239-45 [16403824.001]
  • [Cites] Endocr J. 2005 Dec;52(6):775-9 [16410672.001]
  • [Cites] Clin Endocrinol (Oxf). 2006 Feb;64(2):219-24 [16430724.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Apr;91(4):1397-403 [16449332.001]
  • [Cites] Clin Endocrinol (Oxf). 2006 Mar;64(3):342-51 [16487447.001]
  • [Cites] J Endocrinol Invest. 2005;28(11 Suppl International):21-7 [16625841.001]
  • [Cites] Endocr Rev. 2006 Aug;27(5):485-534 [16705142.001]
  • [Cites] Endocrinology. 2006 Sep;147(9):4438-44 [16740975.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Oct;91(10):3746-53 [16868050.001]
  • [Cites] Clin Endocrinol (Oxf). 2006 Sep;65(3):389-95 [16918962.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Nov;91(11):4482-8 [16940446.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Dec;91(12):4769-75 [16968795.001]
  • [Cites] Nat Clin Pract Endocrinol Metab. 2006 Oct;2(10):552-61 [17024154.001]
  • [Cites] J Clin Endocrinol Metab. 2007 Jan;92(1):172-9 [17062771.001]
  • [Cites] N Engl J Med. 2006 Dec 14;355(24):2558-73 [17167139.001]
  • [Cites] N Engl J Med. 2007 Jan 4;356(1):29-38 [17202453.001]
  • [Cites] N Engl J Med. 2007 Jan 4;356(1):39-46 [17202454.001]
  • [Cites] Eur J Endocrinol. 2007 Jan;156(1):91-8 [17218730.001]
  • [Cites] Clin Endocrinol (Oxf). 2007 Jun;66(6):859-68 [17465997.001]
  • [Cites] N Engl J Med. 2007 Jun 14;356(24):2457-71 [17517853.001]
  • [Cites] Endocrinology. 2007 Dec;148(12):6107-14 [17656461.001]
  • [Cites] J Clin Endocrinol Metab. 2007 Aug;92(8):2861-5 [17682084.001]
  • [Cites] J Clin Endocrinol Metab. 2007 Dec;92(12):4598-601 [17895318.001]
  • [Cites] Mol Cell Endocrinol. 2008 May 14;286(1-2):69-74 [17977644.001]
  • [Cites] Eur J Endocrinol. 2007 Nov;157(5):579-87 [17984237.001]
  • [Cites] Neurosurg Focus. 2007;23(6):E14 [18081479.001]
  • [Cites] Eur J Endocrinol. 2008 Jan;158(1):91-9 [18166822.001]
  • [Cites] Endocr Pract. 2007 Nov-Dec;13(7):726-34 [18194929.001]
  • [Cites] Eur J Endocrinol. 2008 Jul;159(1):1-5 [18456868.001]
  • [Cites] Int J Clin Pract. 2008 Dec;62(12):1864-9 [18462372.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Sep;93(9):3348-56 [18559921.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Sep;93(9):3436-42 [18593770.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Sep;93(9):3515-8 [18611977.001]
  • [Cites] Eur J Endocrinol. 2008 Oct;159(4):R11-4 [18625690.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Oct;93(10):3853-9 [18647806.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Oct;93(10):3777-84 [18682513.001]
  • [Cites] Neurosurgery. 2008 Jun;62(6):1262-9; discussion 1269-70 [18824992.001]
  • [Cites] J Clin Endocrinol Metab. 2009 Jan;94(1):223-30 [18957500.001]
  • [Cites] J Clin Endocrinol Metab. 2009 Jan;94(1):115-22 [18957506.001]
  • [Cites] Endocr Pract. 2008 Sep;14(6):672-7 [18996784.001]
  • [Cites] Clin Endocrinol (Oxf). 2009 Jan;70(1):104-8 [19128367.001]
  • [Cites] J Clin Endocrinol Metab. 2009 Apr;94(4):1118-24 [19141584.001]
  • [Cites] Clin Endocrinol (Oxf). 2009 May;70(5):757-68 [19178516.001]
  • [Cites] J Endocrinol Invest. 2008 Dec;31(12):1119-23 [19246980.001]
  • [Cites] Eur J Endocrinol. 2009 Jun;160(6):1003-10 [19289534.001]
  • [Cites] Clin Endocrinol (Oxf). 2010 Jan;72(1):53-8 [19508591.001]
  • [Cites] Nat Med. 2002 Nov;8(11):1281-7 [12379847.001]
  • [Cites] Endocr Rev. 2003 Feb;24(1):28-47 [12588807.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Jul;93(7):2454-62 [18413427.001]
  • [Cites] Eur J Endocrinol. 2008 May;158(5):595-603 [18426817.001]
  • [Cites] N Engl J Med. 1979 Mar 1;300(9):459-64 [215912.001]
  • [Cites] Clin Endocrinol (Oxf). 1991 Aug;35(2):169-78 [1657460.001]
  • [Cites] J Endocrinol Invest. 1990 Mar;13(3):257-61 [1973178.001]
  • [Cites] Clin Endocrinol (Oxf). 1990 Mar;32(3):275-81 [2160871.001]
  • [Cites] J Clin Endocrinol Metab. 1985 Apr;60(4):698-705 [3882737.001]
  • [Cites] JAMA. 1982 Mar 5;247(9):1320 [6121067.001]
  • [Cites] Ann Intern Med. 1980 May;92(5):613-9 [6247946.001]
  • [Cites] Clin Endocrinol (Oxf). 1981 Nov;15(5):479-84 [6276051.001]
  • [Cites] Endocr Rev. 1993 Aug;14(4):443-58 [7693447.001]
  • [Cites] Clin Endocrinol (Oxf). 1994 Jul;41(1):95-102 [8050136.001]
  • [Cites] Am J Med. 1993 Sep;95(3):305-8 [8396322.001]
  • [Cites] J Clin Endocrinol Metab. 1996 Jul;81(7):2647-52 [8675592.001]
  • [Cites] Drug Saf. 1996 Apr;14(4):228-38 [8713691.001]
  • [Cites] J Endocrinol. 1997 Oct;155 Suppl 1:S23-9; discussion S31-2 [9389992.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Feb;83(2):374-8 [9467544.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Aug;83(8):2730-4 [9709939.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Sep;83(9):3034-40 [9745397.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Oct;83(10):3542-4 [9768661.001]
  • [Cites] Lancet. 1998 Oct 31;352(9138):1455-61 [9808008.001]
  • [Cites] Ann Med. 1998 Oct;30(5):452-9 [9814831.001]
  • [Cites] Eur J Endocrinol. 1998 Nov;139(5):516-21 [9849816.001]
  • [Cites] J Endocrinol Invest. 1999 Apr;22(4):306-9 [10342366.001]
  • [Cites] Front Neuroendocrinol. 1999 Jul;20(3):157-98 [10433861.001]
  • [Cites] Mol Cell Endocrinol. 1999 Nov 25;157(1-2):75-85 [10619399.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Jan;85(1):8-13 [10634356.001]
  • [Cites] N Engl J Med. 2000 Apr 20;342(16):1171-7 [10770982.001]
  • [Cites] Acta Med Austriaca. 2000;27(1):27-31 [10812460.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Jun;85(6):2247-52 [10852458.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Jun;86(6):2779-86 [11397887.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Jul;86(7):2929-34 [11443145.001]
  • [Cites] Endocrine. 2001 Apr;14(3):329-36 [11444429.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Aug;86(8):3568-73 [11502780.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Sep;86(9):4104-8 [11549633.001]
  • [Cites] Endocr Relat Cancer. 2001 Dec;8(4):287-305 [11733226.001]
  • [Cites] Lancet. 2001 Nov 24;358(9295):1754-9 [11734231.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Jan;87(1):99-104 [11788630.001]
  • [Cites] Clin Endocrinol (Oxf). 2002 Jan;56(1):65-71 [11849248.001]
  • [Cites] Eur J Endocrinol. 2002 May;146(5):707-16 [11980628.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Jul;87(7):3013-8 [12107192.001]
  • [Cites] Eur J Endocrinol. 2003 Mar;148(3):325-31 [12611613.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Jul;88(7):3105-12 [12843150.001]
  • [Cites] Ann Intern Med. 1960 Mar;52:560-9 [14426442.001]
  • [Cites] N Engl J Med. 2003 Nov 20;349(21):2023-33 [14627787.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Dec;88(12):5593-602 [14671138.001]
  • [Cites] Pituitary. 2003;6(1):19-27 [14674720.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Feb;89(2):638-45 [14764775.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Feb;89(2):667-74 [14764779.001]
  • [Cites] Clin Endocrinol (Oxf). 2004 Mar;60(3):375-81 [15009004.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Apr;89(4):1577-85 [15070915.001]
  • [Cites] J Clin Endocrinol Metab. 2004 May;89(5):2452-62 [15126577.001]
  • [Cites] Clin Endocrinol (Oxf). 2004 Aug;61(2):209-15 [15272916.001]
  • [Cites] Cancer. 2004 Aug 1;101(3):613-9 [15274075.001]
  • [Cites] J Clin Invest. 2004 Aug;114(3):349-56 [15286801.001]
  • [Cites] Eur J Endocrinol. 2004 Aug;151(2):173-8 [15296471.001]
  • [Cites] Endocr Pract. 2004 May-Jun;10(3):213-25 [15382339.001]
  • [Cites] Neuroendocrinology. 2004;80 Suppl 1:47-50 [15477717.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Mar;90(3):1588-93 [15585549.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Mar;90(3):1340-6 [15585550.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Mar;90(3):1856-63 [15613435.001]
  • [Cites] Eur J Endocrinol. 2005 Mar;152(3):379-87 [15757854.001]
  • [Cites] Am J Physiol Endocrinol Metab. 2005 Aug;289(2):E278-87 [15769796.001]
  • [Cites] Eur J Endocrinol. 2005 Apr;152(4):645-54 [15817922.001]
  • [Cites] Lancet. 2005 May 7-13;365(9471):1644-6 [15885297.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Aug;90(8):4465-73 [15886238.001]
  • (PMID = 20478050.001).
  • [ISSN] 1472-6823
  • [Journal-full-title] BMC endocrine disorders
  • [ISO-abbreviation] BMC Endocr Disord
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2887860
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85. Picard C, Silvy M, Gerard C, Buffat C, Lavaque E, Figarella-Branger D, Dufour H, Gabert J, Beckers A, Brue T, Enjalbert A, Barlier A: Gs alpha overexpression and loss of Gs alpha imprinting in human somatotroph adenomas: association with tumor size and response to pharmacologic treatment. Int J Cancer; 2007 Sep 15;121(6):1245-52

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gs alpha overexpression and loss of Gs alpha imprinting in human somatotroph adenomas: association with tumor size and response to pharmacologic treatment.
  • Gs alpha is paternally silenced in normal pituitary, but Gs alpha imprinting relaxation is found in some tumoral tissue.
  • In addition, Gs alpha mRNA levels are high in some somatotroph adenomas not bearing the active Gs alpha mutant, the gsp oncogene.
  • We compared the expression and imprinting of 4 transcripts of GNAS locus (NESP55, XL alpha s, exon 1A, Gs alpha) of 60 somatotroph adenomas with those of 23 lactotroph adenomas.
  • [MeSH-major] Adenoma / genetics. Drug Resistance, Neoplasm / genetics. GTP-Binding Protein alpha Subunits, Gs / genetics. Genomic Imprinting. Growth Hormone-Secreting Pituitary Adenoma / genetics
  • [MeSH-minor] Antineoplastic Agents, Hormonal / therapeutic use. Blotting, Western. DNA Methylation. Humans. Octreotide / therapeutic use. Prolactinoma / drug therapy. Prolactinoma / genetics. Prolactinoma / pathology. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17514647.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / RNA, Messenger; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs; RWM8CCW8GP / Octreotide
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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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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. Cho MA, Yashar P, Kim SK, Noh T, Gillam MP, Lee EJ, Jameson JL: HoxD10 gene delivery using adenovirus/adeno-associate hybrid virus inhibits the proliferation and tumorigenicity of GH4 pituitary lactotrope tumor cells. Biochem Biophys Res Commun; 2008 Jul 4;371(3):371-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HoxD10 gene delivery using adenovirus/adeno-associate hybrid virus inhibits the proliferation and tumorigenicity of GH4 pituitary lactotrope tumor cells.
  • Prolactinoma is one of the most common types of pituitary adenoma.
  • It has been reported that a variety of growth factors and cytokines regulating cell growth and angiogenesis play an important role in the growth of prolactinoma.
  • HoxD10 has been shown to impair endothelial cell migration, block angiogenesis, and maintain a differentiated phenotype of cells.
  • We investigated whether HoxD10 gene delivery could inhibit the growth of prolactinoma.
  • Rat GH4 lactotrope tumor cells were infected with adenovirus/adeno-associated virus (Ad/AAV) hybrid vectors carrying the mouse HoxD10 gene (Hyb-HoxD10) or the beta-galactosidase gene (Hyb-Gal).
  • Hyb-HoxD10 expression inhibited GH4 cell proliferation in vitro.
  • These results indicate that the delivery of HoxD10 could potentially inhibit the growth of PRL-secreting tumors.
  • This approach may be a useful tool for targeted therapy of prolactinoma and other neoplasms.
  • [MeSH-major] Gene Transfer Techniques. Genetic Therapy. Genetic Vectors. Homeodomain Proteins / genetics. Pituitary Neoplasms / therapy. Prolactinoma / therapy. Transcription Factors / genetics
  • [MeSH-minor] Adenoviridae / genetics. Animals. Cell Proliferation. Cyclin D2. Cyclins / metabolism. Dependovirus / genetics. Fibroblast Growth Factor 2 / metabolism. Mice. Rats. beta-Galactosidase / genetics

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  • (PMID = 18442473.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ccnd2 protein, rat; 0 / Cyclin D2; 0 / Cyclins; 0 / Homeodomain Proteins; 0 / Hoxd10 protein, mouse; 0 / Transcription Factors; 103107-01-3 / Fibroblast Growth Factor 2; EC 3.2.1.23 / beta-Galactosidase
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88. Colao A, Loche S: Prolactinomas in children and adolescents. Endocr Dev; 2010;17:146-59
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prolactinomas in children and adolescents.
  • Prolactinomas are the most common pituitary adenomas in children and adolescents followed by adrenocorticotropic hormone-secreting and growth hormone-secreting adenomas.
  • Diagnosis is generally based on clinical symptoms of primary or secondary gonadal failure, growth delay and/or tumor compressive symptoms.
  • Treatment is based on medical therapy with dopamine agonists, to control prolactin levels and reduce tumor size.
  • Surgery is indicated in patients with tumors resistant to dopamine agonists as well as in those showing severe neurological symptoms at diagnosis.
  • [MeSH-major] Pituitary Neoplasms / therapy. Prolactinoma / therapy

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  • [Copyright] Copyright 2010 S. Karger AG, Basel.
  • (PMID = 19955764.001).
  • [ISSN] 1662-2979
  • [Journal-full-title] Endocrine development
  • [ISO-abbreviation] Endocr Dev
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Ergolines; LL60K9J05T / cabergoline
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89. Al-Futaisi A, Saif AY, Al-Zakwani I, Al-Qassabi S, Al-Riyami S, Wali Y: Clinical and Epidemiological Characteristics of Pituitary Tumours using a Web-based Pituitary Tumour Registry in Oman. Sultan Qaboos Univ Med J; 2007 Apr;7(1):25-30

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical and Epidemiological Characteristics of Pituitary Tumours using a Web-based Pituitary Tumour Registry in Oman.
  • OBJECTIVE: From a recently instituted web-based pituitary tumour registry at Sultan Qaboos University Hospital, Oman, this study explores the results of comprehensive clinical evaluation, hormonal levels, radiological evidence of pituitary mass lesion using magnetic resonance (MRI) and the different treatment modalities.
  • METHODS: All patients who were diagnosed with pituitary mass tumours in our tertiary care endocrinology clinic between January 1998 and February 2006 were registered in the Oman pituitary tumour registry.
  • RESULTS: A total of 160 entries were made into the pituitary tumour registry.
  • There were 81 patients with non-functioning adenomas (50.6%), 59 with prolactinoma (36.9%) eight with acromegaly (5%), seven with craniopharyngioma (4.4%), four with Cushing's disease (2.5%) and one with sarcoidosis (0.6%).
  • Sub-group analyses were done only for the subjects with the 3 most prevalent pituitary tumours (non-functioning adenomas, prolactinomas, and acromegaly).
  • CONCLUSION: To our knowledge, this is the first pituitary tumour registry in the Arabian Gulf countries using a web-based programme.
  • This tumour registry will enable us to characterize clinical and the epidemiological features of pituitary tumours in the Sultanate of Oman.

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  • [Cites] Endocrinol Metab Clin North Am. 1999 Mar;28(1):81-117, vi [10207686.001]
  • [Cites] Medicine (Baltimore). 1999 Jul;78(4):236-69 [10424206.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Jan;85(1):168-74 [10634382.001]
  • [Cites] Ann Intern Med. 1990 Jun 15;112(12):925-31 [2187392.001]
  • [Cites] J Clin Endocrinol Metab. 1996 Oct;81(10):3455-9 [8855784.001]
  • [Cites] Endocrinol Metab Clin North Am. 1997 Dec;26(4):725-40 [9429857.001]
  • [Cites] Ann N Y Acad Sci. 1982;381:6-16 [6953802.001]
  • [Cites] N Engl J Med. 1981 Jan 15;304(3):156-8 [7442734.001]
  • [Cites] Ann Intern Med. 1994 May 15;120(10):817-20 [8154641.001]
  • [Cites] J Clin Endocrinol Metab. 1993 May;76(5):1089-94 [8496297.001]
  • [Cites] Surg Neurol. 1996 Jul;46(1):28-31 [8677484.001]
  • [Cites] Cancer. 1996 Aug 1;78(3):502-10 [8697397.001]
  • (PMID = 21654941.001).
  • [ISSN] 2075-051X
  • [Journal-full-title] Sultan Qaboos University medical journal
  • [ISO-abbreviation] Sultan Qaboos Univ Med J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Oman
  • [Other-IDs] NLM/ PMC3086414
  • [Keywords] NOTNLM ; Clinical / Epidemiology / Oman / Pituitary adenomas / Registry
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90. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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

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  • [CommentIn] Intern Med. 2010;49(17):1839-40 [20823641.001]
  • (PMID = 20686291.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] RWM8CCW8GP / Octreotide
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91. Saveanu A, Jaquet P: Somatostatin-dopamine ligands in the treatment of pituitary adenomas. Rev Endocr Metab Disord; 2009 Jun;10(2):83-90
MedlinePlus Health Information. consumer health - Pituitary Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Somatostatin-dopamine ligands in the treatment of pituitary adenomas.
  • Somatostatin receptors (sst1-5) and dopamine receptor 2 (D2DR) are well expressed and co-localized in several human pituitary adenomas, suggesting possible functional interactions in the control of hormonal hypersecretion and tumor cell growth.
  • The present review describes the expression and functionality of these receptors in the different classes of human pituitary adenomas.
  • The D2DR agonists, bromocriptine and cabergoline, control about 90% of prolactinomas.
  • Such drugs are much less effective in the control of the others pituitary adenomas also expressing ssts and D2DR receptors.
  • Such ligands bearing distinct ssts and DRD2 pharmacophores may synergistically produce an increased control of secretion and/or of proliferation in the different types of pituitary adenomas.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Pituitary Neoplasms / drug therapy. Receptors, Dopamine D2 / agonists. Receptors, Somatostatin / agonists

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  • (PMID = 18651224.001).
  • [ISSN] 1573-2606
  • [Journal-full-title] Reviews in endocrine & metabolic disorders
  • [ISO-abbreviation] Rev Endocr Metab Disord
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Receptors, Dopamine D2; 0 / Receptors, Somatostatin
  • [Number-of-references] 72
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92. Liu T, Joo SH, Voorhees JL, Brooks CL, Pei D: Synthesis and screening of a cyclic peptide library: discovery of small-molecule ligands against human prolactin receptor. Bioorg Med Chem; 2009 Feb 1;17(3):1026-33
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Synthesis and screening of a cyclic peptide library: discovery of small-molecule ligands against human prolactin receptor.
  • Prolactin receptor is involved in normal lactation and reproduction; however, excessive prolactin levels can cause various reproductive disorders such as prolactinomas.
  • Small-molecule antagonists against the human prolactin receptor (hPRLr) thus have potential clinical applications and may serve as useful molecular probes in biomedical research.
  • The identity of a positive bead was revealed by sequencing the linear encoding peptide within the bead by partial Edman degradation/mass spectrometry.

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  • [Cites] Angew Chem Int Ed Engl. 2005 Apr 29;44(18):2760-3 [15830403.001]
  • [Cites] Methods Mol Biol. 1999;112:531-52 [10027275.001]
  • [Cites] J Am Chem Soc. 2005 Oct 19;127(41):14142-3 [16218582.001]
  • [Cites] Biochemistry. 2005 Nov 15;44(45):14932-47 [16274240.001]
  • [Cites] Chem Rev. 2005 Dec;105(12):4441-82 [16351050.001]
  • [Cites] Anal Chem. 2006 Aug 15;78(16):5935-9 [16906744.001]
  • [Cites] Chem Biol Drug Des. 2006 Jul;68(1):3-10 [16923020.001]
  • [Cites] J Am Chem Soc. 2006 Oct 4;128(39):13000-9 [17002397.001]
  • [Cites] Peptides. 2006 Nov;27(11):2567-74 [16730857.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Nov 14;103(46):17462-7 [17090667.001]
  • [Cites] J Med Chem. 2007 Jun 28;50(13):3132-7 [17547386.001]
  • [Cites] ACS Chem Biol. 2007 Sep 21;2(9):625-34 [17894440.001]
  • [Cites] J Biol Chem. 2007 Nov 9;282(45):33118-31 [17785459.001]
  • [Cites] Nature. 2001 Jul 26;412(6845):452-5 [11473322.001]
  • [Cites] J Am Chem Soc. 2002 Jul 3;124(26):7678-80 [12083920.001]
  • [Cites] Nature. 2002 Aug 8;418(6898):658-61 [12167866.001]
  • [Cites] J Biol Chem. 2002 Oct 4;277(40):37512-8 [12167667.001]
  • [Cites] Endocr Rev. 2003 Feb;24(1):1-27 [12588805.001]
  • [Cites] Biochem Biophys Res Commun. 2003 Aug 8;307(4):791-6 [12878179.001]
  • [Cites] Nat Rev Drug Discov. 2003 Dec;2(12):943-4 [14756140.001]
  • [Cites] Antimicrob Agents Chemother. 2004 Apr;48(4):1272-80 [15047529.001]
  • [Cites] J Comb Chem. 2004 May-Jun;6(3):398-406 [15132600.001]
  • [Cites] Antimicrob Agents Chemother. 2004 Sep;48(9):3349-57 [15328096.001]
  • [Cites] Biochemistry. 2004 Nov 2;43(43):13755-65 [15504038.001]
  • [Cites] Can Med Assoc J. 1982 May 1;126(9):1041-6 [7074504.001]
  • [Cites] Nature. 1991 Nov 7;354(6348):82-4 [1944576.001]
  • [Cites] Nature. 1991 Nov 7;354(6348):84-6 [1719428.001]
  • [Cites] Nature. 1994 Dec 1;372(6505):478-81 [7984244.001]
  • [Cites] Biochemistry. 1995 Nov 28;34(47):15430-5 [7492543.001]
  • [Cites] Pept Res. 1995 Jul-Aug;8(4):236-7 [8527877.001]
  • [Cites] J Biol Chem. 1996 Jun 14;271(24):14353-60 [8662911.001]
  • [Cites] Mol Divers. 1996 Aug;1(4):233-40 [9237214.001]
  • [Cites] Mol Divers. 1997-1998;3(3):149-59 [9680646.001]
  • [Cites] Bioorg Med Chem Lett. 1998 Sep 8;8(17):2327-32 [9873536.001]
  • [Cites] Protein Expr Purif. 1999 Feb;15(1):16-23 [10024465.001]
  • [Cites] Endocr Rev. 2005 May;26(3):400-22 [15814850.001]
  • (PMID = 18234500.001).
  • [ISSN] 1464-3391
  • [Journal-full-title] Bioorganic & medicinal chemistry
  • [ISO-abbreviation] Bioorg. Med. Chem.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / GM062820-05A1; United States / NIGMS NIH HHS / GM / R01 GM062820; United States / NIGMS NIH HHS / GM / R01 GM062820-05A1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Ligands; 0 / Peptide Library; 0 / Peptides; 0 / Peptides, Cyclic; 0 / Receptors, Prolactin
  • [Other-IDs] NLM/ NIHMS96200; NLM/ PMC2662701
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93. Morita S, Otsuki M, Izumi M, Asanuma N, Izumoto S, Saitoh Y, Yoshimine T, Kasayama S: Reduced epinephrine reserve in response to insulin-induced hypoglycemia in patients with pituitary adenoma. Eur J Endocrinol; 2007 Sep;157(3):265-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Reduced epinephrine reserve in response to insulin-induced hypoglycemia in patients with pituitary adenoma.
  • Insulin-induced hypoglycemia is used for evaluating GH-IGF-I and ACTH-adrenal axes in patients with pituitary disorders.
  • The aim of this study was to determine whether the response of catecholamine secretion to hypoglycemia is disrupted in patients with pituitary adenoma.
  • METHODS: The study population comprised 23 patients with pituitary adenoma (non-functioning adenoma or prolactinoma).
  • CONCLUSIONS: Impaired epinephrine secretion in response to insulin-induced hypoglycemia was frequently observed in patients with pituitary adenoma.
  • This disorder was especially severe in patients with secondary adrenal insufficiency.

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  • (PMID = 17766707.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Hypoglycemic Agents; 0 / Insulin; X4W3ENH1CV / Norepinephrine; YKH834O4BH / Epinephrine
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94. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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95. Gruszka A, Kunert-Radek J, Pawlikowski M, Stepien H: Serum endostatin levels are elevated and correlate with serum vascular endothelial growth factor levels in patients with pituitary adenomas. Pituitary; 2005;8(2):163-8
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  • [Title] Serum endostatin levels are elevated and correlate with serum vascular endothelial growth factor levels in patients with pituitary adenomas.
  • The purpose of our study was to evaluate serum concentrations of endostatin in patients harbouring various pituitary adenoma types and to examine the relationship of serum endostatin levels to circulating vascular endothelial growth factor (VEGF) levels.
  • Preoperative serum endostatin and VEGF concentrations were measured using competitive enzyme immunoassays in 71 patients with pituitary adenomas (20 somatotropinomas, 3 corticotropinomas, 6 prolactinomas and 42 clinically nonfunctioning pituitary adenomas - CNFPAs) and compared with levels from age-matched controls.
  • Serum endostatin concentrations were significantly higher in all pituitary adenoma types, except for prolactinomas (somatotropinomas: 124 +/- 16; p < 0.02, corticotropinomas: 157 +/- 42; p < 0.02, prolactinomas: 141 +/- 37; p > 0.05, CNFPAs: 169 +/- 11 ng/ml; p < 0.000005 vs 73 +/- 10 ng/ml in controls).
  • There was a significant positive correlation between endostatin and VEGF serum levels in patients with pituitary adenomas (r = +0.322; p = 0.006).
  • The simultaneous elevation of endostatin and VEGF may attenuate the pro-angiogenic action of VEGF and be responsible for rather weak neovascularization of pituitary adenomas.
  • Prospective studies are required to assess the usefulness of circulating endostatin and VEGF as markers of progression or recurrence of pituitary tumors.
  • [MeSH-major] Adenoma / blood. Endostatins / blood. Pituitary Neoplasms / blood. Vascular Endothelial Growth Factor A / blood

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  • (PMID = 16379029.001).
  • [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 / Endostatins; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A
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96. Krysiak R, Okopieh B, Herman ZS: [Verapamil-induced hyperprolactinemia--a case report]. Pol Arch Med Wewn; 2005 Feb;113(2):155-8
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  • Occasionally, verapamil-treated patients experience a slight asymptomatic increase in serum prolactin level.
  • In this article we report the case of 42-year woman with manifest verapamil-induced hyperprolactinemia whose clinical symptoms suggested the occurrence of prolactinoma.
  • A marked increase in prolactin levels and the preserved reactivity of this hormone in dynamic tests suggested that the patient exhibited "hypersensitivity" to verapamil.
  • In the described state of the examined female detection of the disease, verapamil withdrawal and temporary bromocriptine administration have led to a full normalization of patient's clinical status.
  • [MeSH-minor] Adult. Bromocriptine / administration & dosage. Female. Hormone Antagonists / administration & dosage. Humans. Prolactin / blood. Time Factors

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  • (PMID = 16209236.001).
  • [Journal-full-title] Polskie Archiwum Medycyny Wewnetrznej
  • [ISO-abbreviation] Pol. Arch. Med. Wewn.
  • [Language] pol
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Calcium Channel Blockers; 0 / Hormone Antagonists; 3A64E3G5ZO / Bromocriptine; 9002-62-4 / Prolactin; CJ0O37KU29 / Verapamil
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97. Sodi R, Fikri R, Diver M, Ranganath L, Vora J: Testosterone replacement-induced hyperprolactinaemia: case report and review of the literature. Ann Clin Biochem; 2005 Mar;42(Pt 2):153-9
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  • Half of all men with prolactin (PRL)-producing macroadenomas present with hypogonadism, decreased libido and impotence, and therefore require testosterone replacement.
  • However, very little is known about the effect of testosterone on prolactinomas.
  • We report a case of an 18-year-old obese man who presented with hypogonadism and hyperprolactinaemia and underwent a transphenoidal hypophysectomy after a computer tomography scan showed the presence of a suprasellar macroadenoma.
  • On separate occasions, we documented a rise in PRL when testosterone replacement was started and a fall in PRL when testosterone replacement was stopped (r = 0.6090, P = 0.0095).
  • We hypothesize that the exogenous testosterone was aromatized to oestradiol, which stimulated the release of PRL by the anterior pituitary.
  • [MeSH-major] Adenoma / complications. Hyperprolactinemia / chemically induced. Pituitary Neoplasms / complications. Testosterone / adverse effects


98. Kałuzny M, Bolanowski M: [Hyperprolactinemia: etiology, clinical symptoms, and therapy]. Postepy Hig Med Dosw (Online); 2005;59:20-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Hyperprolactinemia is caused in most cases by drugs or it has an organic etiology (pituitary tumor:--prolactinoma).
  • In the medical treatment of a hyperprolactinemic condition dopamine receptors type D2 agonists are used.
  • Such drugs have well-established high therapeutic efficiency (in the vast majority of patients they cause normalization of PRL serum level, tumor shrinkage, and withdrawal of the hyperprolactinemia-related symptoms and tumor mass).
  • This is why they are the first line treatment for prolactinoma.
  • In cases of a lack of pharmacological effect, drug intolerance or resistance, large tumors with accompanying compression symptoms' (tumor mass effect), dynamic tumor enlargement, or if a macroprolactinoma-affected woman desires pregnancy neurosurgery should be considered.

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  • (PMID = 15761382.001).
  • [ISSN] 1732-2693
  • [Journal-full-title] Postepy higieny i medycyny doswiadczalnej (Online)
  • [ISO-abbreviation] Postepy Hig Med Dosw (Online)
  • [Language] POL
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Dopamine Antagonists; 0 / Receptors, Dopamine D2
  • [Number-of-references] 32
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99. Kaltsas GA, Nomikos P, Kontogeorgos G, Buchfelder M, Grossman AB: Clinical review: Diagnosis and management of pituitary carcinomas. J Clin Endocrinol Metab; 2005 May;90(5):3089-99
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical review: Diagnosis and management of pituitary carcinomas.
  • Pituitary carcinomas are rare, making up some 0.2% of all pituitary tumors, but represent a particular challenge to clinical practice.
  • The diagnosis of a pituitary carcinoma requires evidence of metastatic disease, either outside the central nervous system (CNS) or as separate noncontiguous foci within the CNS.
  • They may present as typical pituitary adenomas, which reveal their malignant character only as time progresses, or as peculiarly aggressive tumors ab initio.
  • The majority of carcinomas are secretory, usually arising from corticotroph tumors or prolactinomas, but all histological types and secretory patterns are represented.
  • Chemotherapy in some instances probably prolongs survival, but, in general, their progress from the diagnosis of carcinomatous changes is progressive and inexorable.
  • [MeSH-major] Pituitary Neoplasms / diagnosis. Pituitary Neoplasms / therapy

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  • (PMID = 15741248.001).
  • [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] 9002-60-2 / Adrenocorticotropic Hormone
  • [Number-of-references] 116
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100. Demura M, Yoneda T, Karashima S, Higashikata T, Mabuchi H, Kawano M, Yamagishi M, Takeda Y: A possible new syndrome with double endocrine tumors in association with an unprecedented type of familial heart-hand syndrome: a case report. J Med Case Rep; 2010;4:347

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A possible new syndrome with double endocrine tumors in association with an unprecedented type of familial heart-hand syndrome: a case report.
  • INTRODUCTION: The combination of a pituitary prolactinoma and an aldosterone-producing adrenal adenoma is extremely rare.
  • A large pituitary adenoma with an increased level of serum prolactin was apparent by computed tomography.
  • Computed tomography showed a mass in the right adrenal gland.
  • Similar digital and cardiac abnormalities were detected in our patient's father, and a clinical diagnosis of hereditary heart-hand syndrome was made.
  • Her father had no obvious endocrine tumors, implying that the parent of transmission determined variable phenotypic expression of the disease: heart-hand syndrome with multiple endocrine tumors from the paternal transmission or no endocrine tumor from the maternal transmission.
  • This suggests that the gene or genes responsible for the disease may be under tissue-specific imprinting control.

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  • (PMID = 21034446.001).
  • [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/ PMC2987961
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