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Caroline M Gorvin, Paul J Newey, and Rajesh V Thakker

recently, a germline Asn492Ile PRLR variant that increases receptor activity via the PI3K-Akt pathway was reported to be associated with a higher incidence of prolactinoma ( Gorvin et al. 2018b ). Both the Ile146Leu and Asn492Ile variants are present in

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Shilpa Thakur, Brianna Daley, and Joanna Klubo-Gwiezdzinska

they secrete. These PitNETs are usually benign in nature and can be classified as functional or non-functional, depending on whether or not they secrete hormones ( Theodros et al. 2015 ). Among the PitNETs, prolactinomas are the most common

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H Namihira, M Sato, K Murao, WM Cao, S Matsubara, H Imachi, M Niimi, H Dobashi, NC Wong, and T Ishida

Menin is a protein encoded by the gene mutated in multiple endocrine neoplasia type 1 (MEN1) characterized by multiple endocrine tumors of the parathyroid glands, pancreatic islets and the anterior pituitary, especially prolactinoma. In this study, we examined the effects of menin on human prolactin (hPRL) expression. In rat pituitary GH3 cells stably expressing menin, both PRL gene expression/secretion and thymidine incorporation into DNA were inhibited as compared with mock-transfected cells. The transcriptional activity of PRL promoter in GH3 cells co-transfected with menin was significantly decreased. A deletion mutation (569 delC), which we identified in a Japanese MEN1 family, was introduced into menin. When GH3 cells were transfected with a mutant menin expression vector, inhibition of hPRL promoter activity was partially reversed. These observations suggest that menin inhibits hPRL promoter activity and cell proliferation, raising the possibility that menin might play an important role in the tumorigenesis of prolactinoma.

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M Delhase, P Vergani, A Malur, B Velkeniers, E Teugels, J Trouillas, and E L Hooghe-Peters

ABSTRACT

Adenomas can develop from each cell type of the anterior pituitary. In the normal pituitary, three of these cell types, the GH-, prolactin- and TSH-secreting cells, express the transcription factor Pit-1/GHF-1 which is responsible for prolactin and GH (and probably TSH) cell commitment, differentiation, probably proliferation and gene expression. We have analysed the expression of Pit-1/GHF-1 in a panel of human pituitary adenomas. All GH-, prolactin- and TSH-expressing adenomas studied expressed the Pit-1/GHF-1 factor, as demonstrated by in-situ hybridization and immunocytochemistry. The expression was higher in adenomas than in normal human pituitary. In contrast, ACTH- and LH—FSH-secreting and non-secreting adenomas were negative. Seven transplants of the spontaneous rat prolactinoma SMtTW were also investigated and all were found to be positive.

This further stresses the analogy between these tumours and human prolactinomas. Taken together, the data confirm that Pit-1/GHF-1 expression is restricted to GH-, prolactin- and TSH-expressing cells, and the increased expression in adenomas is compatible with a role of Pit-1/GHF-1 in cell proliferation.

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Diego Ferone, Federico Gatto, Marica Arvigo, Eugenia Resmini, Mara Boschetti, Claudia Teti, Daniela Esposito, and Francesco Minuto

/PRL adenomas ( Panetta & Patel 1995 , Stefaneanu et al . 2001 , Zatelli et al . 2005 , Taboada et al . 2007 , Ferone et al . 2008 , Saveanu et al . 2008 ). The vast majority of prolactinomas express high number of D 2 receptor; however, sst 1 , and

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Monica Fedele and Alfredo Fusco

. 1999 ). B-type cyclins have recently been described as overexpressed in many human pituitary adenomas, with prevalence in prolactinomas ( Wierinckx et al . 2007 , De Martino et al . 2009 b ). Silencing of the gene encoding p16 INK4A by methylation

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Elina Heliövaara, Sari Tuupanen, Manuel Ahlsten, Shirley Hodgson, Ernesto de Menis, Outi Kuismin, Louise Izatt, R J McKinlay Gardner, Sadi Gundogdu, Anneke Lucassen, Johanna Arola, Anne Tuomisto, Markus Mäkinen, Auli Karhu, and Lauri A Aaltonen

provided in Fig. 1 . Figure 1 Schematic RET region illustrating the five genetic findings from familial pituitary adenoma patients. A heterozygous V262A missense change c.785T>C was found in RET Exon 4 in an Italian prolactinoma patient. However, this

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Tamar Eigler and Anat Ben-Shlomo

-specific role of sst receptor subtypes in SRIF-dependent inhibition of GH secretion. PRL secretion SRIF-dependent control of PRL secretion is modest compared with that of GH. Treatment of prolactinoma samples with sst5-selective agonists effectively inhibited

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Erika Peverelli, Giovanna Mantovani, Andrea G Lania, and Anna Spada

existed in a lethal prolactinoma, in which gsp mutation represented the second hit for the transition from prolactinoma to acromegaly ( Lania et al . 2010 ). This reduced oncogenic potential could be explained by the existence of intracellular

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Hong-Wei Chang, Chao-Yuan Huang, Shao-Yu Yang, Vin-Cent Wu, Tzong-Shinn Chu, Yung-Ming Chen, Bor-Shen Hsieh, and Kwan-Dun Wu

, Gemignani et al . 2005 , Campa et al . 2007 ). Transgenic knockout of DRD2 in mice resulted in hyperprolactinemia and prolactinoma ( Kelly et al . 1997 , Saiardi et al . 1997 ). In human studies polymorphisms of dopamine receptors are associated with