Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027819 (neuroblastoma)
 27,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 6-day-old baby boy showed concentration of Ga-67 citrate in both breasts and an abdominal neuroblastoma. The breast uptake was most likely caused by estrogen and prolactin production and passage from the maternal to the fetal circulation.
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PMID:Breast uptake of Ga-67 in a neonate. 161 93

Our studies demonstrate that rat anterior pituitary cells (GH3) are capable of synthesizing and secreting tissue kallikrein together with prolactin and growth hormone. The secretion of prolactin and growth hormone in GH3 cells was measured by two newly developed sensitive radioimmunoassays (RIA), using the polyethylene glycol separation technique. In the direct radioimmunoassay for rat tissue kallikrein, using a polyclonal antiserum which recognizes both active and prokallikrein, the GH3 kallikrein displays parallelism with standard curves of rat urinary kallikrein. The production of immunoreactive kallikrein, prolactin, and growth hormone is time-dependent, and the levels after a 72 h incubation in serum-free media are approximately 12.2 +/- 4.4 ng, 272.2 +/- 33.0 ng, and 475.6 +/- 4.8 ng per 10(6) cells per ml (mean +/- SD, n = 3), respectively. In Western blot analyses, a specific monoclonal antibody to tissue kallikrein (V4D11) identifies GH3-secreted kallikrein as a approximately 39,000 Da protein, slightly larger than approximately 38,000 Da kallikreins of submandibular gland, mouse anterior pituitary cells (AtT 20) or rodent neuroblastoma X glioma hybrid cells (NG108). Kallikrein mRNA in GH3 cells was identified in Northern blot analyses, using a tissue kallikrein cDNA probe. In a RIA using a kallikrein monoclonal antibody (V1C3) recognizing only active kallikrein, kallikrein could not be detected in the media incubated up to 48 h with GH3 cells. However, after trypsin treatment, a time-dependent increase of immunoreactive kallikrein (using monoclonal antibody V1C3), Tos-Arg-OMe esterase, and kinin-releasing activities can be measured in the conditioned media. The activated esterase activity was inhibited by aprotinin and by affinity-purified kallikrein monoclonal antibody (V4D11) in a dose-dependent manner. The data indicated that rat anterior pituitary GH3 cells secrete latent tissue kallikrein, which can be converted to active kallikrein by trypsin. These hormonally responsive cells co-synthesize kallikrein with prolactin and growth hormone and provide a model system for studying the regulation of kallikrein gene expression.
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PMID:Identification of latent tissue kallikrein, prolactin and growth hormone secretion in GH3 pituitary cells using modified radioimmunoassays. 336 Feb 6

The authors report the case of a 40-year-old woman with a 12-year history of irregular menses, amenorrhea, infertility, galactorrhea, a slightly elevated prolactin level, and a slowly growing pituitary adenoma. She developed recent onset of visual symptoms, prompting craniotomy for removal of an intrasellar tumor. Following surgery, her vision and prolactin levels returned to normal. Light microscopic and immunohistochemical examination of the tumor revealed it to be a neuroblastoma, which was immunohistochemically positive for synaptophysin, S-100 protein, and oxytocin. The neoplasm contained prolactin-positive neuroblastic and pituitary epithelial cells. No other pituitary hormones were found. Electron microscopy demonstrated two cell types: one with frequent neuritic processes containing neurosecretory granules and showing synaptic specialization, and another one compatible with epithelial adenohypophyseal cells. A few cells had ultrastructural features that were transitional between neuronal cells and granulated epithelial cells. Agranular folliculostellate cells were also identified. Immunoelectron microscopy demonstrated prolactin granules in the cytoplasm of the epithelial cells, in a few transitional cells, and in scattered neuritic processes. Ultrastructural and immunohistochemical features of the tumor suggested a transformation of pituitary epithelium to neuroblastic cells. Hyperprolactinemia and associated clinical symptoms may in part be attributed to selective prolactin secretion by neoplastic cells that were differentiating into adenomatous pituitary cells and, to a lesser extent, to cells differentiating into a neuroblastic line. Compression of pituitary stalk might also have been a contributory factor to the increased prolactin levels. Moreover, the oxytocin produced by the neuroblastic cells was considered an additional stimulus for prolactin secretion by neoplastic cells or by the normal pituitary.
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PMID:Differentiating neuroblastoma of pituitary gland: neuroblastic transformation of epithelial adenoma cells. Case report. 889 39

The aetiology of neuroblastoma remains obscure, although a number of neuropeptides have been implicated in its pathogenesis. Using the mouse neuroblastoma cell line Neuro2a as a model, we have investigated the mitogenic actions of prolactin (PRL) and two hypothalamo-pituitary-adrenal stress axis hormones, corticotropin-releasing factor (CRF) and corticosterone. Using established polyclonal PRL receptor antisera with immunofluorescence cytochemistry, we show that the Neuro2a cells possess immunoreactive forms of both the long and short forms of the receptor. PRL and CRF were effective as mitogens in Neuro2a cell cultures, where a 10(-7) M concentration of PRL or CRF elicited a two-fold increase in the numbers of cells after 72 h (p < 0.0001). Corticosterone, however, attenuated their proliferation. These data suggest that prolactin may act to increase the proliferation and regulation of neuroblastomas and that the effects of PRL may be modified by hypothalamo-pituitary-adrenal hormones.
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PMID:Expression of prolactin receptors and regulation of cell proliferation by prolactin, corticotropin-releasing factor, and corticosterone in a neuroblastoma cell line. 1223 1

The hematopoietic cytokine erythropoietin (Epo) prevents neuronal death during ischemic events in the brain and in neurodegenerative diseases, presumably through its antiapoptotic effects. To explore the role of different signaling pathways in Epo-mediated antiapoptotic effects in differentiated human neuroblastoma SH-SY5Y cells, we employed a prolactin receptor (PrlR)/erythropoietin receptor (EpoR) chimera system, in which binding of prolactin (Prl) to the extracellular domain activates EpoR signaling in the cytosol. On induction of apoptosis by staurosporine, Prl supports survival of the SH-SY5Y cells expressing the wild-type PrlR/EpoR chimera. In these cells Prl treatment strongly activates the STAT5, AKT, and MAPK signaling pathways and induces weak activation of the p65 NF-kappaB factor. Selective mutation of the eight tyrosine residues of the EpoR cytoplasmic domain results in impaired or absent activation of either STAT5 (mutation of Tyr(343)) or AKT (mutation of Tyr(479)) or both (mutation of all eight tyrosine residues). Most interestingly, Prl treatment does not prevent apoptosis in cells expressing mutant PrlR/EpoR chimeras in which either the STAT5 or the AKT signaling pathways are not activated. In contrast, ERK 1/2 is fully activated by all mutant PrlR/EpoR chimeras, comparable with the level seen with the wild-type PrlR/EpoR chimera, implying that activation of the MAPK signaling pathway per se is not sufficient for antiapoptotic activity. Therefore, the antiapoptotic effects of Epo in neuronal cells require the combinatorial activation of multiple signaling pathways, including STAT5, AKT, and potentially MAPK as well, in a manner similar to that observed in hematopoietic cells.
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PMID:Antiapoptotic effects of erythropoietin in differentiated neuroblastoma SH-SY5Y cells require activation of both the STAT5 and AKT signaling pathways. 1640 71

Proliferins (also termed mitogen-regulated proteins; MRP/PLFs) belong to the prolactin gene family. Mrp/Plfs are involved in angiogenesis of the uterus and placenta and maximally expressed during midgestation and decline through the remainder of the gestation period in mouse placenta. The tissue expressions of Mrp/Plfs are mainly documented in placenta, hair follicles of skin and in wound healing. In this report, we demonstrate that Plf1, Plf1 minus exon3, Plf2 and Mrp3 but not Mrp4 are expressed in mouse whole brain by diagnostic RT-PCR and Western blotting. The expression levels of Mrp/Plf mRNAs in mouse brains were low during the neonatal period, but higher in embryonic and adult stages, indicating Mrp/Plfs expression profiles are different in mouse brain and placenta. Interestingly, endogenous Mrp/Plfs were detected using immunostaining both in mouse brain sections and the neuroblastoma cell line, Neuro-2a cells. The function of PLF1 was explored by expressing exogenous PLF1 in Neuro-2a cells. This resulted in increased microvilli. Neuro-2a cells with stable expression of PLF1 had increased proliferation compared with normal and stable expressing EGFP cells when cell reached saturation density. Together these data, strongly suggest that MRP/PLFs mediate microvilli formation and contribute to cell proliferation of neuroblastoma cells.
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PMID:Proliferin enhances microvilli formation and cell growth of neuroblastoma cells. 1687 75

Abstract Quinacrine, a fluorescent basic molecule, accumulates in secretory granules of pituitary cells, as was revealed by its colocalization with immunoreactive prolactin. Thus quinacrine fluorescence may be used to monitor secretory activity at the single cell level. Rat pituitary cells in primary culture were loaded with quinacrine and stimulated with physiological secretagogues, such as thyrotrophin-releasing hormone or bradykinin, which induced a multiphasic lowering of fluorescence, corresponding to the loss of quinacrine contained in exocytosed granules. Quinacrine was further used in combination with the fluorescent calcium probe fura-2, in order to monitor simultaneously exocytosis and variations in the cytosolic free calcium concentration, [Ca(2+)](i). With an appropriate selection of the excitation wavelengths, in dual excitation microfluorimetry experiments, it was possible to distinguish between fluorescence changes due to altered [Ca(2+)](i) versus quinacrine exocytosis. Transient elevations of [Ca(2+)](i) were provoked in individual pituitary cells by enhancing calcium influx through voltage gated channels. In part of the cells an initial increase in [Ca(2+)](i) coincided with stimulated quinacrine release. The approach was also applied to cells of the neuroblastoma line NCB20, where stimulation with bradykinin caused a transient rise in [Ca(2+)](i), concomitantly with enhanced exocytosis. No increase in exocytosis was ever detected without an elevation of [Ca(2+)](i), suggesting that in both cellular systems, an increase in [Ca(2+)](i), is absolutely necessary, but not sufficient to induce secretion.
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PMID:Simultaneous monitoring of cytosolic free calcium and exocytosis at the single cell level. 1921 61

Neuroblastomas of the sellar region are exceedingly rare. Only 2 cases have previously been reported. Management of these tumours depends on the tumour's primary site, the patient's age and histopathological features. We are reporting the case of a 43-year-old woman who developed progressive bitemporal hemianopsia and visual loss, accompanied by amenorrhea and hyponatremia. Laboratory findings revealed a slightly elevated prolactin level. Cranial MR-imaging displayed an intrasellar and suprasellar lesion with a maximum diameter of 2.5 cm that was suspicious for a pituitary adenoma or tuberculum sellae meningioma. The tumour was approached via a pterional trepanation. Intraoperatively, the tumour was highly vascularized and adhesive to the optic chiasm, the floor of the third ventricle, the hypothalamus and the hypophyseal stalk. Postoperatively, vision improved and prolactin dropped to normal values, but hyponatremia persisted. Histopathological examination revealed a neuroblastoma with strong positivity for synaptophysin and chromogranin, MAP-2 protein and NeuN-antigen in the immunohistochemistry. No pituitary hormone receptors were expressed. The MIB-1 labelling index was positive in 5% of the cell nucleoli. In the further course, the patient underwent radiotherapy of the neuroaxis. A brief review of the literature is presented.
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PMID:Sellar neuroblastoma mimicking a pituitary tumour: case report and review of the literature. 1964 Jun 36

In a variety of species, the LH-secretory response to gonadotropin-releasing hormone (GnRH) is completely suppressed by the combined actions of prolactin (PRL) and dopamine (DA). In sheep, this effect is only observed under long days (nonbreeding season [NBS]). To investigate the level at which these mechanisms operate, we assessed the effects of PRL and bromocriptine (Br), a DA agonist, on the gonadotropin-secretory and mRNA responses to GnRH in pituitary cell cultures throughout the ovine annual reproductive cycle. As expected, the LH-secretory response to GnRH was only abolished during the NBS following combined PRL and Br application. Conversely, the LHB subunit response to GnRH was reduced during both the BS and NBS by the combined treatment and Br alone. Similar results were obtained in pars distalis-only cultures, indicating that the effects are pars tuberalis (PT)- independent. Further signaling studies revealed that PRL and Br alter the LH response to GnRH via convergence at the level of PLC and PKC. Results for FSH generally reflected those for LH, except during the BS where removal of the PT allowed PRL and Br to suppress the FSH-secretory response to GnRH. These data show that suppression of the LH-secretory response to GnRH by PRL and DA is accompanied by changes in mRNA synthesis, and that the photoperiodic modulation of this inhibition operates primarily at the level of LH release through alterations in PKC and PLC. Furthermore, the suppressive effects of PRL and DA on the secretion of FSH are photoperiodically regulated in a PT-dependent manner.
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PMID:Photoperiodic modulation of the suppressive actions of prolactin and dopamine on the pituitary gonadotropin responses to gonadotropin-releasing hormone in sheep. 2230 89

Case 1: A tumor mass involving the rostral part of left cerebrum was found in a two-year-old female budgerigar (Melopsittacus undulatus) at necropsy. Histologically, the neoplastic cells were arranged in sheets or cords and occasionally showed nest growth patterns. These uniform tumor cells had a little cytoplasm and ovoid or round basophilic nuclei with clearly distinct cytoplasmic membranes. The tumor cells were strong diffusely immunostained with both neuron-specific enolase (NSE) and neurofilament protein and partially for synaptophysin. They lacked chromogranin A, glial fibrillary acidic protein (GFAP), vimentin, S-100, and cytokeratin antigen expression. Moreover, they had no reaction to antibodies against pituitary hormones, such as adrenocorticotrophic hormone (ACTH), growth hormone, and prolactin. The histological and immunohistochemical examination determined the tumor as neuroblastoma. Case 2: An extremely enlarged pituitary mass was found above the sella turcica of a male budgerigar. It was soft and well delineated from the adjacent structures. On histological examination, this tumor consisted of a sheet of large closely packed polyhedral cells that had scant to a large amount of pale to strongly eosinophilic cytoplasm. The pleomorphic nuclei were apparently variable in shape, from small round hyperchromatic to very large vesicular forms. The cell boundaries were not clearly distinct. The multifocal immunolabelling of neoplastic cells for NSE, synaptophysin, GFAP, and ACTH appeared, whereas a few cells reacted with vimentin and S-100 and stained negative for other markers, which were also utilized for case 1. Histological and immunohistochemical findings led to identification of corticotroph adenocarcinoma in the pituitary gland.
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PMID:Cerebral neuroblastoma and pituitary adenocarcinoma in two budgerigars (Melopsittacus undulatus). 2231 97


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