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)

Cyclophosphamide is used extensively to treat malignancies. A 5-year-old boy with stage IV neuroblastoma is described who developed a fatal syndrome of inappropriate antidiuretic hormone (ADH) secretion after high dose cyclophosphamide therapy.
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PMID:A fatal case of inappropriate ADH secretion induced by cyclophosphamide therapy. 47 99

Five patients with an unusual encephalopathy, possible secondary to measles virus infection, are described. Features common to these patients are: an existing chronic disease, neurologic deterioration 2 1/2 to 6 months after a measles infection, and death several weeks later. These events occurred when the chronic disease (e.g. leukemia or neuroblastoma) was in remission. That the measles virus was the causative agent is suggested only by finding in brain and extracranial tissues intracytoplasmic and intranuclear inclusions which contained measleslike particles. Additional clinical features seen in each of the five patients were: seizures, hypertension, and the inappropriate secretion of antidiuretic hormone.
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PMID:Encephalopathy following measles infection in children with chronic illness. 127 Nov 91

Insulin and various growth factors (epidermal growth factor (EGF), insulin-like growth factor, fibroblast growth factor, and transforming growth factor alpha), which fail to modify the resting [Ca2+]i in PC12 rat pheochromocytoma and SKNBE human neuroblastoma cells when administered alone, became capable of inducing [Ca2+]i increases when administered a few (4-20) min after another agent, bradykinin. The latter peptide, working through a B2 receptor, caused hydrolysis of polyphosphoinositides and a large, biphasic [Ca2+]i transient (an initial (1-2 min) spike, originated primarily from intracellular stores, followed by a steady-state elevation dependent on Ca2+ influx). Priming by bradykinin of the growth factor effects was quickly dissipated by the addition of a B2 blocker. Activation of other receptors coupled to polyphosphoinositide hydrolysis: muscarinic and purinergic (in PC12 and SKNBE cells); bombesin and vasopressin receptors (in Swiss 3T3 cells), was without effect in priming. Bradykinin-primed, growth factor-induced [Ca2+]i rises in PC12 cells appeared after a 20-30-s delay; they were relatively small, but persistent; their concentration dependence was similar to that of other effects of the factors; and they included both release of Ca2+ from intracellular stores and stimulation of Ca2+ influx, preceded (in PC12 cells) by a transient increase of polyphosphoinositide hydrolysis. Thus the effect of growth factors (possibly dependent on the tyrosine kinase activity of their receptors) consisted in the reinforcement of the transmembrane signaling at B2 receptors. This is the first direct demonstration of a [Ca2+]i rise induced by insulin and insulin-like growth factor-I, and of such an effect of EGF in cell types endowed with a small number of specific EGF receptors.
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PMID:Reinforcement of signal generation at B2 bradykinin receptors by insulin, epidermal growth factors, and other growth factors. 253 35

Dopamine inhibits and serotonin stimulates adenylate cyclase activity in a neuroblastoma X Chinese hamster brain explant cell line (NCB-20). The inhibition of cyclic AMP accumulation by dopamine was blocked by pretreatment of the cells with pertussis toxin. Carbachol and bradykinin stimulated the accumulation of water-soluble inositol phosphates whereas thyrotropin-releasing hormone, vasopressin, neurotensin, and phenylephrine were without effect. Dopamine and serotonin had no significant effect on carbachol-induced phosphoinositide hydrolysis or the levels of the parent lipids within the membrane. Forskolin induced a much larger stimulation of cyclic AMP than did serotonin, and caused an increase in the levels of phosphatidylinositol-4-phosphate and phosphatidyl inositol-4,5-bisphosphate in the cell membrane.
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PMID:Activation of dopamine receptors does not affect phosphoinositide turnover in NCB-20 cells. 303 93

A 28-year-old man with the chronic syndrome of Inappropriate antidiuretic hormone secretion and hypertension was found to have an olfactory neuroblastoma. We demonstrated evidence of elevated circulating arginine vasopressin levels, significantly elevated arginine vasopressin and vasopressin neurophysin levels in the tumor extract, and immunohistochemical staining for arginine vasopressin and vasopressin neurophysin in the tumor cells. The patient's clinical syndrome, including hypertension, resolved following subtotal removal of the tumor and radiation therapy. This study identified olfactory neuroblastoma as a definite cause of ectopic arginine vasopressin secretion causing the syndrome of inappropriate antidiuretic hormone secretion.
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PMID:Chronic syndrome of inappropriate antidiuretic hormone secretion and hypertension in a patient with olfactory neuroblastoma. Evidence of ectopic production of arginine vasopressin by the tumor. 375 13

A 26-year-old woman with the syndrome of inappropriate antidiuresis demonstrated complete recovery following the resection of an olfactory neuroblastoma. Tissue arginine vasopressin levels by radioimmunoassay, immunohistochemical staining of the tissue arginine vasopressin, postoperative normalization of plasma arginine vasopressin levels, and the clinical resolution are evidence in support of a neurally derived tumor being the direct source of neurosecretion of arginine vasopressin rather than neurohypophyseal secretion or secretion from non-neural tissues, as reported to date in the etiology of the syndrome of inappropriate antidiuresis.
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PMID:Neurosecretion of arginine vasopressin by an olfactory neuroblastoma causing reversible syndrome of antidiuresis. 377 95

Twenty years ago it was demonstrated that angiotensin II (Ang II) acts on the brain, which results in an elevation of blood pressure. Ten years later, reninlike activity was discovered in the brain of the rat and dog, which gave rise to the concept of an endogenous brain renin-angiotensin system. In the periphery, the kidney, liver, and lungs work in unison to produce Ang II. Evidence for brain renin, substrate, converting enzyme, and angiotensins is reviewed. New data indicate that the enzyme system for the synthesis of Ang II within the brain may in fact be contained in the cell. All the components for a renin-angiotensin system have now been found in neuroblastoma/glioma cell lines and Ang II is present in primary cell culture of rat brain neurons. The significance of angiotensin in the brain for hypertension is that it may be a stimulus for vasopressin release and sympathetic activation, which can maintain high blood pressure. In the spontaneously hypertensive rat, there is evidence of increased brain angiotensin. Also, experiments with angiotensin-converting enzyme inhibitors show that blockade of brain angiotensin production leads to a long-lasting lowering of blood pressure. The activity of the inhibitors in part appears to be directly on the brain.
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PMID:New evidence for brain angiotensin and for its role in hypertension. 630 29

A patient with a four-year history of unexplained hyponatremia was seen with recurrent nasal discharge and was found to have a typical olfactory neuroblastoma. The clinical laboratory diagnostic studies suggested that the patient's sodium deficiency was secondary to the syndrome of inappropriate antidiuretic hormone. Subsequent resection of the neoplasm led to resolution of the hyponatremia, suggesting that a (tumor-associated) humoral factor, such as vasopressin or a vasopressinlike substance, was responsible for the electrolyte disturbance. A search of the literature disclosed one previous case of vasopressin-secreting nasal neuroblastoma.
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PMID:Hyponatremia secondary to olfactory neuroblastoma. 687 Jun 50

Circulating angiotensin is produced by the action of renin from the kidneys on circulating angiotensinogen. There are other renin-angiotensin systems in various organs in the body, and recent observations raise the intriguing possibility that angiotensin II is produced by a totally intracellular pathway in the juxtaglomerular cells, the gonadotrops of the anterior pituitary, neurons, in the brain, salivary duct cells, and neuroblastoma cells. Circulating angiotensin II levels depend in large part on the plasma concentration of angiotensinogen, which is hormonally regulated, and on the rate of renin secretion. Renin secretion is regulated by an intrarenal baroreceptor mechanism, a macula densa mechanism, angiotensin II, vasopressin, and the sympathetic nervous system. The increase in renin secretion produced by sympathetic discharge is mediated for the most part by beta-adrenergic receptors, which are probably located on the juxtaglomerular cells. Hyperthyroidism would be expected to be associated with increased renin secretion in view of the increased beta-adrenergic activity in this condition, and hypothyroidism would be associated with decreased plasma renin activity due to decreased beta-adrenergic activity. Our recent research on serotonin-mediated increases in renin secretion that depend on the integrity of the dorsal raphe nucleus and the mediobasal hypothalamus has led us to investigate the effect of the pituitary on the renin response to p-chloroamphetamine. The response is potentiated immediately after hypophysectomy, but 22 days after the operation, it is abolished. This slowly developing decrease in responsiveness may be due to decreased thyroid function.
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PMID:Thyroid hormones and renin secretion. 704 Aug 92

A patient with a nasal neuroblastoma was found to have hypertension and severe hyponatraemia. Radiotherapy and cytotoxic chemotherapy were ineffective in reducing the size and vascularity of the neoplasm. Assay of tumor tissue post mortem revealed high levels of arginine vasopressin. The possibility of vasopressin formation to be added to the better known potential hormonal secretory activities of neuroblastomas.
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PMID:Nasal neuroblastoma secreting vasopressin. A case report. 726 Aug 47


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