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)

Adrenal imaging was performed using magnetic resonance (MR) was in 100 patients who had no clinical or biochemical evidence of adrenal abnormality and in 19 patients with 24 adrenal lesions (adenoma in 5, hyperplasia in 2, metastasis in 5, (lung cancer in 1, hepatoma in 4) adrenal cancer in 1, pheochromocytoma in 3, neuroblastoma in 3). Normal adrenal glands showed intermediate intensity between muscle and liver, and were detected in over 90% of cases on T1-weighted images (T1-weighted SE, inversion recovery). Adenomas and hyperplasias had the same intensity as normal glands. Medullary masses showed extreme hyperintensity on T2-weighted images and could be differentiated from cortical masses. Neuroblastomas were detected as hyperintense tumors with intratumoral hemorrhage and necrosis on T2-weighted MR images. Metastatic adrenal tumors from lung cancer were hyperintense on T2-weighted images, while metastasis from hepatoma showed low intensity on the same pulse sequence. In diagnosing adrenal metastasis, we must compare and contrast the tumor intensity and structure with those of the primary lesions. MR is considered a useful modality in characterizing adrenal tissue.
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PMID:[Magnetic resonance imaging of the adrenal gland]. 179 51

We report 93 patients with catecholamine producing tumors that were analyzed at the Hormone Laboratory of the Institute of Cardiology. They are 75 pheochromocytoma patients and 18 children with neuroblastoma. Fluorimetric methods were used to measure urinary and plasma catecholamines on neuroblastoma and pheochromocytoma patients. Dopamine high excretion (mean value 2889 micrograms/24 hs), was constantly observed in the neuroblastoma children as were adrenaline and noradrenaline in the benign and malignant pheochromocytoma patients. The mean values for the malignant tumours were 53 for adrenaline and 1436 micrograms/24 hs for noradrenaline. Structural and biochemical differences of the catecholamine producing tumours are reflected on the clinical manifestations which are observed in the patients bearing such neoplasms.
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PMID:[Catecholamine-producing tumors]. 179 8

We have reported previously that platelet-activating factor (PAF) interacts with the neuronal cell line NG108-15 (neuroblastoma X glioma hybrid) and the pheochromocytoma cell line, PC12. PAF acts on these cells by raising levels of intracellular free calcium ions. In the present report, we extend these studies. PAF induced the vesicular release of adenosine 5'-triphosphate (ATP) from PC12 cells in a dose-dependent manner. The PAF-induced ATP release was inhibited by the PAF antagonists, CV-3988 and CV-6209, and the calcium antagonist prenylamine. The relevance of the interaction of PAF with neuronal cells was investigated further by using brain synaptosomal preparations and primary cortical and neostriatal cells. Nanomolar concentrations of PAF induced calcium transients in aequorin-loaded synaptosomal preparations, and cortical and neostriatal cells were sensitive to the action of PAF. The possible physiological and pathophysiological roles of PAF in brain function are discussed.
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PMID:Calcium ion mobilization in neuronal cells induced by PAF. 181 10

The role of diagnostic [131I/123I]metaiodobenzylguanidine (*I-MIBG) scintigraphy in the management of pheochromocytoma and neuroblastoma is established, but for other neural crest tumors is less defined. Radiopharmaceutical therapy of all these tumors with large activities of suitably radiolabeled MIBG is a compelling concept. In the five years since the first workshop on 131I-MIBG therapy held in Rome, the initial therapeutic promise appears to have been maintained for neuroblastoma and pheochromocytoma. A significant fraction of patients enter partial remission but complete remission is rare and relapse frequent. To date, experience with other neuroendocrine tumors and the use of 125I in place of 131I remains limited. Many promising areas remain incompletely explored. These include development of appropriate in vitro cultures and animal models, basic pharmacological mechanisms, drug interactions, macro- and microdosimetry and human clinical trials. The latter includes determining dose-limiting toxicity of 131I- and 125I-MIBG, treatment of patients at earlier times or stages of disease, optimal integration with other therapy including granulocyte-stimulating factor and marrow transplant rescue from otherwise limiting myelotoxicity. Progress to date has been slow and painstaking, but nevertheless significant, while the future holds both challenges and promise.
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PMID:Summary, conclusions, and future directions of [131I]metaiodobenzylguanidine therapy in the treatment of neural crest tumors. 182 58

We have presented a case of sporadic medullary carcinoma of the thyroid with documentation of localization of tracer 131I-MIBG within the primary neoplasm. A review of the nuclear medicine literature of localization techniques for MCT demonstrates that 131I-MIBG, while an excellent choice for diagnosis of pheochromocytoma and neuroblastoma, produces low yield and unpredictable concentration in other neural crest apudomas, including MCT. A low incidence of true-positive results with 131I-MIBG uptake and a high incidence of false-negative results make this radiopharmaceutical a suboptimal choice for diagnostic studies, but a potentially promising one as a therapeutic agent.
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PMID:Iodine 131 metaiodobenzylguanidine scintigraphy of medullary carcinoma of the thyroid. 185 77

This report describes a retrospective study of 23 patients with incidentally discovered adrenal masses. Two patients with subclinical cortisol secretion developed adrenal insufficiency after removal of benign adenomas. Another patient, who probably harbors an asymptomatic pheochromocytoma, developed a hypertensive crisis when a mass was palpated during aortic vascular surgery. Twelve patients underwent surgery. Seven benign adenomas, an angiomyolipoma, and a cyst were removed. Three patients had malignant masses that include an angiosarcoma, an adrenal adenocarcinoma, and a congenital neuroblastoma. We conclude that hormones, especially cortisol, may be secreted in subclinical amounts by incidentally discovered masses. We recommend a concise laboratory evaluation that includes an overnight dexamethasone suppression test. Based on our interpretation of the literature, we believe masses greater than 3 cm in size should be removed. Patients who do not undergo surgery should have computed tomographic scans repeated for one year and should be reassessed periodically for the development of hormone secretion.
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PMID:Incidentally discovered adrenal masses. 192 30

Human neuroblastoma SK-N-SH-SY5Y (SY5Y) and rat pheochromocytoma PC12 cells are model cell lines used in the study of nerve growth factor (NGF) effect. The effects of NGF are initiated by binding to cell surface receptors (NGFR). The amino acid sequence for NGFR has been deduced based on the identification of a single gene for NGFR. However, there are two kinds of NGF binding activities and several reported molecular weights of NGFR. We report here on the demonstration of NGFR-like proteins from PC12 and SY5Y cells by sequential lectin chromatography, reverse-phase HPLC, and SDS-PAGE analysis of immunoprecipitates obtained with NGFR-specific monoclonal antibodies. For both human and rodent NGFR, there was a tendency for the higher molecular-weight species of NGFR-like proteins to be eluted in more hydrophobic fractions. Also, the expression of different species of NGFR could be modified by treatment with retinoic acid (RA). These results are consistent with the hypothesis that the different molecular species of NGFR may result from the generation of a truncated form of NGFR, the presence of sugar residues on the NGFR protein, dimer formation between NGFR, or the association of NGFR with a receptor-associated protein.
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PMID:Reverse-phase high-performance liquid chromatography of nerve growth factor receptor-like proteins identified with monoclonal antibodies. 196 79

A method for the purification of full-length nerve growth factor receptor (NGFRc) using membranes from three different cell lines was developed. We emphasized recovery of NGFRc that retained specific binding activity. Lipids were required to preserve binding activity during solubilization and throughout the purification procedure. Phosphatidylcholine was used for this purpose. Lectin affinity chromatography followed by high-resolution anion-exchange chromatography was used, and a 3000-fold increase in specific binding activity was obtained for NGFRc from human melanoma A875 membranes. Seven percent of the original binding activity was recovered as pure NGFRc. NGFRc binding activity eluted at 0.35 M NaCl in anion-exchange chromatography of solubilized A875, rat pheochromocytoma PC12, and human neuroblastoma MC-IXC membranes. Eight and three percent of the original binding activity were recovered as highly enriched NGFRc from membranes prepared from PC12 and MC-IXC cells, respectively. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of highly enriched, 125I-labeled NGFRc revealed several protein species. After chromatography, identification of proteins as NGFRc was verified both by immunoprecipitation using receptor-specific monoclonal antibodies and by covalent cross-linking to 125I-NGF using N-hydroxysuccinimidyl-4-azidobenzoate. Predominantly, NGFRc was recovered as a mixture of species of 80 and 160-180 kDa. Small amounts of larger species as well as smaller species were observed, consistent with minor amounts of receptor aggregation and proteolysis occurring during purification.
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PMID:Two-step purification of full-length nerve growth factor receptor and maintenance of receptor-specific binding activity. 196 21

Little is known about the prevalence and significance of ras gene activation in neural crest tumors such as neuroblastomas, pheochromocytomas, and medullary thyroid cancers (MTCs). Therefore, we analyzed DNA from 10 human neuroblastoma cell lines and 10 primary human pheochromocytomas for activating mutations in N-ras, H-ras, and K-ras. We also studied DNA from 24 primary neuroblastomas and 10 MTCs for N-ras mutations. ras genes were analyzed by direct sequencing of specific DNA fragments amplified by the polymerase chain reaction. With the exception of the SK-N-SH cell line, the examined ras gene sequences were normal in all the neuroblastomas, pheochromocytomas, and MTCs tested. A single point mutation was identified at codon 59 (GCT(ala)----ACT(thr)) in one N-ras allele in an SK-N-SH subline. Interestingly, this mutation is different from the activating codon 61 mutation which resulted in the initial identification of N-ras from SK-N-SH DNA. Therefore, we analyzed the sequences of earlier passages and sublines of the SK-N-SH cell line, but mutations at codon 59 or 61 were not detected, suggesting that neither mutation was present in the primary tumor. Our results indicate that N-ras mutations may occur spontaneously during in vitro passage of cell lines but rarely, if ever, occur in primary neuroblastomas, pheochromocytomas, and MTCs. In addition, we have not found H-ras or K-ras mutations in any neuroblastoma cell line or primary pheochromocytoma.
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PMID:Low frequency of ras gene mutations in neuroblastomas, pheochromocytomas, and medullary thyroid cancers. 199 49

Radiodinated meta-iodobenzylguandine (MIBG) is increasingly used for the diagnosis and targeted radiotherapy of neuro-adrenergic tumors. We have investigated various conditions for specific tumor loading and prolonged retention of this radiopharmaceutical in poorly differentiated SK-N-SH neuroblastoma and highly differentiated PC-12 pheochromocytoma cells. At a constant value of drug concentration x incubation time, short incubations were superior to protracted incubations for maximal cell loading. This effect was most pronounced in the SH-N-SH neuroblastoma cells. In highly differentiated pheochromocytoma cells, the levels of MIBG storage remained high and unchanged during incubations up to 46 hr in label-free medium, while primitive SK-N-SH cells lost 40-50% of accumulated drug by diffusion. In PC-12 cells, susceptibility of stored MIBG to exocytotic release induced by acetylcholine or K+ was similar to that of natural norepinephrine (NE) and prevented by the Ca(++)-channel blockers verapamil and nifedipine. Conversely, granule-poor SK-N-SH cells were insensitive to exocytotic release of MIBG. Uptake and retention capacities were minimally impaired by an externally delivered radiation dose of 5 Gy to mimic the radiobiological effect of 131I-MIBG in tumors. In pre-irradiated cultures, drug uptake was even stimulated, probably due to enrichment in non-proliferating cells. An autoradiographic comparison of the (sub)cellular distributions of 3H-norepinephrine and 125I-MIBG showed that routine conditions of cell fixation and sample processing do not yield reliable results regarding localization of MIBG.
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PMID:Pharmacokinetics and intracellular distribution of the tumor-targeted radiopharmaceutical m-iodo-benzylguanidine in SK-N-SH neuroblastoma and PC-12 pheochromocytoma cells. 204 5


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