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)

The effect of acetylcholine, 3,4-dihydroxyphenylethylamine, prostaglandin (PGE1), guanosine triphosphate (GTP), and divalent ions on adenylate cyclase activity in homogenates of ""differentiated" and malignant mouse neuroblastoma cells was studied. The sensitivity of adenylate cyclase to acetylcholine and 3,4-dihydroxyphenylethylamine markedly increased in adenosine cyclic 3:5-monophosphate-induced differentiated neuroblastoma cells. Although 3,4-dihydroxyphenylethylamine stimulated adenylate cyclase activity in malignant neuroblastoma cells, it failed to do so in X-irradiation induced differentiated cells. PGE1 and GTP stimulated adenylate cyclase activity in malignant and adenosine cyclic 3:5-monophosphate induced differentiated neuroblastoma cells to about the same level. GTP protentiated the PGE1 effect in differentiated concentrations of magnesium and manganese inhibited adenylate cyclase activity; this effect was more pronounced in differentiated cells than in malignant cells. Calcium stimulated adenylate cyclase activity in malignant and differentiated cells to about the same level. There was no significant difference in the values of Km and Vmax of neuroblastoma cells. This study shows that the sensitivity of adenylate cyclase to neurotransmitters and divalent ions (magnesium and manganese) and the sensitivity of PGE1 stimulated enzyme activity to GTP increase in adenosine cyclic 3:5-monophosphate-induced differentiated neuroblastoma cells. Therefore, we suggest that the reverse may be true during malignant transformation of nerve cells.
Cancer Res 1975 Jan
PMID:Effect of neurotransmitters, Guanosine triphosphate, and divalent ions on the regulation of adenylate cyclase activity in malignant and adenosine cyclic 3':5'-monophosphate-induced "differentiated" neuroblastoma cells. 16 67

Intravenous urography with total body opacification, and tomography as required, often give the most information toward evaluating abdominal masses in children. Ultrasonography is a noninvasive procedure which defines normal structures and differentiates cystic and solid tumors. The combination of these studies gives sufficient information about renal tumors to plan for possible surgery. Arteriography is not necessary for the diagnosis of Wilms' tumor, nor its surgical or medical management. Pseudotumor of the kidney is due to focal cortical hyperplasia. It can be diagnosed by nephrotomography, renal arteriography or renal scanning. The latter method is most accurate and has the lowest morbidity. Aortography is advisable in the evaluation of a patient with pheochromocytoma in an attempt to locate multiple tumors. Determining the extent of abdominal neuroblastoma by angiography and lymphangiography does not appear to influence the mode of therapy, not the survival rate; therefore, invasive diagnostic procedures do not appear to be indicated in neuroblastoma. Angiography is necessary in the evaluation of liver cancer. If one lobe is determined to be free of disease, lobectomy is a possible cure. Splenic cysts and choledochal cysts can be diagnosed by noninvasive methods such as ultrasonography or radioisotope scanning. Arteriography and percutaneous opacification are not necessary to make these diagnoses.
Cancer 1975 Mar
PMID:The evaluation of abdominal masses in children with emphasis on noninvasive methods. A roentgenographic approach. 16 41

5-(3,3-Dimethyl-1-triazeno)imidazole-4-carboxamide (NSC-45388) was administered to 46 children with various solid tumors which were resistant to conventional therapy. Two or more courses of NSC-45388 were administered to 13 of 18 children with neuroblastoma, seven of 11 children with rhabdomyosarcoma, three of four children with Wilms' tumor, one of three children with Ewing's tumor, and six of ten children with miscellaneous neoplastic disorders. Major toxic effects included nausea, vomiting, decreased hemoglobin level, thrombocytopenia, and leukopenia. A therapeutic regimen of 200-450 mg/m2/day for 5 consecutive days can be administered safely every 22 days. Objective responses were observed in three children with neuroblastoma and in one child with rhabdomyosarcoma. This drug has minimal but definite activity as a single agent in children with advanced neuroblastoma and rhabdomyosarcoma and should be evaluated further in combination therapy.
Cancer Chemother Rep
PMID:5-(3,3-Dimethyl-1-triazeno)imidazole-4-carboxamide (NSC-45388) in the treatment of solid tumors in children. 16 36

For establishment of a reproducible model of human neuroblastoma, 2 to 5 million of established neuroblastoma cell lines (SK-N-SH, SK-N-MC) were injected s.c. or i.p. into 20 nu/nu mice of a predominantly Swiss back-ground. Following latency periods of 8 to 21 days, tumors developed at the injection site and grew to 4-ml volumes within 3 weeks. Histologically, the tumors resembled the original metastases from which the tumors were derived; however, the SK-N-SH appeared to have evidence of morphological differentiation. When compared to monolayer culture, the heterotransplanted SK-N-SH tumor had decreased dopamine-beta-hydroxylase activity and elevated cyclic adenosine 3':5'-monophosphate phosphodiesterase activity. Activity of cyclic adenosine 3':5'-monophosphate phosphodiesterase in the transplanted SK-N-MC tumor was not appreciably different from the activity in the cultured cells. Serum dopamine-beta-hydroxylase levels in the mice bearing SK-N-SH tumor increased threefold. The SK-N-MC cultured cells lacked dopamine-beta-hydroxylase and did not alter existing serum levels in the SK-N-MC tumor-bearing mice. 67Ga injected i.v. was found to localize in the tumor after 24 hr. Human neuroblastoma in the nude mouse can be a reproducible and informative model for tumor pharmacology, screening, radionuclides, tumor localization and imaging, and investigating morphological differentiation.
Cancer Res 1975 Sep
PMID:Human neuroblastoma in nude mice. 16 65

The practical value of cytologic examination in the clinical management of children with cancer was determined by analyzing 2,363 cytologic specimens collected during a two year period. The specimens included cerebrospinal fluid, pleural and peritoneal effusions, urine and tracheal aspirates from 347 children with cancer. Malignant tumor cells were detected in 266 specimens obtained from 106 children with the following malignant neoplasms: leukemia 44/133, malignant lymphoma 13/64, soft tissue sarcoma 13/48, neuroblastoma 13/26, Wilms' tumor 4/18, malignant teratoma 4/13, osteogenic sarcoma 7/11, Ewing's sarcoma 2/10, brain tumor 5/6 and retinoblastoma 1/1. No malignant cells were detected in fluids from 18 patients with other tumors. The malignant cells were identified most ofter in spinal fluid, pleural and peritoneal effusions. Cytologic examination appears to be of value in the clinical management of children with cancer.
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PMID:Diagnostic value of cytologic specimens obtained from children with cancer. 16 27

A clone of neuroblastoma cells has been selected for its ability to survive and multiply at 40 degrees C. This temperature-resistant clone, like clones of neuroblastoma cells selected for resistance to dibutyryladenosine 3':5'-monophosphate (Bt2-Ado-3':5'-P) showed an increased tumorogenicity in animals and an increased saturation density at 37 degrees C. The Ado-3':5'-P-binding proteins and Ado-3':5'-P-dependent protein kinases from the temperature-resistant and non-resistant cells have been partially purified by chromatography on a DEAE-cellulose column. The Ado-3':5'-P-binding proteins from temperature-resistant cells were more sensitive to temperature than the binding proteins from non-resistant cells. After incubation of binding proteins from resistant cells at 37 degrees C, the specific activity of Ado-3':5'-P-binding to proteins was decreased about 50% and the apparent association constant (Ka) for Ado-3':5-p-binding was decreased from 7.4 X 10(7)M-1 to 4.4 x 10(7)M-1. There was no such decrease with binding proteins from non-resistant cells. A decrease in the activity of binding proteins from the temperature-resistant cells, but not of those from non-resistant cells, was also found when the proteins were stored at 2 degrees C. Treatment with 2-mercaptoethanol made binding proteins from the resistant cells less temperature-sensitive. In the absence of added Ado-3:5-P the protein kinase activity from the temperature-resistant cells was about 50% of the activity from non-resistant cells. Kinase activity was increased by addition of Ado-3:5-P and there was a greater increase with kinases from resistant cells. The maximum protein kinase activity was found in the presence of 10muM Ado-3':5'-P for the temperature-resistant cells and 0.1 muM Ado-3':5'-P for the non-resistant cells. The results indicate that the temperature sensitivity of Ado-3':5'-P-binding proteins, and the activity of protein kinase from cells selected for resistance to high temperature, are similar to those of cells selected for resistance to Bt2-Ado-3':5'-P. It is suggested that the temperature sensitivity of Ado-3':5'-P-binding proteins and the activity of Ado-3':5'-P-dependent protein kinases are involved in the regulation of malignancy and of cell growth at different temperatures.
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PMID:Temperature sensitivity of cyclic-adenosine-3':5'-monophosphate-binding proteins, activity of protein kinases and the regulation of cell growth. 17 35

Trigerminal ganglia of 4 adult albino mice of the NMRI outbred stock were examined by electron microscopy. In all animals, about 10% of the neurons contained intracisternal A particles. Isolated structures resembling intracisternal A particles could be detected in atleast 50% of the nerve cells and in a few Schwann cells. Budding at the cell surface and/or extracellular type-C particles were not observed. An intracerebrally transplanted mouse C1300 neuroblastoma was likewise studied. Most tumor cells exhibited large numbers of intracisternal A particles having the same ultrastructure as the particles in trigeminal neurons. In addition, budding and extracellular type-C particles were occasionally observed.
J Natl Cancer Inst 1975 Dec
PMID:Intracisternal A and C particles in mouse neurons: a thin-section study of normal trigeminal ganglion and C1300 neuroblastoma. 17 70

Dexamethasone stimulates type C virus production induced by iododeoxyuridine (IdUrd) from several murine cell lines: uninfected BALB cells, virally transformed nonproducer K-BALB cells, mouse neuroblastoma N-4 cells, and rat tumor XC cells. Dexamethasone also stimulates virus production from BALB cells newly infected by some murine leukemia or leukemia sarcoma viruses, from a murine myelogenous leukemic cell line (M-1) producing type C virus, from K-BALB(l) cells (K-BALB producing cells previously induced by IdUrd), and from K-BALB cells rescued by Rauscher leukemia virus. However, this stimulatory effect is not universal, since we observed that dexamethasone did not stimulate virus production from BALB cells newly infected by B-tropic virus, from S2CL3 cells producing N-tropic virus (a clone of spontaneously transformed BALB cells), from virus producing normal rat kidney cells, and from a mouse adrenal gland tumor Y-1 cell line chronically producing type C virus. Some estrogenic hormones that do not have any stimulatory effect on virus production from BALB or K-BALB cells induced by IdUrd stimulate virus production from normal rat kidney cells induced by IdUrd. When there is no stimulation of virus production in a cell system by steroid hormones, very often there is some inhibitory activity. Furthermore, we observed that in JLSV10 cells chronically producing Rauscher leukemia virus and in K-BALB cells newly infected by Rauscher leukemia virus, virus production is enhanced by dexamethasone when the cells are still producing a low titer of virus but is not enhanced when the cells are producing a high titer of virus.
Cancer Res 1976 Jun
PMID:A survey on the effect of steroid hormone on type C virus production from cultured murine cells. 17 41

Extracts were made from Walker 256 carcinoma, spontaneous rat mammary adenocarcinoma, Wilms' tumour, human neuroblastoma and human haemangioma. Chromatography of the extracts on Sephadex G-100 yielded four fractions, A, B, C and D. Injection of fractions B and C resulted in the growth of new capillaries in the subcutaneous fascia or rats. Controls, e.g. similar extracts of rat liver or human kidney, did not induce neovascularisation. The endothelium of newly-formed blood vessels contained many mitotic figures. A limitation of this method is that it is qualitative only. In order to develop a quantitative in vitro assay for a tumour angiogenesis factor (TAF), short-term primary cultures were initiated from adult rat brain white matter, as cells from such cultures were shown to be vascular in origin. Addition of fractions containing TAF (B and C) which were active in vivo failed to stimulate thymidine uptake by the cells. The possible reasons for this failure and the therapeutic potential of TAF in cancer control are discussed.
Int J Cancer 1976 May 15
PMID:Tumour angiogenesis factor (TAF) in human and animal tumours. 17 10

The binding of adenosine cyclic 3':5'-monophosphate (cyclic AMP) with soluble (100,000 X g supernatant), pellet, and total homogenate proteins from cyclic AMP-induced "differentiated" mouse neuroblastoma cells increased by about two-fold. The extent of binding with soluble proteins was higher than that with pellet proteins. The binding of cyclic AMP with soluble proteins from 5'-adenosine monophosphate-treated, serum-free medium-treated, sodium butyrate-treated, 6-thioguanine-treated, or X-irradiated neuroblastoma cells did not significantly change. When the soluble proteins containing bound cyclic [3H]AMP were filtered through a Sephadex G-25 column, the relative amount of protein-bound cyclic [3H]AMP in differentiated cells was greater than that in malignant cells, but the amount of free cyclic [3H]AMP was correspondingly less. The electrophoretic characteristics of cyclic AMP-binding proteins of differentiated and malignant cells were identical. There were two binding peaks, but the extent of binding at each peak was relatively high in differentiated neuroblastoma cells. An increase in cyclic AMP binding occurred 24 hr after treatment of neuroblastoma cells with prostaglandin E1. This increase was completely blocked by cycloheximide but not by actinomycin D. The binding was heat labile and sensitive to protease action. These data indicate that the increase in binding in differentiated cells is due to an elevation in the levels of binding proteins. The binding of cyclic AMP with soluble proteins from rat glial cells and mouse L-cells did not significantly change after treatment with prostaglandin E1 or an inhibitor of cyclic AMP phosphodiesterase. Cyclic AMP and guanosine cyclic 3':5'-monophosphate bind with the same proteins, but cyclic AMP has about 10-fold higher binding affinity than does guanosine cyclic 3':5'-monophosphate.
Cancer Res 1976 Jul
PMID:Binding of cyclic nucleotides with proteins in malignant and adenosine cyclic 3':5'-monophosphate-induced "differentiated" neuroblastoma cells in culture. 17 1


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