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)

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.
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PMID:5-(3,3-Dimethyl-1-triazeno)imidazole-4-carboxamide (NSC-45388) in the treatment of solid tumors in children. 16 36

Friend mouse erythroleukemia cells (T3c1-2 and its subline 5000) can be induced to synthesize hemoglobin after treatment with 1.5% (vol/vol) dimethylsulfoxide. When these cells are fused with nonerythroid cells (namely, mouse neuroblastoma or L cells) hemoglobin induction is extinguished. In order to determine if the nucleus of the nonerythroid cell is necessary for this extinction, fusions were performed between mouse erythroleukemia cells and enucleated neuroblastoma or L cells. Hemoglobin induction was reduced or eliminated in clones of these hybrids even after 6 months of continuous culture. These results suggest that the cytoplasm of nonerythroid cells contains factor(s) that extinguish hemoglobin inducibility in erythroleukemic cells and that this new phenotype can be inherited.
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PMID:Extinction of hemoglobin inducibility in Friend erythroleukemia cells by fusion with cytoplasm of enucleated mouse neuroblastoma or fibroblast cells. 26 3

Evidence suggests that nitric oxide (NO) may mediate, at least in part, excitotoxic effects of excessive N-methyl-D-aspartate (NMDA) receptor activation both in vivo and in vitro. In the present experiments, NMDA-induced excitotoxicity has been studied in CHP100 neuroblastoma cell cultures. Application of NMDA (0.25-1.5 mM) produced concentration-dependent cell death. These effects were antagonized by co-application of dizocilpine (MK801), a selective and non-competitive NMDA receptor complex antagonist. Protection from NMDA-induced lethal effects was also afforded by N omega-nitro-L-arginine methyl ester, a potent NO-synthase inhibitor, and by hemoglobin, a NO-trapping agent. In addition, substitution of L-arginine, normally present in the exposure solution with its D-isomer, abolished the cell death induced by the excitotoxin. In conclusion, the present experiments support the suggestion that excitotoxic effects induced by NMDA receptor stimulation involve L-arginine-NO pathway activation.
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PMID:Evidence that CHP100 neuroblastoma cell death induced by N-methyl-D-aspartate involves L-arginine-nitric oxide pathway activation. 128 60

Twenty of 109 children (age, one day to 14 years) with neuroblastoma studied over an eight-year period initially presented with orthopaedic complaints. Patients were grouped into four categories: hip pain, a nonspecific limp, limb weakness, or back pain. The largest group involved the hip, and their conditions were most often misdiagnosed as suppurative arthritis. The initial hemoglobin level was the most consistent laboratory finding that suggested malignancy. This anemia was contrasted to that found in 74 children diagnosed with septic arthritis of the hip that presented during the same period. The anemia in the children with neuroblastoma was much more pronounced; in retrospect, it could have suggested a malignant process early in the evaluation.
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PMID:Pediatric update #16. The orthopaedic presentation of neuroblastoma. 214 70

Accumulation of cyclic GMP in cultured rat lung fibroblasts was used to test the hypothesis that N1E-115 neuroblastoma cells produce an endothelium-derived relaxing factor (EDRF)-like activity. By using this assay, the production of an EDRF-like activity in homogenates and cytosolic fractions of N1E-115 neuroblastoma cells was observed. Detection of the activity required the presence of superoxide dismutase and was inhibited by hemoglobin. Production of the EDRF-like factor was dependent on L-arginine and NADPH. The apparent Km for L-arginine was 1.25 microM and the apparent Km for NADPH was 1.67 microM. The production of the EDRF-like activity was inhibited by the L-arginine analogs, NG-monomethyl-L-arginine and NG-nitro-L-arginine, with apparent Ki values of 1.0 and 0.3 microM, respectively.
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PMID:Production of an EDRF-like activity in the cytosol of N1E-115 neuroblastoma cells. 215 50

Anthracyclines such as Adriamycin (ADR) and daunomycin markedly inhibit cell growth in vivo and in vitro. These studies demonstrate that 30 microM hemin, which induces hemoglobin synthesis in human and murine erythroleukemia cells in culture, markedly decreases the cytotoxicity of ADR in a variety of hemopoietic cell lines (K562, HEL-1, MEL-745, HL-60, and U937) and in erythroid burst-forming cells from normal human marrow. Hemin failed to protect four of the five nonhemopoietic cell lines tested, including MCF-, breast adenocarcinoma cells, C-205 colon carcinoma cells, mouse 3T3 fibroblasts, and mouse kidney VERO cells. Hemin did protect human neuroblastoma IMP-32 cells from ADR cytotoxicity; however, this nonhemopoietic cell line undergoes dendrite formation in response to hemin induction. Cytofluorographic analysis of cellular ADR content and labeling studies with [3H]daunomycin demonstrated that hemin decreases the intracellular accumulation of these anthracyclines by more than 50% in K562 erythroleukemia cells. These studies indicate that small doses of hemin prevent intracellular accumulation of anthracyclines and thereby markedly reduce anthracycline toxicity to cells. Since this protective effect is observed preferentially with hemopoietic cells, it is possible that this finding could be exploited to protect the bone marrow from the cytotoxic action of anthracyclines during therapy for nonhemopoietic tumors.
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PMID:Prevention of anthracycline-induced cytotoxicity in hemopoietic cells by hemin. 370 75

Serum vitamin B12, serum and red cell folate and serum vitamin B12 binding proteins were determined in 18 patients with neuroblastoma, with ages ranging from 8 months to 14 years. A mean value of serum vitamin B12 level was slightly but not significantly lower than that of the normal subjects but all of them had serum vitamin B12 levels over 150 pg/ml. There was no relationship between serum vitamin B12 levels and hemoglobin, hematocrit or white cells. Transcobalamin I (TCI) was significantly increased resulting in slightly elevated UBBC and normal TBBC levels in these patients. This could be a compensatory mechanism for the low serum vitamin B12 by increasing the unsaturated vitamin B12 binding capacity of TCI. All these findings indicated that the status of vitamin B12 in patients with neuroblastoma was within the normal limits. Treatment of neuroblastoma by giving a high dose of vitamin B12 would therefore not give any direct therapeutic effect. Both serum and red cell folate concentrations were significantly lower in the group of patients. As only 2 out of 18 patients had low serum folate and none of them had red cell folate lower than the lower limit of normal subjects; therefore these patients were only in the state of negative folate balance.
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PMID:Folic acid, vitamin B12 and vitamin B12 binding proteins in patients with neuroblastoma. 378 6

A double-antibody radioimmunoassay for human neuron-specific enolase (NSE) was developed, using rabbit antiserum against the gamma subunit of enolase purified from human brain. Intra-assay variance was 3.8-5.1% and inter-assay variance 4.3-7.3%, and recovery of NSE added to normal serum was 100.2% on average. Normal serum NSE levels for 451 adults ranged from 3.6 to 10.8 ng/ml (mean 6.6 ng/ml). Antibodies raised against the gamma gamma enolase isozyme did not cross-react with the alpha alpha and beta beta isozymes at concentrations of 1,000 ng/ml, but showed a cross-reactivity of 41.5% (theoretically 50%) with the alpha gamma isozyme. It was also shown that hemolysis of 160 mg/dl hemoglobin can add 5.73 ng/ml of NSE to the true level. The coefficient of correlation between the radioimmunoassay and the sandwich enzyme immunoassay [1] was 0.99 (n = 21), and values determined by the RIA were about twice those obtained by the EIA. Serum NSE was abnormally high in 42 of 52 patients (80.8%) with small cell lung carcinoma, and in all 38 children with neuroblastoma.
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PMID:Radioimmunoassay development for human neuron-specific enolase: with some clinical results in lung cancers and neuroblastoma. 389 69

A 4 year-old child being treated for neuroblastoma developed erythroblastopenia. We used specific erythroid lineage markers (hemoglobin and spectrin) and in vitro erythroid colony assays to characterize this hematologic picture and discuss its relationships with the disease and its treatment.
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PMID:[Erythroblastopenia in a child during treatment of a neuroblastoma]. 391 40

Serum and tumor tissue of a patient with neuroblastoma contained an abnormal isoenzyme of lactate dehydrogenase (LDH; EC 1.1.1.27), which, on agarose gel electrophoresis, migrated between LDH-2 and LDH-3 with a mobility the same as that of the extra LDH isoenzyme found in normal human erythrocytes. On surgical removal of the tumor, the high total LDH activity (775 U/L) in the serum of the patient rapidly decreased to normal (70-220 U/L), and the abnormal LDH isoenzyme was no longer detected. The total LDH activity of the abnormal LDH isoenzyme per gram of hemoglobin in the tumor tissue was 26 times that of erythrocytes, suggesting that the abnormal isoenzyme originated mainly from the tumor cells themselves rather than the erythrocytes contained in the tumor tissue. This first report on the appearance of the abnormal LDH isoenzyme in a patient with neuroblastoma suggests that this abnormal LDH isoenzyme may have some significance as a marker enzyme for neurogenic tumors.
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PMID:Abnormal lactate dehydrogenase isoenzyme in serum and tumor tissue of a patient with neuroblastoma. 396 74


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