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)

Two glycolytic enzymes, PHI and LDH, have been evaluated in 18 children affected by leukemia or solid tumors: 11 patients had just initiated therapy, 3 patients were about to initiate therapy, while 4 patients were out of therapy. The analysis of the data obtained has shown a good correlation with the course of the disease: we have found values above the normal range in patients with a favorable course of the disease (bone marrow relapse or CNS involvement in leukemic children; relapse or metastasis in solid tumors) almost always before it was possible to demonstrate by clinical and laboratory studies the inhanchement of tumoral cells growth. This was true in all patients except two children affected by neuroblastoma, who were in a favorable immunological status (presence in the serum of free specific antibodies), and who were out of therapy. In these patients the abnormal high values of PHI were interpretated as an index of necrotic phenomena of micrometastasis of tumor cells induced by specific committed T-lymphocytes. Values of PHI and LDH in the normal range were found in patients whose disease demonstrated a favorable course. The AA. suggest the introduction of these enzymatic parameters which may be a useful index of the efficacy of the chemotherapy in the follow-up of oncologic patients.
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PMID:[Behavior of phosphoisomerase and lactate dehydrogenase in pediatric oncological pathology]. 23 78

Total serum LDH activity and isoenzyme distribution were studied in children with neuroblastoma at the time of hospital admission. The total LDH was determined in 26 cases, and 20 (77%) of them showed elevation of its activity. On the other hand, in 9 of these 26 cases, the isoenzyme distribution was determined along with the total LDH. All 9 cases, 4 of them with normal total LDH activity, showed an abnormal isoenzyme pattern with a percentage increase in the intermediate fractions (malignant pattern). The results suggest the usefulness of the determination of serum LDH isoenzymes as a screening procedure in children with malignant tumors including neuroblastoma.
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PMID:Serum lactate dehydrogenase isoenzyme pattern in neuroblastoma. 97 80

The toxic effect of the Parkinsonism-producing neurotoxin MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) was investigated using a neuronal cell culture system, namely, neuroblastoma X glioma hybrid NG 108-15. The cells were able to metabolize MPTP into its active metabolite MPP+ (1-methyl-4-phenylpyridinium ion) and to convert its derivative, 2'-methyl MPTP, to the corresponding pyridinium ion. Degenerative changes were observed in NG 108-15 cells when they were examined with a phase-contrast microscope following exposure to MPTP, MPP+, or 2'-methyl MPTP. These compounds also caused an increased leakage of LDH from the treated cells. An enhanced release of [14C]adenine nucleotides was observed from treated cells which were prelabeled with [14C]adenine. The cell death as indicated by the leakage of LDH and the release of adenine nucleotides was markedly reduced in the presence of a high concentration (25 mM) of glucose in the medium. MPTP and MPP+ induced a drastic depletion in cell ATP content prior to cell death. The ATP depletion was also reduced by the presence of a high concentration of glucose. In contrast, tetraphenylborate, a lipophilic anion, highly potentiated the ATP depletion and the subsequent cell death induced by MPTP. Thus, ATP depletion could be a major factor in MPTP-induced neuronal cell death.
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PMID:MPTP-induced ATP depletion and cell death in neuroblastoma X glioma hybrid NG 108-15 cells: protection by glucose and sensitization by tetraphenylborate. 199 18

Evidence is presented that LDH virus infection of mice results in drastic changes in several immune activities. Serum IFN titer and splenic NK activity are increased during the acute phase of infection. NK stimulation is mediated by IFN-alpha,beta since injection of an antibody against murine IFN-alpha,beta is able to abolish the effect. IL-2 production is inhibited throughout the study period following injection of LDH virus (14 days), although a partial recovery is observed during the second week. Similarly, IL-2 receptor expression and MLC responsiveness are suppressed. This suppression lasts for 2 and 7 days respectively after injection. Addition of recombinant IL-2, but not of indomethacin, to the MLC cultures restores the proliferation rate. Not only proliferation but also cytotoxic cell generation in MLC is diminished during the first week after LDH virus injection. Again, this response is normalized at day 14. Additional observations indicate that LDH virus is present in murine neuroblastoma. This explains some of the previously described effects of this tumor on the cellular immune system of the host.
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PMID:Cellular immunity changes caused by LDH virus: analogy with observations of neuroblastoma-bearing mice. 244 3

Twenty neuroblastoma and 4 nonneuroblastoma patients were studied by 131I-MIBG imaging. The primary tumor was detected in 89% of patients (8/9) before therapy. Bone marrow metastasis was also visualized in 4 of the 8 patients with primary positive scan. True negative results were obtained in 4 nonneuroblastoma patients. After therapy, of 10 tumor-bearing patients, eight showed positive scans and 9 of 12 lesions (75%) were visualized. The accuracies of presence or absence of neuroblastoma were compared between 131I-MIBG imaging and several tumor markers. The accuracies before and after therapy were as follows: 131I-MIBG imaging; 92% (12/13), 88% (15/17), serum NSE; 80% (4/5), 93% (13/14), serum LDH; 92% (11/12), 76% (13/17), urinary VMA; 54% (7/13), 56% (9/16), and urinary HVA; 77% (10/13), 56% (9/16). It appears that 131I-MIBG imaging is useful for both locating and excluding neuroblastoma. In addition, 131I-MIBG imaging appears to be the most efficient diagnostic and follow up study for neuroblastoma when it is combined with measurements of serum NSE.
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PMID:[Clinical evaluation of I-131 metaiodobenzylguanidine (MIBG) imaging in suspected neuroblastoma]. 281 Sep 11

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

The specific activity of lactate dehydrogenase (LDH; EC 1.1.1.27) is induced two-fold by l-norepinephrine (NE) in C6TK- rat glioma cells, but not in NA mouse neuroblastoma cells or various other nonglial cells. Previous reports have shown that the induction is mediated by cyclic AMP (cAMP) and possibly protein phosphorylation, and that it requires RNA and protein synthesis. To study the block to LDH induction in nonglial cells, we hybridized C6TK- cells with NA cells and isolated a hybrid clone in which LDH is inducible by NE. Mouse and rat LDH from hybrid cells were separated by electrophoresis and quantitated by two independent methods, and it was found that mouse and rat LDH were induced equally when cells were exposed to NE. The results suggest that inducibility of LDH is not determined by a cis-acting control at the gene level, but rather by the presence or absence of an earlier component in the cAMP-mediated induction system, and that the induction system acts indiscriminately on all active LDH gene copies in the cell.
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PMID:Induction of both rat and mouse lactate dehydrogenase in hybrids between inducible rat glioma and uninducible mouse neuroblastoma cells. 625 3

Neuroblastoma (NB) is a common tumor of childhood, presenting "unique" characteristics: i.e., different prognosis in relation to age, high rate of metastases at diagnosis, capacity of spontaneous regression, strong immunogenicity. The embryologic derivation of NB has been recently clarified: NB derives from the embrional sympathetic nervous tissue; its enzymatic activity is determined mainly by environmental factors. A number of clinical and laboratory aspects influence the fate of children with NB: extention of disease and age are the most important, followed by site of primary, histology, pattern of metastatic spread, immunologic characteristics. Among laboratory tests, many are correlated with the clinical course: urinary excretion of sympathetic amines, serum levels of ferritin, C3 complement fraction, LDH, IgM, neurono-specific enolase. In the recent years the development of monoclonal antibodies techniques has greatly improved. In NB, a number of membrane molecule determinants have been discovered, against which specific monoclonal antibodies can be profitably directed for diagnostic and therapeutic purposes. NB cells grow in vitro in the soft agar system; in this assay resistance and sensitivity of tumor cells can be tested with sufficient accuracy and may predict drug effect in vivo. Therapy of disseminated neuroblastoma is unsatisfactory till now. Promising techniques include autologous or allogeneic bone marrow infusion following supralethal chemotherapy, and administration of substances, such as retnoids, able to promote neuroblastoma cells differentiation in vivo.
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PMID:[Neuroblastoma]. 639 28

Prognosis of neuroblastoma is primarily dependent on the stage of disease. While stages 1 to 3 show a survival rate of 94 to 66%, stage 4 has a survival rate below 20%. The most important prognostic factor is the extent of disease. Age, LDH, resectability of primary tumor, cytologic and molecular parameters are defined to have a prognostic impact as well. A stage- and risk-adapted therapy of neuroblastoma needs a thorough assessment of all these factors.
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PMID:[Neuroblastoma: diagnosis and therapy]. 748 25

The prognosis for patients with neuroblastoma is related to the age and stage at time of presentation, as well as to the presence or absence of biological markers such as N-myc amplification and the degree of DNA ploidy. However, previous studies have shown that neuroblastoma in the thoracic site also is a favorable prognostic indicator, in that children with mediastinal neuroblastoma have a better survival rate, regardless of age or stage at time of presentation. This study was designed to evaluate the biological differences between thoracic and nonthoracic neuroblastoma with respect to N-myc amplification, DNA index as a measure of DNA ploidy, serum lactate dehydrogenase levels, and serum ferritin levels. Patients enrolled in the Pediatric Oncology Group study protocols for neuroblastoma were evaluated retrospectively, and log-rank analysis allowed the impact of each biological variable on survival to be determined for each cohort of patients. There were 1,335 neuroblastoma patients in the data base; 227 had thoracic-site neuroblastoma. Through analysis, it was apparent that patients with thoracic neuroblastoma have better survival rates than do their nonthoracic counterparts (P < .0001), and they are less likely to have N-myc amplification (P = .001), more likely to have an LDH level of less than 1,500 (P < .0001), and usually have a DNA index of greater than 1 (P < .003). Both thoracic and nonthoracic patients have low serum ferritin levels (86% of thoracic versus 83% of nonthoracic patients).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Biological variables in thoracic neuroblastoma: a Pediatric Oncology Group study. 773 54


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