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 prolonged exposure to ammonia on fluid-phase, receptor-mediated, and adsorptive (non specific) endocytosis in cultured neuroblastoma (Neuro-2a) cells were studied using fluorescein-labeled dextran, concanavalin A conjugated with fluorescein isothiocyanate, and cationized ferritin as tracers. Ammonia treatment increased the rate of endocytosis of cationized ferritin as well as the number of cell elements involved in the process. Moreover, the number of cytoplasmic components containing acid phosphatase activity was also found to increase following ammonia treatment. In contrast, flow-cytometric analyses showed that, under experimental conditions, exposure to ammonia did not alter the intralysosomal pH and had little effect on the fluid-phase and receptor-mediated endocytosis of fluorescein-labeled dextran and concanavalin-A fluorocrome, respectively.
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PMID:Effects of prolonged exposure to ammonia on fluid-phase, receptor-mediated, and adsorptive (non specific) endocytosis in cultured neuroblastoma cells. A flow-cytometry and cytochemical study. 244 72

As neuroblastoma, the most common solid tumour in childhood, may contain all the constituents of the catecholamine biosynthesis cascade, some of these constituents may be produced in excess in a varying mixture reflecting the wide variability in expression of differentiated features of the tumour. We have measured plasma levels of norepinephrine (NE), epinephrine (E), dopamine (DA) and 3,4-dihydroxyphenylalanine (DOPA), and plasma activities of dopamine beta-hydroxylase (DBH) and aromatic L-amino acid decarboxylase (ALAAD) in 18 patients with neuroblastoma, in 13 at various times during the course of their disease. Activities of serum lactic dehydrogenase (LDH), serum levels of ferritin (FER) and neuron-specific enolase (NSE), and urinary vanilmandelic acid (VMA) were also determined. NE, E and DBH were found not to reflect tumour activity. In untreated active neuroblastoma DOPA or ALAAD (10 out of 10) or both (six out of 10) were clearly elevated. In all 13 patients where samples were obtained during chemotherapy, ALAAD activities fell within the normal range, while DOPA decreased more slowly. During relapse, DOPA and, especially, ALAAD, rapidly increased; in all six patients who had a relapse both DOPA and ALAAD were elevated. In complete remission (eight patients), ALAAD was normal in all patients, but DOPA remained elevated in the one patient who later experienced a relapse. Our preliminary conclusion is that combined measurements of plasma ALAAD and DOPA may be useful markers for neuroblastoma activity at diagnosis, but even more so in indicating residual disease (DOPA) and in the early detection of relapse (ALAAD).
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PMID:Combined measurements of plasma aromatic L-amino acid decarboxylase and DOPA as tumour markers in diagnosis and follow-up of neuroblastoma. 250 83

Elevated serum ferritin levels have been reported in patients with malignant tumors and especially in those with neuroblastoma or breast carcinoma. The presence of the iron-storing compounds ferritin and hemosiderin in these tumors was therefore investigated. Some neuroblastomas, mostly of patients with advanced stages of disease, contained numerous ferritin particles randomly dispersed in the cytosol. Iron was also seen as ferritin clusters in the cytosol and as ferritin or hemosiderin in siderosomes. Morphometric study of ferritin particles as well as of the features of the siderosomes enabled the identification of two major types of iron-containing cells. In breast carcinoma most electron-opaque iron was found in siderosomes, with few ferritin particles being in the cytosol. The study points toward the hitherto unrevealed ultrastructure of cytosiderosis in neoplasms, the biological importance of which remains largely unknown.
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PMID:Iron and neoplasia: ferritin and hemosiderin in tumor cells. 279 88

Serum ferritin is known to be one of the tumor markers for neuroblastoma. Serum ferritin is elevated in most children with neuroblastoma who are in stages III or IV, but it is not elevated in those in stage I or II. It has also been observed that iron load caused by blood transfusion shows a greater effect on serum ferritin levels than tumor activity due to neuroblastoma. Thus, serum ferritin increases in a linear fashion in children given repeated blood transfusions but the levels increase exponentially in children who have bulky neuroblastomas. Thus, serum ferritin values must be interpreted with caution in patients with advanced stages of neuroblastoma who inevitably require blood transfusions. The authors propose that the pretransfusion and posttransfusion serum ferritin values be in comparison with other tumor markers such as urinary VMA, urinary HVA, and neuron specific enolase. The serum ferritin level should not be used as a sole indicator of tumor activity in neuroblastoma.
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PMID:Serum ferritin in stage IV neuroblastoma. 318 16

Patients with widespread neuroblastoma (NB) frequently have elevated serum ferritin levels, and recently anti-NB effects of the iron chelator deferoxamine (DFO) have been reported. We have investigated the effect of DFO on human bone marrow NB cells from two untreated children with Evans Stage IV disease. DFO treatment caused dose- and time-dependent cytotoxicity of NB cells, with maximal killing at exposure to 50 micron DFO for 72 h. Cytotoxicity was prevented by cotreatment with stoichiometric amounts of iron salts and reversible by removal of DFO or addition of iron salts within 48 h of treatment. Additionally, DFO inhibited clonal growth of human bone marrow NB cells in methylcellulose in a time- and dose-dependent manner. These effects were also prevented by cotreatment with iron salts. Thus, DFO has potent antitumor effects on human NB cells which appear to be related to iron deprivation. DFO should be considered for further preclinical evaluation as an anti-NB agent.
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PMID:Deferoxamine inhibition of human neuroblastoma viability and proliferation. 319 93

Spontaneous maturation of Stage IVS neuroblastoma has been postulated as a mechanism for its favorable prognosis, but this has rarely been documented pathologically. We report on a patient with congenital Stage IVS neuroblastoma who had extensive subcutaneous and bone-marrow involvement. Serial photographs, biopsies, and vanillomandelic acid determinations documented the tumor's initial progression which was followed by spontaneous maturation and involution of the patient's disease over a 6-year period. No cytotoxic therapy was administered. Favorable biologic prognostic factors were documented, including tumor DNA and protein analyses for N-myc amplification or overexpression and analysis for serum neuron-specific enolase and ferritin. Implications for management and therapy of Stage IVS neuroblastoma are discussed with reference to this case and the recent literature.
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PMID:Complete pathologic maturation and regression of stage IVS neuroblastoma without treatment. 329 64

The ultrastructure of neuroblastoma was examined using unstained sections so that ferritin particles could be identified by the electron density of their iron cores. Ferritin and hemosiderin were found in ten of 11 neuroblastomas that were examined when the patients first presented. The study was therefore expanded to an additional group of children, including some diagnosed by noninvasive procedures and given chemotherapy before the excision of their tumors. In this second group 12 of 20 specimens contained ferritin and hemosiderin in variable amounts. In both groups there was a tendency for patients with advanced disease to have increased amounts of iron compounds in the tumor tissue (Stage III and particularly Stage IV). Most Stage IV patients also had elevated serum ferritin levels. However, based on the available heterogenous material, no absolute relationship could be established between age, disease stage, tumoral storage iron, and the level of serum ferritin. The presence of ferritin in neuroblastoma may be linked to the elevated serum ferritin levels and may be implicated in tumorigenesis.
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PMID:Neuroblastomas contain iron-rich ferritin. 336 71

Serum ferritin frequently is elevated in patients with neuroblastoma. Isoferritins extracted from neuroblastoma tumors and cells in culture show a wide range from basic (rich in L subunit) to acidic (rich in H subunit) isoferritins. Total ferritin is a combination of basic and acidic isoferritins. Forty-four serum samples from 25 patients with neuroblastoma were measured for basic and acidic isoferritin levels by radioimmunoassay using antibodies to liver (basic) ferritin and HeLa (acidic) ferritin. Normal ranges for basic and acidic serum ferritins were 7 to 142 ng/ml (median, 30 ng/ml) and 0 to 12 ng/ml (median, 3.4), respectively. Basic ferritins in the 44 neuroblastoma sera ranged from 0 to 1460 ng/ml, and acidic ferritins, 0 to 40 ng/ml. Sera with high levels of acidic ferritins always had increased basic ferritins. Thus, acidic/basic ferritin ratios were nearly constant, less than 0.3 in all sera. There was a significant linear correlation between basic and acidic isoferritins (r = 0.833). These results suggest that neuroblastoma tumors produce both basic and acidic isoferritins and release them into circulation. However, there is no acidic ferritinemia not accompanied by basic ferritinemia. Therefore, the commercial assay for basic isoferritin currently seems sufficient for clinical prognostic purposes.
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PMID:Basic and acidic isoferritins in the sera of patients with neuroblastoma. 340 87

Serum ferritin is present in two forms--a glycosylated form that results from active secretion by cells and a nonglycosylated form that is directly released by damaged cells. Glycosylated ferritin binds to concanavalin A (Con A) through the glucose and/or mannose residues of the molecule. Patients with neuroblastoma frequently present at diagnosis with abnormally elevated levels of serum ferritin. The ferritin levels will, however, return to normal with clinical remission, suggesting that the tumor is the origin of the elevated ferritin. With the use of a Con A binding assay, an investigation was made as to whether the increased levels of serum ferritin at diagnosis in neuroblastoma patients resulted from active secretion by the tumor or were the consequence of direct release of ferritin from damaged tissue. Serum samples were collected at diagnosis from 36 children with neuroblastoma and from 16 normal healthy subjects. Tissue ferritins were purified from normal human liver, placenta, HeLa cells, human neuroblastoma, and hepatoma cells grown in culture. Serum and tissue ferritins were measured before and after binding with Con A. Sixty-three percent of serum ferritin from neuroblastoma patients and 66% of serum ferritin from normal subjects were bound to Con A, suggesting that they were glycosylated and were likely to have been secreted. On the other hand, only 28% of tissue ferritin were bound to Con A. Furthermore, most patients showed abnormally elevated levels of serum ferritin, and 63% of these ferritins were bound to Con A. These results are compatible with the hypothesis that much of the elevated ferritin in sera of patients with neuroblastoma seen at diagnosis is the result of secretion of ferritin by the tumor.
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PMID:Source of increased ferritin in neuroblastoma: studies with concanavalin A-sepharose binding. 345 40

Known prognostic factors in neuroblastoma were analyzed in 124 children to determine which were independent and which were most useful in predicting outcome. The following factors were analyzed: age, sex, stage of disease, serum neuron-specific enolase (NSE), serum ferritin, E-rosette inhibition, urinary catecholamines, and histologic type according to the criteria of Shimada. Estimates of survival were calculated using the method of Kaplan and Meier. The overall survival for 124 patients was 60% at 2 years. There were significant differences in survival by pathology, age, NSE, ferritin, vanilmandelic acid (VMA): homovanillic acid (HVA) ratio, and stage. There was a strong association among NSE, age, stage, and ferritin. Using the recursive partitioning approach, it was possible to subdivide patients into three groups (based on diagnostic values of ferritin, age, and stage) with a good, intermediate, and poor prognosis and estimated 2-year survival of 100%, 62%, and 19%, respectively. Further analysis could not be done because of small numbers in the subgroups, but the results suggest that combinations of age, stage, serum ferritin, and histologic type may be able to define two populations: favorable with 80% + 2-year survival and unfavorable with less than 20%.
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PMID:Prognostic factor in neuroblastoma. 356 48


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