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)

Heat shock-induced alterations in protein synthesis and the cytoskeleton of two mammalian cell types have been investigated. A hyperthermic treatment of 30 min at 43 degrees C causes an accumulation of heat shock proteins (HSPs). The apparent molecular weights of HSPs of Reuber H35 hepatoma cells and of N2A neuroblastoma cells are 28 000, 65 000, 68 000, 70 000, 84 000, 100 000 D and 68 000, 70 000, 84 000 and 100 000 D respectively. Hyperthermia induces the disruption of microfilaments in hepatoma cells. Microtubules and intermediate filaments (vimentin and cytokeratin) remain intact. In neuroblastoma cells microfilaments remain intact whereas microtubules become disorganized after heat shock. As a result vimentin is found as a perinuclear aggregate. These cells were still able to synthesize heat shock proteins after pretreatment with cytoskeleton disrupting drugs such as dihydroxycytochalasin B and colchicine. Therefore it is concluded that the alterations in the cytoskeleton observed after the heat treatment are unlikely to be the cause of heat shock protein synthesis. Our results suggest that these heat shock-induced alterations in the cytoskeleton can be considered as a part of the heat shock response.
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PMID:Studies on a possible relationship between alterations in the cytoskeleton and induction of heat shock protein synthesis in mammalian cells. 242 73

Interferon-gamma-induced tryptophan metabolism of human macrophages was compared to ten human neoplastic cell lines of various tissue origin and to normal dermal human fibroblasts. Tryptophan and metabolites were determined in supernatants of cultures, after incubation for 48 h, by high-performance liquid chromatography with ultraviolet and fluorescence detection. With the exception of two cell lines (Hep G 2, hepatoma and CaCo 2, colon adenocarcinoma) in all of the ten other cells and cell lines tryptophan degradation was induced by interferon-gamma. Five of these ten formed only kynurenine (SK-N-SH, neuroblastoma; T 24, J 82, bladder carcinoma; A 431, epidermoid carcinoma; normal dermal fibroblasts), three formed kynurenine and anthranilic acid (U 138 MG, glioblastoma; SK-HEP-1, hepatoma; A 549, lung carcinoma). Only one line, A 498 (kidney carcinoma) showed the same pattern of metabolites as macrophages (kynurenine, anthranilic acid and 3-hydroxyanthranilic acid). Interferon-gamma regulated only the activity of indoleamine 2,3-dioxygenase. All other enzyme activities detected were independent of interferon-gamma, as shown by the capacity of the cells to metabolize L-kynurenine or N-formyl-L-kynurenine. Increasing the extracellular L-tryptophan concentration resulted in a marked induction of tryptophan degradation by macrophages. Contrarily, a significant decrease of the tryptophan degrading activity was observed when the extracellular L-tryptophan concentration was increased 2-fold with SK-N-SH, T 24 and J 82, 4-fold with A 431 and A 549 and 10-fold with U 138 MG and SK-HEP-1. The activity was unaffected by extracellular L-tryptophan with dermal fibroblasts and A 498. Though interferon-gamma was the most potent inducer of tryptophan metabolism, interferon-alpha and/or -beta showed small but distinct action on some of the cells. In all cells which reacted to interferon-gamma by enhanced expression of class I and/or class II major histocompatibility complex antigens tryptophan degradation was also inducible. These results demonstrate that induction of indoleamine 2,3-dioxygenase is a common feature of interferon-gamma action, that the extent of this induction is influenced by extracellular L-tryptophan concentrations and that indoleamine 2,3-dioxygenase is the only enzyme in the formation of 3-hydroxyanthranilic acid from tryptophan which is regulated by interferon-gamma.
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PMID:Characteristics of interferon induced tryptophan metabolism in human cells in vitro. 250 Sep 76

A panel of seven murine monoclonal antibodies reactive with human hepatocellular carcinoma (HCC) cell line, SK- HEP-1, resulted in the definition of four distinct antigen systems, designated HB4, HB5, HB1 and HJ2. HB4 antigen was found to be expressed specifically on HCC cell lines and fresh HCC specimens but not on normal liver. Immunoprecipitation tests suggest that the HB4 epitope may be a heat-stable carbohydrate determinant on a high molecular mass molecule. HB5 antigen was found to have less-restricted expression on a panel of normal adult tissues and on melanoma, astrocytoma, sarcoma, neuroblastoma and epithelial cancer cell lines. In fetal and adult liver, HB5 antigen localized to bile canaliculi and ducts. Under reducing conditions, three mAbs detected a Mr 140,000 glycoprotein using lysates of [125-I], [3-H]-glucosamine and [35-S]-methionine labeled SK-HEP-1 cells. Under non-reducing conditions an additional component of greater than Mr 200,000 was also detected. HB1 antigen was found on almost all monolayer cell lines and not on most cultured suspension cells. This antigen was also detected on cultured HCC cells inoculated into nu/nu mice. Immunoprecipitation experiments revealed that the HB1 antigen is a bimolecular complex with an Mr 170,000 alpha chain and Mr 130,000 beta chain under non-reducing conditions, and three subunits of Mr 140,000, Mr 30,000 and Mr 130,000 under reducing conditions. Two antibodies reacted with epitopes on the alpha chain. HJ2 antigenic determinant is a heat-stable component which could not be immunoprecipitated. This most widely expressed antigen was found in secreted form in many of the cells and tissues examined. These antibodies introduce new antigens which may serve as useful markers for the diagnosis, classification and investigation of HCC and other liver diseases.
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PMID:Serological analysis and biochemical characterization of monoclonal antibodies defining antigens of human hepatocellular carcinoma. 255 3

By restriction fragment length polymorphism (RFLP) analysis, it was found that loss of heterozygosity (LOH) at three different chromosomal loci, 3p, 13q, and 17p, occurs simultaneously in nearly 100% of small-cell lung carcinomas (SCLC). This was observed even in stage I tumors and an untreated tumor, and it occurred prior to NMYC amplification. The common region of LOH on chromosome 3p was 3p14-24.1, and this region was also frequently lost in carcinoma of the uterine cervix (100% at D3S2 on 3p14-21) as well as renal cell carcinoma (56% at ERBA beta on 3p22-24.1), suggesting the presence of tumor suppressor gene(s) for these cancers in this region. On chromosome 13, LOH was observed commonly in the region between 13q12 and 13q22, including the RB locus on 13q14, and normal RB protein was not detected in any of 9 SCLC cell lines by immunoprecipitation analysis. The common region of LOH on chromosome 17 was 17p13 and is the same as that in colon carcinoma and osteogenic sarcoma. Since LOH is supposed to unmask the recessive mutation of tumor suppressor gene in the remaining allele, these results may imply that at least six genetic alterations are necessary to convert a normal cell into a fully malignant cancer cell in SCLC. RFLP analysis was performed on several other types of human cancers, including carcinoma of the uterine cervix, neuroblastoma, hepatocellular carcinoma, pheochromocytoma, and stomach cancer to determine the chromosomal loci of putative tumor suppressor genes in each tumor. Chromosomal loci showing frequent LOH were different among these tumors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Multiple genetic alterations in small-cell lung carcinoma. 257 37

Preproenkephalin A (PPA) mRNA expression was studied by Northern blot and in situ hybridization in cell lines (rat glioma C6, rat hepatoma HTC, human neuroblastoma IMR32, mouse neuroblastoma NS20Y, rat fibroblast FR3T3, human bladder carcinoma EJ, human vulva carcinoma A431, myelocytic leukemia HL60, rat adrenal carcinoma Y1) and in brain tumours (implanted C6 cells). C6 glioma in cell culture, as well as in brain tumours, expressed high levels of PPA mRNA as compared to the caudate nucleus of the rat brain. EJ and FR3T3 cell lines also expressed the PPA mRNA, which was not detectable in A431, Y1, NS20Y, IMR32, HTC, HL60 cell lines as well as in the rat liver. This observation provides an interesting model to study the mechanisms by which the malignant transformation can induce in glial cells the derepression of a gene which is usually expressed in neurons or in neuron-like cells.
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PMID:Expression of the preproenkephalin A gene in tumor cells and brain glioma: a northern and in situ hybridization study. 273 83

We have isolated a heme protein from canine midbrains that possesses potent peroxidase activity. This enzyme catalyzes the oxidation of dopamine to neuromelanin in the presence of H2O2. We have further shown that the isolated peroxidase possesses potent cytotoxic activity in the presence of superoxide or H2O2 and Cl-. The enzyme possesses an endogenous NAD(P)H oxidase activity that can promote the cytotoxic activity by virtue of its production of superoxide. Other enzymes such as dihydroorotate dehydrogenase and galactose oxidase, which produce O2- and H2O2, respectively, are also effective in promoting the cytotoxic activity of the brainstem peroxidase. Although rat erythrocytes were routinely used as the target cell, other cell types, including rat hepatoma and mouse neuroblastoma cells, are also susceptible to the toxic action of the peroxidase. The cytotoxic action of the brainstem peroxidase is dramatically enhanced by kainic acid and is significantly enhanced by Mn2+, whereas dopamine was found to be a potent inhibitor of the cytotoxic activity. Based on these findings, we postulate a central role for the brainstem peroxidase in dopamine metabolism as well as in the biochemical and anatomical changes associated with Parkinson's disease.
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PMID:Neuromelanogenic and cytotoxic properties of canine brainstem peroxidase. 302 61

A total of 452 cases of childhood malignant solid tumors were treated over the last twenty years at the National Children's Hospital. These included 175 cases of neuroblastoma, 64 cases of Wilms' tumor, 65 cases of malignant lymphoma, 45 cases of soft tissue sarcoma, 31 cases of hepatoma, 20 cases of malignant teratoma, 17 cases of testicular tumor, 7 cases of ovarian tumor and 28 cases of other forms of malignant solid tumor. Bone metastasis was observed in 62 of 175 cases of neuroblastoma, 3 of 64 cases of Wilms' tumor, one of 65 cases of malignant lymphoma, 4 of 45 cases of soft tissue sarcoma, one case of pulmonary blastoma and one case of osteogenic sarcoma, giving a total occurrence of bone metastasis in 72 of the 452 cases. The main sites of bone metastasis in neuroblastoma were the skull (61.4%), femur (56.8%), orbit (27.3%) and spine (22.7%). The average values of serum calcium and alkaline phosphatase activity showed no significant difference. The patients with bone metastasis were treated with a combination of radiation therapy and intensive chemotherapy, resulting in temporary improvement. The survival of patients with stage IV neuroblastoma with bone metastasis was worse than that of similar patients without bone metastasis.
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PMID:[Bone metastasis of malignant solid tumors in childhood]. 303 15

The data on 26 patients with solitary metastatic lesions arising in cortical bone were studied. Nineteen patients were over 50 years of age. In 19 patients, the cortical metastasis was the first indication of the presence of a primary malignant condition. In seven cases, cortical metastases developed in patients with a known primary tumor. The primary tumors involved were eight renal cell carcinomas, six bronchogenic carcinomas, two carcinomas of the gastrointestinal tract, one osteosarcoma, one neuroblastoma, one melanoma, one hepatoma, one carcinoma of the breast, and one thyroid carcinoma. In four cases, the primary tumor remained unknown. A metastatic origin should be considered in the differential diagnosis of an osteolytic lesion arising in the cortex of a long bone, especially in older patients and in patients with a known primary malignant condition. The cortical bone metastases encountered in this study did not originate solely from bronchogenic carcinoma, as has been reported by other authors. Cortical metastases are probably less rare than has been hitherto assumed.
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PMID:Cortical bone metastases. 317 2

In order to investigate the function of heat shock protein 84 (hsp84) we have isolated the protein from mouse neuroblastoma cells and raised a polyclonal antiserum which was affinity-purified. The specificity of the antibody was established by immunoprecipitation and immunoblotting. Immunofluorescence studies revealed both a cytoplasmic and a nuclear localization of hsp84 in five different mammalian cell lines (mouse neuroblastoma cells and fibroblasts, rat hepatoma cells, and HeLa cells). In none of the five cell lines were found significant differences in the total cellular levels of hsp84 before and immediately after a heat shock (4 h, 42 degrees C) by immunoblot quantification. Furthermore after heat shock the fluorescence of anti-hsp84-labeled nuclei was increased relative to that of the surrounding cytoplasm. The increased fluorescence disappeared upon reincubation at 37 degrees C. The heat-induced increase in contrast between cytoplasmic and nuclear fluorescence could be explained by a combination of three factors: (a) decrease in nuclear projection area, (b) increase in cytoplasmic projection area, and (c) translocation of hsp84. The contribution of these factors to the increase after heat treatment was different for the cell lines.
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PMID:Localization and quantitation of hsp84 in mammalian cells. 329 74

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


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