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)

Binding of type C neurotoxin (C1 toxin) from Clostridium botulinum (strain Stockholm) to neuroblastoma cell lines was studied by using biotinylated anti-toxin antibody and avidin-biotinylated peroxidase complex. The neurotoxin bound with high efficiency to mouse neuroblastoma (NS-20Y and NIE-115) cells and to hybridomas of rat glioblastoma and mouse neuroblastoma (NG108-C15) cells. The toxin bound little to human neuroblastoma, rat astrocytoma, and nonneural cell lines. Binding of the neurotoxin to NG108-C15 cells was inhibited by gangliosides (GT1b and GM1) and by monoclonal antibodies (CA-12 and C-9), although inhibition was not complete. Sequential preincubation of C1 toxin with GT1b and CA-12 caused complete inhibition. A Scatchard plot of binding of 125I-labeled C1 toxin to NG108-C15 cells showed a hyperbolic curve. Monoclonal antibody CA-12 but not C-9 neutralized the lethal activity of the toxin toward mice. Only C-9 clearly inhibited toxin binding to GT1b. These results suggest that NG108-C15 cells have at least two kinds of receptors for C1 toxin. From the results of binding tests with neuraminidase-, pronase-, and trypsin-treated NG108-C15 cells, the chemical nature of the high-affinity site was presumed to be a glycoprotein containing sialic acid. GT1b may have an important role in low-affinity sites.
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PMID:Binding of Clostridium botulinum type C neurotoxin to different neuroblastoma cell lines. 253 34

The case of a 48-year-old male patient is reported in whom a primary malignant cerebral neoplasm was cured by its neurosurgical removal and by postoperative radiotherapy and chemotherapy. Initially, from the results of the examination of frozen and paraffin section, the tumour was considered to be a glioblastoma multiforme. Electronmicroscopy, immunohistochemistry and review of the light microscopy of the original biopsy sample after his death by suicide four-and-a-half years later showed the neoplasm to have been a primary cerebral neuroblastoma rather than a glioblastoma. The diagnosis of glioblastoma multiforme, which depends upon multiple non-specific microscopic findings, such as necrosis, abnormal blood vessels, anaplasia and the pleomorphism of tumour cells, often is imprecise. Our experience underlines the need for comprehensive neuropathological studies of malignant cerebral neoplasms, including transmission electronmicroscopy and immunohistochemistry. This is of particular importance in view of the dismal prognosis of glioblastoma multiforme and of the palliative, rather than curative, treatment programmes that frequently are indicated for this tumour. The value of our report is to demonstrate that a cerebral neuroblastoma, which potentially is curable, may be mistaken easily for a glioblastoma-even by competent neuropathologists.
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PMID:High-grade cerebral neuroblastoma: a case study. 254 39

The combined effects of Acyclovir [9-(2'-hydroxyethoxymethyl)guanine; ACV] and human interferon-alpha (IFN-alpha) on replication of the herpes simplex virus type I (HSV-1) were determined in human neural cell lines, neuroblastoma (IMR), glioblastoma (118MGC), and glioma (U251MG). HSV-1 grew well in all these cells, with final yields of more than 1 x 10(6) PFU/ml. In terms of virus-yield reduction, ACV was found to be highly effective in IMR, moderately effective in U251MG, but ineffective in 118MGC. By contrast, IFN-alpha reduced the virus yield significantly in 118MGC and in U251MG, but did not in IMR. Combined application of ACV and IFN-alpha strongly inhibited the virus replication in all three cell lines with various degrees of synergism or additive effect. These results were also confirmed by immunofluorescent examinations. The sensitivity of HSV-1 to ACV or IFN-alpha was found to be different among the three different cell types. By combining the two agents, the virus growth was strongly suppressed in all the cells. These results suggest the importance of combination therapy for severe type of herpes simplex encephalitis in clinical practice.
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PMID:Combined effects of acyclovir and human interferon-alpha on herpes simplex virus replication in cultured neural cells. 255 47

To determine whether the amplification of the proto-neu oncogene (also called c-erbB-2) plays a role in tumorigenicity, we previously generated an NIH 3T3 transfectant (DHFR/G-8) that carried the amplified proto-neu gene. The DHFR/G-8 cells exhibited normal morphology. Their growth curve was similar to that of NIH 3T3 cells but was different from that of the B104-1 cell, and NIH 3T3 transfectant that carries the activated neu oncogene. When injected into nude mice, B104-1 cells produced tumors within 2 weeks, whereas the DHFR/G-8 cells did not produce tumors until 3 months after injection, and the NIH 3T3 cells did not produce any tumors even after 3 months. The tumors produced by the injection of the DHFR/G-8 cells were excised and grown in culture. The cells derived from the tumors were of transformed morphology and highly tumorigenic. The DNAs from the tumor cells were transfected into NIH 3T3 cells. The transfection resulted in foci on the NIH 3T3 monolayer. Southern analysis indicated that the foci derived from the transfection contained the neu gene. Using oligonucleotides as probes, the neu gene in the foci was found to carry a single-point mutation identical to the one previously found in the rat neuroblastoma and glioblastoma induced by the ethylnitrosourea. We conclude that the DNA region encoding the transmembrane domain of neu is a hot spot for converting the proto-neu gene into an activated oncogene and that amplification of the proto-neu gene facilitates mutation of the hot spot.
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PMID:Amplification of the proto-neu oncogene facilitates oncogenic activation by a single point mutation. 256 34

By fusion of mouse NS1 myeloma cells with splenocytes from a BALB/c mouse immunized with human melanoma cells, an IgG1 monoclonal antibody, designated as 140.72, was produced. By the mixed hemadsorption antibody binding assay, 140.72 was shown to react with 17 of 20 melanoma cell lines and with 5 of 14 carcinoma cell lines. This antibody also reacted with 3 of 3 normal melanocyte cultures in much lower titers. It did not react with any of 35 other normal and malignant lines, including neuroblastoma, glioblastoma, sarcoma, teratoma, fibroblast, and lymphoid cell lines. Absorption with fresh melanoma and carcinoma homogenates confirmed the results of direct tests. Fetal reactivity of antibody 140.72 was determined by positive absorption with 10 of 11 tissue homogenates derived from different fetuses of 10-16 weeks' gestation. The reactivity of this antibody was completely removed by absorption with a highly purified preparation of carcinoembryonic antigen (CEA) derived from a colon carcinoma. The antigenic activity was detected in the culture medium of reactive cell lines. Immunoprecipitation analyses of melanoma and carcinoma cells indicated that the antigenic determinant recognized by antibody 140.72 is on a glycoprotein with an apparent molecular weight of 95,000-150,000 common to both serologically reactive cell types. Additionally, a 200,000-molecular-weight glycoprotein corresponding to the CEA molecule was detected only on the reactive carcinoma cells. These data confirmed previous findings obtained with polyclonal anti-CEA antisera for the existence of shared CEA-related antigenic determinants on human carcinomas and melanomas and provided additional molecular characterization of these glycoproteins. Further characterization of the molecules bearing the antigenic determinant recognized by antibody 140.72 should be performed with a view to exploring its potential in the immunodiagnosis and immunotherapy of patients with melanoma.
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PMID:Monoclonal antibody recognizing human melanoma-carcinoma cross-reacting oncofetal antigen epitopically associated with carcinoembryonic antigen. 258 73

Based on the two mutation hypothesis in the development of retinoblastoma, loss of heterozygosity (LOH) of specific chromosome has been implicated in the presence of tumor suppressor gene. Studies on the LOH in different types of tumors revealed that LOH of each chromosome might play a different role in the multistep process of carcinogenesis: LOH of some chromosomes may play an etiological role in the development of some tumors, while that of other chromosomes or the same chromosome in other tumors, may play a role in the progression of tumors. LOH of chromosome 13 is an example for the former cases, and the latter cases involve LOH of chromosome 17 in colorectal carcinoma and osteosarcoma, chromosome 10 in glioblastoma, chromosome 1 in neuroblastoma and malignant melanoma, and chromosome 11 in breast carcinoma. These studies indicates that the progressive or concerted LOH could be a measure of the highly malignant or metastatic potentiality. However, it should be borne in mind that, especially in polyploid tumors, LOH also occurs as a random event following the polyploidization-segregation process.
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PMID:[Loss of heterozygosity in the progression of tumors]. 267 92

FK 973, a new substituted dihydrobenzoxazine, was obtained by chemical modification of a novel antibiotic which was isolated from the fermentation products of streptomyces sandaensis No. 6897. FK 973 had cytotoxic effects against in vitro cultured human and murine glioma cells. The concentration of FK 973 required to inhibit cell growth by 50% was 0.06-5 micrograms/ml, after 2-day exposure of this drug against human glioblastoma (ONS-6, 12, 23, and ONS-12/ACNU), human medulloblastoma (ONS-76, 81), human neuroblastoma (ST), and murine glioblastoma (RSV-M glioma). FK 973 showed antitumor efficacy in the meningeal gliomatosis models by RSV-M glioma cells. The median survival time (MST) of models treated by FK 973 (i.t.) was 30 days. However, the MST of control group was 23 days. In the in vitro neurotoxicity test, FK 973 proved to be slightly more toxic than ACNU and MTX, but it had no crucial problems, compared with ADM.
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PMID:[Antitumor efficacy of FK 973 on malignant glioma cells]. 275 17

Transforming growth factor (TGF)-beta 1 is a polypeptide that is assumed to play a fundamental role in the growth of both normal and neoplastic cells. TGF-beta 2 is a closely related polypeptide, originally described as glioblastoma cell-derived T cell suppressor factor (G-TsF) due to its immunosuppressive activity. Expression of the genes for TGF-beta 1 and G-TsF/TGF-beta 2 was examined in tumor cells and was found to be different in several cell lines and tissues that were tested. Whereas two glioblastoma cell lines expressed both TGF-beta 1 and G-TsF/TGF-beta 2 mRNA, one melanoma and neuroblastoma cell lines showed only TGF-beta 1 mRNA which in the case of the neuroblastoma required cycloheximide treatment for its detection. The coordinate expression of the genes for TGF-beta 1 and G-TsF/TGF-beta 2 in glioblastoma was not paralleled by secretion of both polypeptides as only G-TsF/TGF-beta 2 but not TGF-beta 1 was identified in supernatants of glioblastoma cells. These data provide evidence for a post-transcriptional level of regulation for production of the two forms of TGF-beta. As mRNA for G-TsF/TGF-beta 2 was also identified in fresh surgically removed human glioblastoma tissue, G-TsF/TGF-beta 2 may also be secreted within the tumor in vivo. Unlike glioblastoma, human fetal brain tissues or adult brain specimens studied did not express detectable levels of TGF-beta mRNA. Impaired cell-mediated immunity is an established finding in patients with glioblastoma. Secretion of G-TsF/TGF-beta 2 by tumor cells in vivo may contribute to decreased immune surveillance for tumor development, as well as neovascularization of the tumor tissue.
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PMID:Immunosuppression and transforming growth factor-beta in glioblastoma. Preferential production of transforming growth factor-beta 2. 280 98

The relationship between cell surface sialylation and platelet-activating activity was studied in two tumor cell lines of human origin, the SKNMC neuroblastoma line and the U87MG glioblastoma line. Their platelet-activating activity was evaluated in two different experimental systems, one that measures platelet aggregation and the other that quantifies platelet thrombus formation on vascular subendothelium under flow conditions. Our results demonstrate that, for the SKNMC line, the loss of 30% of surface sialic acid induced a significant reduction in its platelet-activating capacity. Upon recultivation desialylated SKNMC cells did not regenerate surface sialic acid and did not restore their initial values of platelet aggregation and platelet thrombus formation. Conversely, removal of 35% sialic acid from the surface of U87MG cells did not affect their pattern of platelet activation in either system tested. These results demonstrate that there is a correlation between cell surface sialylation and the capacity of SKNMC cells to activate platelets. The lack of effect of desialylation on U87MG-induced platelet activation indicates that different surface components may be the modulators of the interactions of these tumor cells with platelets. Our results support the hypothesis that heterologous mechanisms regulate platelet-tumor cell interactions and that tumor cell sialic acid may be only one of the aspects involved in such interactions.
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PMID:Cell surface sialylation of two human tumor cell lines and its correlation with their platelet-activating activity. 288 Jun 61

A defective subacute sclerosing panencephalitis (SSPE) virus which had been passaged in human embryonic lung cells was transferred to cultures of three neural cell types: neuroblastoma, oligodendroglioma and glioblastoma. The growth characteristics of the virus in these cells were essentially similar to those in non-neural cells. On the other hand, a marked difference in neurovirulence was noticed for the virus grown in neural cells when examined by intracerebral inoculation into mice. The virus passaged in neuroblastoma and oligodendroglioma cells showed high neurovirulence, inducing an acute encephalitis, whereas the virus passaged in human embryonic lung cells and that in glioblastoma cells did not show neurovirulence. These results suggest that the virus recovered its neurovirulence after passage in certain human neural cells.
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PMID:Growth of defective subacute sclerosing panencephalitis viruses in human neural cells and their neurovirulence in mice. 298 73


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