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 various stages of divergent neuroepithelial differentiation were studied in the solid transplants of a transplantable mouse testicular teratoma (OTT-6050) maintained in both ascitic and solid forms. They included: a) areas of undifferentiated medullary epithelium corresponding to the rare human medulloepithelioma; b) areas of neuroblastic differentiation corresponding to neuroblastoma, with more mature neuronal differentiation corresponding to ganglioneuroma or, when mixed with glial elements, to ganglioglioma; and c) more mature neuroglial areas resembling astrocytoma, oligodendroglioma or ependymoma, as well as more primitive areas corresponding to ependymoblastoma. In tissue culture using collagen-coated coverslips, astrocytic differentiation was found in the outgrowth zone after 15 days, confirmed by immunofluorescence with antibodies to an astroglia-specific protein. In organ culture systems, glial components, including ependymal structures, were preserved in tumor explants, and astrocytic differentiation, as expressed by glial fiber formation, was increased after 4 to 6 weeks in vitro. No neuronal differentiation was demonstrable, however. The neuroepithelial component of this experimental teratoma may provide a model for the study of neoplastic neuroepithelial differentiation.
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PMID:An experimental mouse testicular teratoma as a model for neuroepithelial neoplasia and differentiation. I. Light microscopic and tissue and organ culture observations. 16 76

Tumors of the human nervous system (neuroblastomas, an ependymoma, a medulloblastoma, and a Schwannoma) obtained during surgery have been cultured organotypically by the method of Wolff. The tumors retained characteristic morphology, organization and patterns of behavior in vitro, and one neuroblastoma gave rise to a growing long-term culture. Long-term organotypic culture, where maintenance of tissue organization and growth occur together, is recommended for the study of neoplasms of the nervous system.
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PMID:Organ culture of human nervous system tumors. 17 38

The case histories of 273 patients with primary neoplasms of the central nervous system seen in The New York Hospital and Memorial Hospital during the years 1968 through 1973 were reviewed. Neoplastic cells were identified in cytologic preparations obtained from 76 patients. These include patients with meningioma, astrocytoma, glioblastoma multiforme, oligodendroglioma, ependymoma, medulloblastoma, neuroblastoma, retinoblastoma, pineoblastoma, and pituitary adenoma. It is concluded that there are certain suggestive cellular features of these neoplasms in cytologic preparations, but additional studies are needed to establish the cytomorphologic characteristics which may aid in the differential diagnosis of primary intracranial neoplasms from extracranial neoplasms which are metastatic to the central nervous system.
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PMID:Cytology of primary neoplasms of the central nervous system. 26 57

The literature on chemical induction and natural occurrence of neurogenic tumors in mice and some unpublished data from our laboratories are reviewed. Neurogenic tumors are a minor component of the total tumorigenic response of mice to alkylating agents such as ENU and MNU. In comparison with rats, a given dose of ENU induces a much lower incidence of neurogenic tumors in mice, and the mean latency is much longer than in rats. Although most neurogenic tumors induced by ENU in mice by either transplacental or direct postnatal exposure are of glial or Schwann cell origin, as in rats, and occur most frequently in the cerebrum or cranial nerves, respectively, medulloblastomas of the cerebellum also occur in treated mice. Transplacental and neonatal exposure to ENU were much more effective in inducing neurogenic tumors than treatment later in life. Ependymomas were not seen in mice, although they are common in ENU-treated rats. Neuroblastoma of the adrenal medulla, a common human pediatric tumor, has not been induced to either species, but it does occur spontaneously in mice. The induction by ENU of medulloblastomas demonstrates that this rodent equivalent of an embryonal tumor of the human nervous system can result from exposure to exogenous chemical agents.
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PMID:Transplacental and neonatal induction of neurogenic tumors in mice: comparison with related species and with human pediatric neoplasms. 38 62

Selected examples of neoplasms of the central nervous system are reviewed in which the electron microscope has been instrumental in establishing the diagnosis. These include ependymoma, ependymoblastoma, epithelial cyst, paraganglioma in the cauda equina and cerebellar neuroblastoma.
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PMID:Some contributions of electron microscopy to the diagnosis of brain tumors. 67 76

Infectivity of human T-lymphotropic virus type I (HTLV-I) to human nervous tissue cells was explored using co-cultivation with X-irradiated, HTLV-I-producing MT2 cells. Examined cells included normal cerebellar cells, brain tumor cells (astrocytoma, medulloblastoma, meningioma, hemangioblastoma, and schwannoma), and various cell lines (astrocytoma, ependymoma, oligodendroglioma, medulloblastoma, and neuroblastoma). Successful HTLV-I infection was confirmed immunohistochemically using monoclonal antibodies to HTLV-I p19, p24, and pX product. All cell lines and primary cultures from normal cerebellar tissues and brain tumors could be infected with HTLV-I. Double immunostaining showed that glial fibrillary acidic protein-, S-100 protein- or vimentin-positive cells were susceptible to infection. Neurofilament- or neuron-specific enolase-positive cells in medulloblastoma could also be infected. Reverse-transcriptase assay revealed the productive infection in U251-MG (astrocytoma) and KG-IC (oligodendroglioma) lines. Co-cultivated U251-MG cells formed syncytial polykaryons after serial passages, and polymerase chain reaction assay detected HTLV-I genome in U251-MG syncytial polykaryons and p19+ mononuclear cells. HTLV-I viral RNA was also detected in infected U251-MG cells by in situ hybridization. These data show that HTLV-I may have a wide spectrum of infectivity in human nervous tissues.
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PMID:Infectivity of human T-lymphotropic virus type I to human nervous tissue cells in vitro. 138 59

Mouse myeloma cells were fused with spleen cells from mice that had been immunized with a human ependymoma derived cell line, KMS II. Hybridomas producing monoclonal antibodies (MAbs) were screened and cloned. Specificity of the antibody was determined by enzyme-linked immunosorbent assay (ELISA) and/or indirect immunofluorescence assay. One of the MAbs, designated Ep-C4 (subclass = IgG1), reacted with two cell lines derived from ependymoma but did not react with 17 cell lines derived from other types of brain tumor nor with 4 neuroblastoma cell lines or 19 cell lines derived from carcinoma, hematopoietic tumors and amnion. Indirect immunofluorescence and immuno-electron microscopy studies revealed that the antigen recognized by MAb Ep-C4 was located on cell surface membrane. The membrane antigen of KMS II cells, immunoprecipitated by MAb Ep-C4, was a protein of 81,000 dalton. The reactivity of MAb Ep-C4 was further examined using immunofluorescence and/or immunoperoxidase methods and frozen sections and short-term cultures of various types of brain tumors. No cross-reactivity with normal adult or fetal brain tissues was detected by absorption assay and immunoperoxidase staining. Our results suggest that the antigen defined by MAb Ep-C4 is specific for ependymoma cells, and different from the antigens of glioma cells or other neuroectodermal-derived cells previously described.
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PMID:Monoclonal antibody against ependymoma-derived cell line. 154 75

An investigation of 749 deaths occurring among 4082 patients surviving at least five years after the diagnosis of childhood cancer in Britain before 1971 has been undertaken. Of the 738 with sufficient information the numbers of deaths attributable to the following causes were: recurrent tumour, 550 (74%), a second primary tumour, 61 (8%), a medical condition related to treatment of the tumour, 49 (7%), an traumatic death unrelated to the tumour or its treatment, 34 (5%), finally, any other cause unrelated to the tumour or its treatment, 44 (6%). Less than 10% of five year survivors of non-Hodgkin lymphomas, neuroblastoma, retinoblastoma, Wilms' tumour, or a soft tissue sarcoma died of recurrent tumour during the next 15 years, while more than 25% of five year survivors of Hodgkin's disease, ependymoma, medulloblastoma, and Ewing's tumour died of recurrent tumour during the corresponding period. Almost 50% of five year survivors of acute lymphoblastic leukaemia died of recurrent disease during the corresponding 15 years, a large proportion of deaths being due to central nervous system relapse in an era before central nervous system prophylaxis was routinely given. Comparison of the mortality observed with that expected from mortality rates in the general population indicated three times the expected number of deaths from non-neoplastic causes. Five times the expected number of deaths from cardiovascular causes were observed, these were predominantly myocardial infarction and cerebrovascular accidents. There was no evidence of an excess in the number of suicides observed, but there were three times the expected number of deaths from accidents observed after central nervous system tumours. Two groups of patients were identified whose deaths were potentially avoidable. Seven patients with craniopharyngioma and panhypopituitarism presented with addisonian crises during periods of stress not adequately covered by exogenous corticosteroids. In the other group were children who received radiotherapy and later developed problems related to radiation fibrosis. We emphasize that our investigation relates to patients diagnosed with childhood cancer before 1971. The pattern of mortality that will emerge after recent treatment regimens, in which chemotherapy is being used more extensively, is likely to be different from that observed in our study.
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PMID:Late deaths after treatment for childhood cancer. 227 Sep 44

Calcineurin is one of the calmodulin binding proteins and a Ca2+-dependent and calmodulin-stimulated phosphoprotein phosphatase. We used antisera to the calcineurin as a cell-type-specific marker in order to identify neuronal cells in the rat brain and human neoplasms. In normal rat brain slices, basal ganglia were stained macroscopically, and other areas such as cerebral cortex, corpus callosum, cerebellar cortex, granular layer and pyramidal tract of the spinal cord were lightly identified as well. Under the light microscope, it was found that only the neuronal cells were stained, and astrocytes, oligodendrocytes, ependymal cells and vessels were not. Intracellular distribution of the staining showed various patterns and staining intensity of varying degree. Using the PAP method, localization of the calcineurin in formalin-fixed, paraffin-embedded tissues were studied in 65 human intracranial neoplasms, and in 11 human extracranial neoplasms. The neuronal elements of neuroblastoma, ganglioglioma, ganglioneuroma and retinoblastoma were clearly stained. In contrast, glioblastoma, astrocytoma, oligodendroglioma, ependymoma, meningioma, neurinoma, pituitary adenoma, craniopharyngioma, hemangioblastoma, hamartoma, lymphoma and mesenchymal tumor were all negative. Two cases out of 5 medulloblastomas were stained, but others were not. Although positive tumors disclosed various staining patterns and intensities, these results indicated that calcineurin could be a new neuronal marker in human brain tumors.
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PMID:Calcineurin as a neuronal marker of human brain tumors. 242 51

The incidence of primary and metastatic cutaneous malignant solid tumors was investigated in a pediatric dermatology department. Among 25,000 first time patients seen between 1971 and 1985, 19 had cutaneous malignant solid tumors with an annual incidence of 0.7 for every 1,000 pediatric dermatology patients. Nine cases had primary cutaneous tumors and 10 cases metastatic tumors. The majority of patients were infants (zero to two years). The tumors found were rhabdomyosarcoma, six cases; basal-cell carcinoma, four cases; neuroblastoma, three cases; malignant melanoma, two cases, squamous-cell carcinoma, dermatofibrosarcoma, atypical fibroxanthoma and myxopapillary ependymoma, one case of each. Predisposing factors for the developing of malignancy were present in 42% of patients.
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PMID:[Incidence of malignant, primary and metastatic solid skin tumors at a pediatric dermatology service]. 266 91


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