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 surface antigenic characteristics of human glial brain tumor (HGBT) cells were studied by complement-dependent cytotoxic antibody assays and indirect membrane immunofluorescence. Eight permanent, well-characterized cell lines derived from human gliomas were used for analysis with antisera raised by hyperimmunization of nonhuman primates (Macaca fascicularis) with glioblastoma multiforme tissue or established HGBT cells lines. Exhaustive absorption of these antisera to remove predominantly antispecies activity rendered HLA nonreactive "preabsorbed" antisera, which reacted with a large panel of gliomatous and nongliomatous human tumor cells; 1 carcinoma, 2 sarcomas, 2 melanomas, 1 neuroblastoma, and 8 HGBT cell lines. Four lymphoblastoid lines and 2 carcinomas were unreactive. After further absorption with a human osteogenic sarcoma cell line, the antisera demonstrated significant levels of reactivity for 8 tested HGBT cell lines and no longer reacted with the nongliomatous cultured tumor cells lines. Therefore, extensive absorption of nonhuman primate anti-human glioma sera removed all activity for the nongliomatous cell lines tested, but it left significant reactivity against a glial tumor cell line-associated antigen(s) present on all 8 human glioma cell lines tested.
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PMID:Surface antigenic characteristics of human glial brain tumor cells. 7 98

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

Recently the authors have identified a major component of Rosenthal fibers as alpha B-crystallin, a major lens protein. In the current study the authors investigated the expression of alpha B-crystallin in four cultured glioma cell lines and in 115 human neuroectodermal tumors. alpha B-crystallin was expressed differentially by those glioma cell lines, but not by neuroblastoma cell lines. Northern blot analysis revealed two distinct messages for alpha B-crystallin in C-6, whereas only a single message in U-373MG and G26-24. In human surgical specimens positive immunostaining was frequently observed in the following brain tumors: pilocytic astrocytoma of the juvenile type, anaplastic astrocytoma, glioblastoma multiforme, and subependymal giant cell astrocytoma. The astrocytic elements of mixed oligoastrocytomas, glioblastomas with sarcomatous components, and gangliogliomas were likewise strongly stained. In contrast, little immunoreactivity was observed in ependymal and choroid plexus tumors. Thus, alpha B-crystallin is mainly expressed by astrocytic tumors among neuroectodermal neoplasms, without regard to the presence of Rosenthal fibers.
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PMID:Preferential expression of alpha B-crystallin in astrocytic elements of neuroectodermal tumors. 165 7

The bcl2 protooncogene was originally discovered because of its involvement in t(14;18) chromosomal translocations frequently found in non-Hodgkin's lymphomas. The expression of this gene is reported to be highly tissue specific, with bcl2 mRNAs being readily detectable only in hematolymphoid tissues and brain. To explore the possible involvement of bcl2 in neural tumors, we surveyed a variety of tumor cell lines for the presence of the p26-BCL2 protein by immunoprecipitation and immunoblotting methods. Very high levels of BCL2 protein were found in three of nine neuroblastoma (NB) cell lines examined; these levels of p26-BCL2 were comparable to lymphoma cell lines that contain a t(14;18). Despite the impressive relative amounts of BCL2 protein, however, no structural alterations or changes in the methylation status of bcl2 genes were detected in these NB cell lines by conventional Southern blotting. Of the other NB cell lines surveyed, three contained intermediate levels of BCL2 and another three cell lines had little or no detectable BCL2 protein, raising the possibility that determination of relative levels of BCL2 protein may help to segregate neuroblastomas into groups with different biological and clinical characteristics. BCL2 protein levels were not influenced by induction of neuronal differentiation with nerve growth factor in two of the two cell lines examined [SH-SY5Y (high BCL2); GICAN (low BCL2)] and did not correlate with N-MYC gene amplification or expression of nerve growth factor receptors. NB cell lines that contained little or no detectable BCL2 protein, however, tended to contain significant proportions of flat epithelioid cells, whereas bcl2-expressing cell lines were composed primarily of neuronal-like cells, suggesting that expression of this protooncogene correlates with the differentiation characteristics of these tumor cell lines. In addition to NBs, lower levels of BCL2 protein were also found in a variety of other neural crest-derived tumors and tumor cell lines, including some neuroepitheliomas, Ewing's sarcomas, neurofibromas, and melanomas. With regard to tumors of central nervous system origin, bcl2 expression was absent from most medulloblastomas but was detected at moderate to low levels in a retinoblastoma and some glioblastoma multiforme cell lines. Taken together, these findings imply that bcl2 protooncogene expression is differentially regulated within the various lineages of cells that give rise to the nervous system.
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PMID:Differential expression of bcl2 protooncogene in neuroblastoma and other human tumor cell lines of neural origin. 174 26

Multiple genetic changes take place during tumor development and progression. These genetic changes result in inactivation of tumor suppressor genes and activation of proto-oncogenes. Frequent genetic changes observed in gliomas are losses of chromosomal regions on 9p, 10q, 13q, 17p and on 22. Loss of 10q is seen in more than 80% of the glioblastoma multiforme (GBM) tumors suggesting the presence of a gene critical for GBM formation on this chromosome. Amplification of epidermal growth factor receptor gene and expression of platelet derived growth factor and fibroblast growth factor genes are also common among gliomas. The most common genetic abnormality found in medulloblastomas is loss of 17p. The C-myc gene is amplified in a few primary tumors, but the incidence of amplification is higher in medulloblastoma derived cell lines. These findings suggest that the same two genetic processes, gene amplification and regional chromosomal loss, which characterize other primitive childhood neuroectodermal tumors such as retinoblastoma and neuroblastoma are also important in medulloblastomas.
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PMID:Genetic alterations in glioma and medulloblastoma. 178 30

Human brain tumors (obtained as surgical specimens) and nude mouse-borne human neuroblastomas and gliomas were analyzed for sigma and opioid receptor content. Sigma binding was assessed using [3H]1,3-di-o-tolylguanidine (DTG), whereas opoid receptor subtypes were measured with tritiated forms of the following: mu, [D-ala2,mePhe4,gly-ol5]enkephalin (DAMGE); kappa, ethylketocyclazocine (EKC) or U69,593; delta, [D-pen2,D-pen5]enkephalin (DPDPE) or [D-ala2,D-leu5]enkephalin (DADLE) with mu suppressor present. Binding parameters were estimated by homologous displacement assays followed by analysis using the LIGAND program. Sigma binding was detected in 15 of 16 tumors examined with very high levels (pmol/mg protein) found in a brain metastasis from an adenocarcinoma of lung and a human neuroblastoma (SK-N-MC) passaged in nude mice. kappa opioid receptor binding was detected in 4 of 4 glioblastoma multiforme specimens and 2 of 2 human astrocytoma cell lines tested but not in the other brain tumors analyzed.
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PMID:Sigma and opioid receptors in human brain tumors. 197 2

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

Three adult patients had cerebral malignant gliomas composed predominantly of small cells and displaying many areas of palisading necrosis, which are usually characteristic of glioblastoma multiforme. Light and electron microscopy, however, revealed tumour cells with neuritic processes, while astrocytic differentiation was convincingly excluded. It is suggested that palisading necrosis is not pathognomonic of glioblastoma multiforme and that high grade cerebral neuroblastoma should be considered in the differential diagnosis. The need for comprehensive light and electron microscopic studies for the accurate classification of gliomas is stressed.
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PMID:Cerebral gliomas with palisading necrosis: glioblastoma multiforme or high grade cerebral neuroblastoma? A light and electron microscopical study of three cases. 284 Jun 28

Diffuse astrocytomas of the cerebrum, cerebellum, brain stem, and spinal cord are classified into three groups according to the degree of tumor anaplasia. These groups are the astrocytoma, anaplastic astrocytoma, and glioblastoma multiforme. Juvenile pilocytic astrocytomas have a better prognosis and are clinically and biologically distinct from the diffuse, fibrillary astrocytomas. The prognosis of astrocytomas depends not only on histologic characteristics, but also age of the patient, location of the tumor, and extent of surgical resection. The pattern of invasion into surrounding brain distinguishes gliomas from metastatic carcinomas and sarcomas. Topographic correlations have shown that malignant gliomas may invade the brain for distances of up to several centimeters from the enhancing rim seen on CT scan. However, the junction between glioblastoma and adjacent brain may also be fairly abrupt, with a peripheral margin of less than 1 mm. Recurrent glioblastomas are more widely invasive and often extend into areas that appear normal on CT scan. The optimal site for tumor biopsy corresponds to areas of contrast enhancement. Primitive neuroepithelial tumors are malignant neoplasms with a poor prognosis. They tend to recur locally and metastasize throughout the neuraxis via the CSF. It remains controversial whether these tumors should be classified as a single entity with the potential for differentiation along different cell lines, or whether the categories of neuroblastoma, spongioblastoma, ependymoblastoma, pineoblastoma, and medulloblastoma should be retained as specific entities. The medulloblastoma is the most common of these neoplasms, its clinicopathologic features are well characterized, and the current 5-year survivals of 50 to 60 per cent are better than for other "primitive" neoplasms. Glial fibrillary acidic protein is a specific marker for immature, reactive, and neoplastic astrocytes and ependymal cells. Although the absence of GFAP in a neoplasm does not exclude an astrocytic origin, the presence of GFAP indicates astrocytic or ependymal differentiation. This has important diagnostic applications. The expression of GFAP is used to distinguish astrocytic neoplasms from epithelial or mesenchymal tumors that may on occasion mimic a glioma. The detection of GFAP is also useful in the investigation of tumor histogenesis and differentiation both in vivo and in vitro. Although meningiomas exhibit a wide variety of histologic patterns, most tumors exhibit similar biologic and clinical behavior regardless of the histologic subtype.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Pathologic analysis of primary brain tumors. 300 88

The distribution of the glial fibrillary acidic protein (GFAP) was investigated in sections of 131 paraffin-embedded brain neoplasms obtained at surgery or at autopsy. The unlabeled antibody immunoperoxidase (peroxidase-antiperoxidase, PAP) method was used. Equally good results were obtained from 17-year-old material and from recent material derived at surgery or autopsy and fixed with Bouin fluid or phosphate-buffered formalin. The perikaryons and processes of reactive astrocytes showed the most intense stain for GFAP. Positive reaction to antibody against GFAP of varying intensity was demonstrated in astrocytomas of various grades of malignancy (32 of 32), glioblastoma multiforme (10 of 10), subependymal giant cell astrocytoma (1 of 1), ependymoma (2 of 10), subependymoma (4 of 4), and astrocytes in mixed neoplasms (8 of 8). In two neoplasms diagnosed as malignant astrocytomas and in four neoplasms diagnosed as glioblastoma multiforme, GFAP stain was limited to a few neoplastic cells. Usually the stain was more intense over processes than in perikaryons, with the exception of gemistocytic astrocytomas and the giant cells in glioblastoma multiforme, which showed an equally intense stain over perikaryons and processes. The periphery of Rosenthal fibers was intensely positive for GFAP. In astrocytic neoplasms the number of GFAP-positive cells and the intensity of the stain were inversely proportional to the degree of malignancy. In the following neoplasms the reaction for GFAP was negative: oligodendroglioma (3), oligodendroblastoma (1), medulloblastoma (3), medulloepithelioma (1), neuroblastoma (1), pineocytoma (1), typical teratoma of the pineal (1), fibrosarcoma (1), pituitary adenoma (2), craniopharyngioma (1), chordoma (1), chemodectoma of globus jugulare (1), metastatic carcinoma (17), and lymphoma (8). In one of 18 meningiomas, endogenous peroxidase activity was seen in mast cells. All meningiomas studied were negative for GFAP. In one of six neurinomas a positive reaction for GFAP was detected over processes. The authors concluded that the immunostain for GFAP is useful in the diagnoses of astrocytic neoplasms and of mixed gliomas.
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PMID:Immunocytochemical study of the glial fibrillary acidic protein in human neoplasms of the central nervous system. 628 Nov 68


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