Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017636 (glioblastoma)
 18,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The invasiveness of human intracranial tumours was studied in an organ culture system. Biopsies from six glioblastomas, four astrocytomas, two mixed gliomas, one ependymoma, four meningiomas and two carcinoma metastases were cut into fragments of 0.5 mm diameter, and placed in agar overlay tissue culture. The tumour specimens formed spheroids which were co-cultured with cell aggregates or fragments from fetal rat brain for up to 10 days in vitro. The invasiveness of the glioblastoma spheroids was characterised by a gradual destruction of normal brain tissue by tumour cells, followed by replacement of normal tissue by these cells. Co-cultures from two glioblastomas showed lesions in the normal brain tissue in areas removed from the tumour cells. Tumour spheroids from four glioblastomas totally destroyed the normal brain tissue without any change in the original tumour spheroid configuration. The low-grade gliomas were less invasive than the glioblastomas. The meningiomas and the metastases were non-invasive. This organ culture assay appeared to reflect the in situ invasive behaviour of the brain tumours examined. It is suggested that it may be used for evaluating the aggressiveness of individual brain tumours with the specific aim of correlating clinical data with the biological character of the tumour.
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PMID:Interaction between human brain tumour biopsies and fetal rat brain tissue in vitro. 208 53

The present study determined which oncogenes (N-myc, c-myc, v-sis, or v-fos) were amplified and which messenger ribonucleic acids (mRNA's) accumulated in 10 primary human brain tumors of neuroectodermal origin. The tumors included four glioblastomas multiforme, one mixed glioma (astrocytoma grade I and ependymoma), one astrocytoma grade II, one cystic cerebellar astrocytoma, one ependymoma, one ganglioglioma, and one medulloblastoma. The relative amounts of polyadenylated (poly(A)+) RNA's homologous to these genes and their copy number were determined using the RNA and deoxyribonucleic acid blot hybridization techniques. The N-myc and v-sis probes hybridized strongly to the poly(A)+ RNA from the same recurrent glioblastoma with gene amplifications (N-myc 80 copies; v-sis three to four copies). The c-myc probe hybridized strongly to the recurrent medulloblastoma without gene amplification. The amplification or abundant accumulation of mRNA's homologous to their oncogenes may be involved in tumorigenesis or the aggressiveness of these malignant brain tumors of neuroectodermal origin and may be good molecular indicators of an extremely malignant state in these tumors.
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PMID:Proto-oncogene analyses in brain tumors. 254 Dec 27

A case of congenital glioblastoma arising from the cerebellum is presented with special reference to microspectrophotometric deoxyribonucleic acid (DNA) analysis of the tumor cells. Seven cases of this condition are already in the literature. The prognosis is poor and most of the reported cases survive no more than 2 months. Cytofluorophotometric DNA studies were helpful in elucidating the extreme heterogeneous distribution of DNA contents of the tumor cells, suggesting a biological aggressiveness probably related to the rate of proliferation.
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PMID:Congenital glioblastoma of the cerebellum with cytofluorometric deoxyribonucleic acid analysis. 381 Apr 44

The brains of 50 adults with supratentorial glioblastoma multiforme were studied post mortem. The cytologic compositions of the neoplasms were examined in each of three sites: (1) in and around the original tumor bed; (2) zones of infiltration of contiguous structures; and (3) implants in the subarachnoid and/or ventricular spaces. For this purpose, six different cell types were defined: small anaplastic cells (SAC), small fibrillated cells (SFC), fibrillated astrocytes (FA), pleomorphic astrocytes (PA), gemistocytic astrocytes (GA), and large bizarre cells (LBC). In 16 cases with marked mass effect in the original tumor bed entirely due to the neoplasm, the cytologic composition of the neoplasm was predominantly SAC (14 cases) and SFC (2 cases). The prevalence of these two cellular types was evident in the infiltrated regions in 36 of 42 cases, and in the metastatic foci of 11 of 13 cases. In 10 of 11 cases in which there was mild or no mass effect, only limited infiltration in the ipsilateral hemisphere, and no metastases, the neoplasms were composed of a combination of FA, PA, GA, and LBC. The observations suggest that, in spite of the glioblastoma's cytologic heterogeneity, the pathologic substrate of aggressiveness in this malignant glioma is related largely to the proliferation of a population of small anaplastic cells. On the basis of this observation, as well as the consideration of certain clinical and therapeutic variables, an outline is presented summarizing the history of the glioblastoma multiforme from treatment until the time of death.
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PMID:Correlations between cytologic composition and biologic behavior in the glioblastoma multiforme. A postmortem study of 50 cases. 631 12

The patterns of clinical-and autopsy-documented tumor spread were evaluated for 15 patients with biopsy-proven infratentorial (8 cerebellar, 2 brainstem, 5 intramedullary spinal cord) glioblastoma. No patient developed clinical nor autopsy evidence of subarachnoid dissemination, even though no patient had received craniospinal axis irradiation. Fully 14 of the 21 previously reported patients with subarachnoid dissemination from infratentorial glioblastoma had this diagnosis made only at autopsy. The overall poor prognosis at present (8% 3-year survival from the present series and recent literature) along with the demonstrated pattern of local-regional aggressiveness as the major form of initial spread and post-irradiation recurrence, suggests that routine craniospinal axis irradiation may not be indicated for most patients with infratentorial glioblastoma.
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PMID:Infratentorial glioblastoma: the role of neuraxis irradiation. 710 42

Despite its usefulness in adults with cerebral gliomas, indications for thallium-201 single-photon emission computed tomography (SPECT) in pediatric brain tumor patients are not well defined. We prospectively compared thallium SPECT with gadolinium-enhanced MR (Gd-MR) to determine if thallium SPECT provides clinically useful information that cannot be derived from Gd-MR. We studied 24 pediatric brain tumor patients, 7 at presentation and 17 during therapy. MR imaging included T2 and pre- and postgadolinium T1 images. Thallium SPECT was done within 48 h of MR imaging; thallium indices were calculated for 12 of 14 lesions which showed thallium uptake. Surgery and/or clinical follow-up are available in all patients. The tumors included pilocytic astrocytoma (7), medulloblastoma (5), brainstem glioma or glioblastoma (4), germinoma (3), optic glioma (2), mixed glioma (1), primitive neuroectodermal tumor (1), and choroid plexus carcinoma (1). Among the primary tumors, compared to MR, thallium SPECT was false-negative for tumor in 1 patient and true-positive in 6 patients. Among the patients studied while on therapy, compared to MR, thallium SPECT was true-negative for tumor in 7, true-positive in 5, false-negative in 3, and false-positive in 2. In both groups of patients, thallium SPECT underestimated tumor burden as nonenhancing regions of the tumors were not thallium-avid. Thallium indices did not correlate with histologic grade, biologic aggressiveness, or tumor type. We were unable to establish indications for the use of thallium SPECT in this setting as there was little clinically useful information derived from thallium SPECT that was not provided by Gd-MR.
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PMID:Comparison of gadolinium-enhanced MR and thallium-201 single photon emission computed tomography in pediatric brain tumors. 788 93

The GLI gene encodes a transcription factor harboring five zinc finger motifs that bind to DNA in a sequence-specific manner. The gene was originally identified because of its amplification in a human glioblastoma, and previous studies have shown it to be amplified in a significant proportion of mesenchymal tumors, such as childhood sarcomas. Here we evaluate GLI gene expression in bone and soft tissue sarcomas of adult patients. Samples from 40 patients (37 sarcomas and 3 benign mesenchymal tumors) and samples of 15 normal mesenchymal tissues were examined for GLI gene amplification and expression by Southern hybridization, reverse transcription-PCR of tissue RNA, and immunohistochemistry, using a new polyclonal GLI antibody developed against an epitope outside of the zinc finger region. In contrast to childhood sarcomas, amplification of the GLI gene was not observed in sarcomas of adult patients. Although GLI gene expression in sarcomas was significantly higher than that in normal mesenchymal tissues (P < 0.0001), the levels were very variable. Attempts to correlate the expression data with different pathophysiological parameters only showed a significant relationship to tumor grade. Based on these data, increased levels of GLI gene expression may be indicative of the aggressiveness of the tumor.
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PMID:GLI gene expression in bone and soft tissue sarcomas of adult patients correlates with tumor grade. 1021 97

The aggressiveness of human gliomas appears to be correlated with the upregulation of interleukin 6 (IL-6) gene. Using quantitative PCR methods, we detected amplification and expression of the IL-6 gene in 5 of 5 primary glioblastoma samples and in 4 of 5 glioblastoma cell lines. This finding suggests that the amplification of IL-6 gene may be a common feature in glioblastomas and may contribute to the IL-6 over-expression.
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PMID:IL-6 gene amplification and expression in human glioblastomas. 1150 89

Overexpression of the erbB family of receptor tyrosine kinases has been implicated in a variety of tumors including breast, lung, prostate, and brain. Most solid tumors express one or more of these receptors, which can often be related to tumor aggressiveness and poor patient prognosis. CI-1033, a pan-erbB tyrosine kinase inhibitor, is a clinically promising agent that is active against all four members of the erbB receptor tyrosine kinase family. In vitro studies of human cancer cell lines indicate that CI-1033 results in prompt, potent, and sustained inhibition of tyrosine kinase activity. This inhibition is highly selective for erbB1 (epidermal growth factor receptor), erbB2, erbB3, and erbB4 without inhibiting tyrosine kinase activity of receptors such as platelet-derived growth factor receptor, fibroblast growth factor receptor, and insulin receptor, even at high concentrations. Treatment of athymic nude mice bearing xenografts of human A431 epidermoid carcinoma, H125 non-small cell lung carcinoma, and SF-767 glioblastoma results in highly significant suppression of tumor growth. The major toxicity in animals is diarrhea, which is more severe at higher doses. In animal models, all side effects are reversible on cessation of treatment. Thus, CI-1033, which is currently undergoing phase I clinical trials, holds significant potential for use in a broad range of solid tumors.
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PMID:CI-1033, a pan-erbB tyrosine kinase inhibitor. 1170 99

We show that high-grade astrocytic tumors with high levels of galectin-1 expression are associated with dismal prognoses. The immunohistochemical analysis of galectin-1 expression of human U87 and U373 glioblastoma xenografts from the brains of nude mice revealed a higher level of galectin-1 expression in invasive areas rather than non-invasive areas of the xenografts. Nude mice intracranially grafted with U87 or U373 cells constitutively expressing low levels of galectin-1 (by stable transfection of an expression vector containing the antisense mRNA of galectin-1) had longer survival periods than those grafted with U87 or U373 cells expressing normal levels of galectin-1. Galectin-1 added to the culture media markedly and specifically increased cell motility levels in human neoplastic astrocytes. These effects are related to marked modifications in the organization of the actin cytoskeleton and the increase in small GTPase RhoA expression. All the data obtained indicate that galectin-1 enhances the migratory capabilities of tumor astrocytes and, therefore, their biological aggressiveness.
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PMID:Galectin-1 modulates human glioblastoma cell migration into the brain through modifications to the actin cytoskeleton and levels of expression of small GTPases. 1212 37


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