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  • 1
    Electronic Resource
    Electronic Resource
    MOLECULAR PATHOLOGY OF MALIGNANT GLIOMAS (2006)
    Palo Alto, Calif. : Annual Reviews
    Annual Review of Pathology: Mechanisms of Disease (2006) 1 (2006), S. 97-117 
    Details
    ISSN: 1553-4006
    Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Topics: Medicine
    Notes: Malignant gliomas, the most common type of primary brain tumor, are a spectrum of tumors of varying differentiation and malignancy grades. These tumors may arise from neural stem cells and appear to contain tumor stem cells. Early genetic events differ between astrocytic and oligodendroglial tumors, but all tumors have an initially invasive phenotype, which complicates therapy. Progression-associated genetic alterations are common to different tumor types, targeting growth-promoting and cell cycle control pathways and resulting in focal hypoxia, necrosis, and angiogenesis. Knowledge of malignant glioma genetics has already impacted clinical management of these tumors, and researchers hope that further knowledge of the molecular pathology of malignant gliomas will result in novel therapies.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1146/annurev.pathol.1.110304.100043
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  • 2
    Electronic Resource
    Electronic Resource
    Oncolytic virus therapy of multiple tumors in the brain requires suppression of innate and elicited antiviral responses (1999)
    [s.l.] : Nature America Inc.
    Nature medicine 5 (1999), S. 881-887 
    Details
    ISSN: 1546-170X
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] The occurrence of multiple tumors in an organ heralds a rapidly fatal course. Although intravascular administration may deliver oncolytic viruses/vectors to each of these tumors, its efficiency is impeded by an antiviral activity present in complement-depleted plasma of rodents and humans. Here, ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/11320
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  • 3
    Electronic Resource
    Electronic Resource
    Amplification of the cyclin-dependent kinase 4 (CDK4) gene is associated with high cdk4 protein levels in glioblastoma multiforme (1996)
    Springer
    Acta neuropathologica 92 (1996), S. 70-74 
    Details
    ISSN: 1432-0533
    Keywords: Key wordsCDK4 ; Gene amplification ; Protein level ; LOH12q ; Brain tumors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Genetic alterations on the long arm of chromosome 12, including both gene amplification and allelic loss, are associated with malignant progression of human gliomas. The region of the chromosomal arm 12q that is amplified in malignant gliomas contains the CDK4 gene, a cell cycle regulatory gene which promotes cell division. To evaluate the frequency of CDK4 gene amplification, we analyzed a series of 355 brain tumors using a quantitative non-radioactive polymerase chain reaction assay. CDK4 gene amplification occurred in 9 of 81 glioblastomas (11%), but was rare in other neoplasms, including low-grade and anaplastic gliomas, meningiomas, medulloblastomas and metastatic carcinomas (only 6 of 274 cases). There was no correlation between CDK4 gene amplification and allelic loss of chromosome 12. To assess the significance of CDK4 gene amplification, we analyzed protein extracts from 37 glioblastomas by Western blotting with a commercially available polyclonal antibody to cdk4. All tumors with CDK4 gene amplification showed high cdk4 expression levels, whereas no increased cdk4 expression was seen in glioblastomas without CDK4 gene amplification. These data support the functional activity of CDK4 gene amplification in glioblastoma multiforme and point to an important role of CDK4 gene amplification in a subset of glioblastomas.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050491
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  • 4
    Electronic Resource
    Electronic Resource
    Prediction of central nervous system embryonal tumour outcome based on gene expression (2002)
    [s.l.] : Macmillian Magazines Ltd.
    Nature 415 (2002), S. 436-442 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Embryonal tumours of the central nervous system (CNS) represent a heterogeneous group of tumours about which little is known biologically, and whose diagnosis, on the basis of morphologic appearance alone, is controversial. Medulloblastomas, for example, are the most common malignant brain ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/415436a
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  • 5
    Electronic Resource
    Electronic Resource
    Deletions on the long arm of chromosome 17 in pilocytic astrocytoma (1993)
    Springer
    Acta neuropathologica 86 (1993), S. 81-85 
    Details
    ISSN: 1432-0533
    Keywords: Pilocytic astrocytoma ; Loss of heterozygosity ; Chromosome 17 ; Tumor suppressor gene ; Neurofibromatosis type 1
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Pilocytic astrocytomas are the most common astrocytic tumors of childhood and differ clinically and histopathologically from those astrocytomas that affect adults. Studies of adult astrocytic tumors have revealed allelic losses on chromosomes 10, 17p, 19q and alterations in the epidermal growth factor receptor (EGFR) gene. We have previously examined pilocytic astrocytomas for allelic losses on chromosomes 10 and 19q and for amplification of the EGFR gene, but did not detect genomic alterations at these loci. In the present study we assayed 20 pilocytic astrocytomas for loss of allelic heterozygosity of chromosome 17p, including one locus in the p53 tumor suppressor gene. In addition, because pilocytic astrocytomas frequently affect patients with neurofibromatosis type 1 (NF1) and the NF1 gene has been mapped to 17q11.2, we also examined multiple loci on the long arm of chromosome 17. Allelic loss was observed on chromosome 17 in four cases (three sporadic, one NF1); all lost portions of the long arm in chromosome 17, and one tumor lost the short arm as well. One tumor showed an interstitial delection on the long arm that included the region of the NF1 gene. These data suggest the presence of a tumor suppressor gene on 17q that is associated with pilocytic astrocytomas. A potentiel candidate for this gene is the NF1 tumor suppressor gene.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00454903
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  • 6
    Electronic Resource
    Electronic Resource
    Molecular genetic alterations in pleomorphic xanthoastrocytoma (1996)
    Springer
    Acta neuropathologica 91 (1996), S. 293-297 
    Details
    ISSN: 1432-0533
    Keywords: Key words Astrocytoma ; Epidermal growth factor ; receptor ; Glioma ; p53 ;  Loss of heterozygosity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Pleomorphic xanthoastrocytoma (PXA) is a low-grade glioma that may recur as a malignant diffuse astrocytoma such as glioblastoma (GBM). While the molecular genetic basis of diffuse astrocytomas has been studied extensively, PXAs have not been analyzed in detail. We, therefore analyzed DNA from archival primary and recurrent PXAs from eight patients (three grade II PXAs without recurrence, one grade II PXA with recurrence as grade II PXA, two grade II PXAs with progression to GBM, and two grade III anaplastic PXAs with recurrence as grade III anaplastic PXA or GBM) for genetic changes associated with diffuse astrocytomas. Single-strand conformation polymorphism analysis of p53 exons 5–8 revealed migration shifts in two cases, one primary PXA without recurrence and one recurrent grade II PXA in which the primary tumor did not show a shift. DNA sequencing showed two missense mutations in codons 220 (exon 6) and 292 (exon 8), respectively, mutations which have not been previously noted in astrocytomas. Differential polymerase chain reaction analysis demonstrated epidermal growth factor receptor gene amplification in only one tumor, a GBM without allelic loss of chromosome 10 that was the second GBM recurrence of an initial grade II PXA. Loss of heterozygosity studies on tumors from five patients, using three microsatellite polymorphisms on chromosome 10q and three on chromosome 19q, did not disclose allelic loss in any recurrent tumor. These findings suggest that the genetic events that underlie PXA formation and progression may differ significantly from those involved in diffuse astrocytoma tumorigenesis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050428
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  • 7
    Electronic Resource
    Electronic Resource
    Accumulation of wild-type p53 in astrocytomas is associated with increased p21 expression (1997)
    Springer
    Acta neuropathologica 94 (1997), S. 21-27 
    Details
    ISSN: 1432-0533
    Keywords: Key words p21 ; p53 ; Astrocytoma ; Single-strand ; conformation polymorphism ; Immunohistochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Approximately one quarter of human astrocytomas show immunohistochemical positivity for p53 protein but lack p53 gene mutations, which could reflect either an accumulation of wild-type p53 protein or an inadequate sensitivity of mutation detection. Since wild-type p53 up-regulates p21 expression, increased p21 expression in those astrocytomas with p53 accumulation in the absence of mutations would argue that the protein was wild type in these tumors. We therefore compared p21 expression with p53 gene and protein status in 48 primary human astrocytomas. Single-strand conformation polymorphism analysis and direct sequencing of the p53 gene showed mutations in 11 tumors (22.9%), while immunohistochemistry revealed positive staining in 19 cases (39.6%). Those tumors with p53 immunopositivity in the absence of p53 mutation had significantly increased p21 expression when compared to either mutant p53 or p53-immunonegative cases. Neither p53 nor p21 status correlated with proliferation indices, as assessed by Ki-67 immunohistochemistry. These results support the hypotheses that functionally wild-type p53 accumulates in some astrocytomas, and that alternative cell cycle checkpoints (such as the p16 pathway) may be more important than p21 in regulating proliferation in astrocytomas.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050667
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  • 8
    Electronic Resource
    Electronic Resource
    Co-expression of Fas and Fas ligand in malignant glial tumors and cell lines (1998)
    Springer
    Acta neuropathologica 95 (1998), S. 287-290 
    Details
    ISSN: 1432-0533
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Fas ligand (FasL) is involved in tumor evasion from the immune system. We analyzed 22 human gliomas for expression of FasL and its receptor, Fas. Positive FasL and Fas immunoreactivity was detected in 13 out of 22 tumors by Western blotting and in 15 out of 22 tumors by immunohistochemistry. Immunohistochemistry also showed that Fas and FasL expression was confined to tumor cells. Co-expression of these molecules was confirmed by Western blotting and immunohistochemistry in 4 of 7 glioma cell lines. Co-expression of FasL and Fas within tumor cells suggests that their contribution in vivo to the process of immune system evasion and tumor cell apoptosis is complex and probably involves additional factors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050799
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  • 9
    Electronic Resource
    Electronic Resource
    ANOVA, a putative astrocytic RNA-binding protein gene that maps to chromosome 19q13.3 (1997)
    Springer
    Neurogenetics 1 (1997), S. 31-36 
    Details
    ISSN: 1364-6753
    Keywords: Keywords: chromosome 19, glioma, NOVA, RNA-binding
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: ABSTRACT Exon amplification from cosmids mapping to the glioma tumor suppressor gene candidate region on chromosome 19q13.3 yielded an exon with high homology to a portion of the NOVA1 gene, which encodes a neuron-specific RNA-binding protein recognized by the paraneoplastic syndrome antibody anti-Ri. Screening of a human brain cDNA library with this exon identified a 1.9 kb cDNA with extensive homology to NOVA1, including three nearly identical KH domains characteristic of a subtype of RNA-binding proteins. Northern blots demonstrated expression of a 2.5 kb mRNA in brain, but in no other tissues. In situ hybridization on human cerebral cortex showed mRNA expression restricted to astrocytes. We have therefore named the gene ANOVA, for astrocytic NOVA1-like gene. Southern blotting and single strand conformation polymorphism analyses did not show tumor-specific alterations of this gene in gliomas and RT-PCR studies showed expression in glioma cell lines, suggesting that ANOVA is not the chromosome 19q glioma tumor suppressor gene. Given that two cloned paraneoplastic antigens are neuronal RNA-binding proteins and that glial proteins may act as paraneoplastic antigens, the ANOVA product may be a target antigen in one of the undefined human paraneoplastic syndromes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s100480050005
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  • 10
    Electronic Resource
    Electronic Resource
    Cerebral primitive neuroectodermal tumor in an adult, with spinal cord metastasis after 18-year dormancy (1990)
    Springer
    Journal of neuro-oncology 9 (1990), S. 77-80 
    Details
    ISSN: 1573-7373
    Keywords: primitive neuroectodermal tumor ; neuroblastoma ; central nervous system tumors ; metastasis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A cerebral primitive neuroectodermal tumor in a 40-year-old man recurred as a metastasis to the spinal cord after an 18-year dormant period. The metastatic tumor showed features of neuronal differentiation. The clinical course and pathologic findings are discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00167072
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