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  • Articles: DFG German National Licenses  (5)
  • Ganglioglioma  (2)
  • Non-radioactive in situ hybridization  (2)
  • Astrocytoma  (1)
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  • Articles: DFG German National Licenses  (5)
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  • 1
    Electronic Resource
    Electronic Resource
    Ganglioglioma: a detailed histopathological and immunohistochemical analysis of 61 cases (1994)
    Springer
    Acta neuropathologica 88 (1994), S. 166-173 
    Details
    ISSN: 1432-0533
    Keywords: Ganglioglioma ; Hamartia ; Proliferation ; Ki-67 ; p53
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Gangliogliomas are tumors composed of intimately admixed neuronal and glial components and account for approximately 1% of all brain tumors. Here we report the histopathological findings in 61 gangliogliomas. Epilepsy was the most common presenting symptom. Most gangliogliomas were located in the temporal lobes (74%). Thirteen percent of the gangliogliomas were associated with glioneuronal hamartias. There was considerable variation in neuronal size and density, presence of binucleated neurons, calcifications, desmoplasia, lymphocytic infiltrate, pilocytic differentiation, Rosenthal fibers, location, or histological uniformity. Fifteen percent of the gangliogliomas contained areas of purely astrocytic differentiation. All tumors were examined immunohistochemically for an aberrant p53 tumor suppressor gene product and for the presence of nuclear antigens associated with cell proliferation (Ki-67, Ki-S1, proliferating cell nuclear antigen). In 45 of 61 cases (74%) labeling indices for Ki-67 were less than 1%. Nuclear labeling for Ki-67 was observed exclusively in the astrocytic component. Gangliogliomas with very large neurons had higher Ki-67 labeling indices and occurred in younger patients than gangliogliomas with small-or intermediate-sized neurons. None of the tumors had an aberrant expression of p53. The observations suggest that gangliogliomas may arise from glioneuronal hamartias through neoplastic transformation of the astrocytic component.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00294510
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Hippocampal loss of N-methyl-D-aspartate receptor subunit 1 mRNA in chronic temporal lobe epilepsy (1995)
    Springer
    Acta neuropathologica 89 (1995), S. 446-450 
    Details
    ISSN: 1432-0533
    Keywords: N-Methyl-D-aspartate receptor ; Epilepsy ; Non-radioactive in situ hybridization ; Hippocampus ; Ammon's horn sclerosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The hippocampal distribution of mRNA for the N-methyl-D-aspartate (NMDA) receptor subunit 1 (NR 1) was examined by non-radioactive in situ hybridization in 21 archival formalin-fixed and paraffin-embedded surgical specimens from patients with pharmacoresistant chronic epilepsy and in normal control specimens obtained at autopsy. Using the digoxigenin-labeling procedure, ribonucleotide probes were found to be significantly more sensitive than synthetic oligonucleotide probes. In normal autopsy specimens and in surgical specimens without Ammon's horn sclerosis there was intense NR 1 expression in a great majority of the dentate gyrus granular cells. Many neurons in the hippocampal pyramidal cell layer also revealed a strong signal intensity. The strata oriens and moleculare of Ammon's horn and the molecular layer of the dentate gyrus contained only few labeled neurons. In the subiculum and entorhinal cortex most neurons throughout various layers were positive. In hippocampal specimens of patients with chronic epilepsy there was a loss of NR 1-positive cells that was closely related to the overall neuronal loss in the respective specimen and to Ammon's horn sclerosis. These data suggest that the loss of NR 1 expression is a secondary phenomenon rather than an event that is relevant for the pathogenesis of epileptic seizures.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00307650
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    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Hippocampal loss of N-methyl-D-aspartate receptor subunit 1 mRNA in chronic temporal lobe epilepsy (1995)
    Springer
    Acta neuropathologica 89 (1995), S. 446-450 
    Details
    ISSN: 1432-0533
    Keywords: Key wordsN-Methyl-D-aspartate receptor ; Epilepsy ; Non-radioactive in situ hybridization ; Hippocampus ; Ammon's horn sclerosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The hippocampal distribution of mRNA for the N-methyl-D-aspartate (NMDA) receptor subunit 1 (NR1) was examined by non-radioactive in situ hybridization in 21 archival formalin-fixed and paraffin-embedded surgical specimens from patients with pharmacoresistant chronic epilepsy and in normal control specimens obtained at autopsy. Using the digoxigenin-labeling procedure, ribonucleotide probes were found to be significantly more sensitive than synthetic oligonucleotide probes. In normal autopsy specimens and in surgical specimens without Ammon's horn sclerosis there was intense NR1 expression in a great majority of the dentate gyrus granular cells. Many neurons in the hippocampal pyramidal cell layer also revealed a strong signal intensity. The strata oriens and moleculare of Ammon's horn and the molecular layer of the dentate gyrus contained only few labeled neurons. In the subiculum and entorhinal cortex most neurons throughout various layers were positive. In hippocampal specimens of patients with chronic epilepsy there was a loss of NR1-positive cells that was closely related to the overall neuronal loss in the respective specimen and to Ammon's horn sclerosis. These data suggest that the loss of NR1 expression is a secondary phenomenon rather than an event that is relevant for the pathogenesis of epileptic seizures.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00307650
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    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Expression and distribution of vascular endothelial growth factor protein in human brain tumors (1997)
    Springer
    Acta neuropathologica 93 (1997), S. 109-117 
    Details
    ISSN: 1432-0533
    Keywords: Key words Vascular endothelial growth factor ; Brain tumor ; Astrocytoma ; Angiogenesis ; Vascularization
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Marked neovascularization is a hallmark of many neoplasms in the nervous system. Recent reports indicate that the endothelial mitogen vascular endothelial growth factor (VEGF) may play a critical role in the regulation of vascular endothelial proliferation in malignant gliomas. Using novel monoclonal antibodies to the VEGF polypeptide we have determined the expression and cellular distribution of VEGF protein in a representative series of 171 human central nervous system (CNS) tumors by immunohistochemistry and immunoblotting. In agreement with previous in situ hybridization data, 19 out of 20 glioblastomas (95%) showed immunoreactivity for VEGF, whereas both the percentage of immunoreactive tumors and the extent of immunoreactivity for VEGF were significantly lower in astrocytomas. Of the pilocytic astrocytomas (WHO grade I) 44% were immunoreactive for VEGF, but we observed several cases with pronounced vascular proliferates in the absence of VEGF. In ependymomas, meningiomas, hemangioblastomas, and primitive neuroectodermal tumors, there was no correlation between VEGF expression, vascular endothelial proliferation and the grade of malignancy. Oligodendrogliomas and the oligodendroglial component of mixed gliomas lacked immunoreactive VEGF, indicating that endothelial growth factors other than VEGF may regulate tumor angiogenesis in these neoplasms. Western blot analysis showed a predominant VEGF protein species of 23 kDa and confirmed the immunohistochemical data in all cases. Our findings demonstrate that VEGF is expressed in a wide spectrum of brain tumors in which it may induce neovascularization. However, other angiogenic factors also appear to contribute to the vascularization of CNS neoplasms.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050591
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    The CD34 epitope is expressed in neoplastic and malformative lesions associated with chronic, focal epilepsies (1999)
    Springer
    Acta neuropathologica 97 (1999), S. 481-490 
    Details
    ISSN: 1432-0533
    Keywords: Key words Stem cell ; Tumor ; Malformation ; Epilepsy ; Ganglioglioma
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The etiology and pathogenesis of complex focal lesions associated with chronic, intractable epilepsy are largely unknown. Some data indicate that malformative changes of the central nervous system may preceed the development of gangliogliomas and other epilepsy-associated neoplasms. In the present immunhistochemical study, we have examined epilepsy-associated lesions for CD34, a stem cell marker transiently expressed during early neurulation. Surprisingly, most tissue samples from patients with chronic epilepsy (n = 262) revealed neural cells immunoreactive for CD34. Prominent immunoreactivity was detected in gangliogliomas (74%), low-grade astrocytomas (62%) and oligodendrogliomas (59%). Only 52% of non-neoplastic, malformative pathologies, such as glio-neuronal hamartias or hamartomas showed solitary or small clusters of CD34-immunoreactive cells. None of the adult control tissues (n = 22), none of the specimens obtained from the developing human brain (n = 44) and none of those tumor samples from patients without epilepsy (n = 63) contained CD34-immunoreactive neural cells. However, a malignant teratoma with microscopic features of early neural differentiation displayed a focal CD34-immunoreactive staining pattern. The majority of CD34-immunoreactive cells co-localized with S-100 protein and a small subpopulation was also immunoreactive for neuronal antigens. CD34 may, thus, represent a valuable marker for the diagnostic evaluation of neoplastic and/or malformative pathological changes in epilepsy patients. The CD34 immunoreactivity of these lesions indicates an origin from dysplastic or atypically differentiated neural precursors. Further studies may elucidate the functional significance of CD34 expression during the pathogenesis of epilepsy-related focal lesions as well as during neurogenesis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010051017
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    Paper (German National Licenses)
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