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  • 1
    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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  • 2
    Electronic Resource
    Electronic Resource
    Tumor induction by ras and myc oncogenes in fetal and neonatal brain: modulating effects of developmental stage and retroviral dose (1993)
    Springer
    Acta neuropathologica 86 (1993), S. 456-465 
    Details
    ISSN: 1432-0533
    Keywords: Retroviral vectors ; Oncogene-ras-myc ; Grafting ; Brain tumors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Introduction into fetal rat brain cells of a replication-defective retroviral vector harboring v-Ha-ras and v-gag-myc rapidly causes the induction of highly malignant undifferentiated neuroectodermal tumors following transplantation into the brains of syngeneic hosts [Wiestler, et al. (1992) Cancer Res. 52: 3760–3767]. In the present study, we have investigated the modulating effect of the developmental stage of neural target cells and of the dose of the retroviral vector used in the grafting experiments. Exposure of fetal cells from embryonic day (E)12 or E14 produced a 100% incidence of malignant neuroectodermal tumors which led to the death of recipient animals after a median latency period of 32 days. A 100-fold reduction of the virus dose from 2.062×106 to 2.062×104 focus-forming units/ml resulted in a lower tumor incidence of 25%. Of six neural grafts exposed to v-Ha-ras and v-myc at E16, only one showed evidence of tumorigenesis (low-grade astrocytoma and hemangioma). All other transplants were morphologically normal for observation periods of 26 weeks, indicating a marked loss of transforming activity of ras and myc in more advanced stages of brain development. In retrovirus-exposed donor cells which caused the development of neural tumors in recipient rats, malignant transformation was also evident during culture in vitro, usually after 9–12 days. Oncogene complementation was also studied in the newborn rat brain. After microinjection of the retroviral vector into the brain at postnatal day (P)0, P1 and P3, 5 out of 20 animals (25%) developed a total of seven brain tumors. Histopathologically, three of these neoplasms were malignant neuroectodermal tumors which, in contrast to those induced in fetal brain transplants showed evidence of focal glial and/or neuronal differentiation. In addition, we observed one oligodendroglioma, two hemangiomas and a malignant hemangioendothelioma. These data indicate that neural precursor cells and endothelia of the rat brain represent the major target cells for the complementary action of ras and myc and that the use of target cells from later developmental stages (E16 and postnatal) leads to the induction of both primitive and more differentiated neoplasms.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00228580
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  • 3
    Electronic Resource
    Electronic Resource
    Neuropathological findings in 224 patients with temporal lobe epilepsy (1993)
    Springer
    Acta neuropathologica 86 (1993), S. 433-438 
    Details
    ISSN: 1432-0533
    Keywords: Temporal lobe epilepsy ; Hippocampal sclerosis ; Ganglioglioma ; Hamartoma ; Amygdalo-hippocampectomy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract During the period between 1976 and 1990, 247 patients with pharmaco-resistant complex partial seizures and a documented unilateral epileptogenic area in the mediobasal temporal lobe underwent a selective amygdalo-hippocampectomy procedure at our institution. Biopsy specimens from 224 patients (91% of the total) were available for a retrospective histopathological and immunohistochemical review. The tissue specimens of 23 patients without evidence for a macroscopic lesion have been used for neurochemical studies and could not be evaluated histopathologically. The most common temporal lobe pathology were neoplasms in 126 patients, i.e. 56%. Tumor entities observed included 23 astrocytomas (18% of all tumors), 17 gangliogliomas (13%), 15 oligodendrogliomas (12%), 15 cases of glioblastoma multiforme (12%), 13 pilocytic astrocytomas (10%), 12 oligo-astrocytomas (10%), 11 anaplastic astrocytomas (9%) and 20 tumors of various other histologies. In 23 specimens (10%), small foci of oligodendroglia-like clear cells were found. The frequent association of these foci with low-grade gliomas or neural hamartomas raises the possibility that these structures may serve as precursor lesion for neuroepithelial tumors of the temporal lobe. In 98 cases, pathological changes of non-neoplastic origin were encountered. The most common diagnoses in this group included hippocampal gliosis/sclerosis (49 cases, 22%) and vascular malformations (20 cases, 9%). Hamartomas, i.e. focal accumulations of dysplastic neuro-glial cells were diagnosed in 14 patients (6%). In only four cases have we not been able to detect any microscopic pathology. These results indicate that a high proportion of pharmaco-therapy-resistent complex-partial seizures are caused by neoplasms of the temporal lobe, some of which appear to the strikingly overrepresented in this group of patients.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00228577
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  • 4
    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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  • 5
    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: Key words: 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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  • 6
    Electronic Resource
    Electronic Resource
    Hippocampal loss of the GABAA receptor a1 subunit in patients with chronic pharmacoresistant epilepsies (1994)
    Springer
    Acta neuropathologica 88 (1994), S. 313-319 
    Details
    ISSN: 1432-0533
    Keywords: Key words Epilepsy ; Gamma aminobutyric acid ; Receptor ; Ammon's horn sclerosis ; Hippocampus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Alterations of gamma aminobutyric acid (GABA)-mediated neurotransmission have been implicated in the pathogenesis of epilepsies. Here we examine the distribution of the GABAA receptor in the hippocampus of 78 surgical specimens from patients with chronic pharmacoresistant focal epilepsies. The receptor was localized immunohistochemically with the monoclonal antibody bd-24 which selectively recognizes the α1 subunit of the GABAA receptor. The results were compared with the receptor distribution of 28 normal hippocampal specimens obtained at autopsy. In the great majority of the surgical specimens a loss of GABAA receptor immunoreactivity was present in CA1 (92.3  %), CA4 (78.2  %), the dentate granular cell layer (70.5  %) and the molecular layer of the dentate gyrus (65.4  %). The subiculum revealed a normal staining pattern in all but 4 cases. In no instance did we observe an increase of immunoreactivity in any region or cell population. The decrease of GABAA receptor immunoreactivity was closely related to neuronal loss in the respective specimen and to Ammon's horn sclerosis. There was no correlation between GABAA receptor loss and the patient's age at surgery, duration of seizures, age at onset of seizures and to the presence or absence of secondary generalized tonic clonic seizures. The data suggest that the observed loss of GABAA receptor immunoreactivity 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/BF00310375
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  • 7
    Electronic Resource
    Electronic Resource
    Correlated stage- and subfield-associated hippocampal gene expression patterns in experimental and human temporal lobe epilepsy (2003)
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 18 (2003), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Epileptic activity evokes profound alterations of hippocampal organization and function. Genomic responses may reflect immediate consequences of excitatory stimulation as well as sustained molecular processes related to neuronal plasticity and structural remodeling. Using oligonucleotide microarrays with 8799 sequences, we determined subregional gene expression profiles in rats subjected to pilocarpine-induced epilepsy (U34A arrays, Affymetrix, Santa Clara, CA, USA; P 〈 0.05, twofold change, n = 3 per stage). Patterns of gene expression corresponded to distinct stages of epilepsy development. The highest number of differentially expressed genes (dentate gyrus, approx. 400 genes and CA1, approx. 700 genes) was observed 3 days after status epilepticus. The majority of up-regulated genes was associated with mechanisms of cellular stress and injury – 14 days after status epilepticus, numerous transcription factors and genes linked to cytoskeletal and synaptic reorganization were differentially expressed and, in the stage of chronic spontaneous seizures, distinct changes were observed in the transcription of genes involved in various neurotransmission pathways and between animals with low vs. high seizure frequency. A number of genes (n = 18) differentially expressed during the chronic epileptic stage showed corresponding expression patterns in hippocampal subfields of patients with pharmacoresistant temporal lobe epilepsy (n = 5 temporal lobe epilepsy patients; U133A microarrays, Affymetrix; covering 22 284 human sequences). These data provide novel insights into the molecular mechanisms of epileptogenesis and seizure-associated cellular and structural remodeling of the hippocampus.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1460-9568.2003.02993.x
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  • 8
    Electronic Resource
    Electronic Resource
    Primary manifestation of Hodgkin’s disease in the central nervous system (1998)
    Springer
    Virchows Archiv 432 (1998), S. 477-481 
    Details
    ISSN: 1432-2307
    Keywords: Key words Hodgkin’s disease ; Central nervous system ; Proliferation ; Apoptosis ; bcl-2
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  A 62-year-old woman presented with loss of memory and a mild hemiparesis. Neuroradiology demonstrated a left frontoparietal tumour. Biopsy specimens of this lesion revealed intracerebral Hodgkin’s lymphoma, a diagnosis supported by immunohistochemical reactions of the tumour cells for the CD30 antigen. Additional cell cycle studies revealed a high proliferative activity of the tumour cells in association with absence of apoptosis. There was no evidence that overexpression of bcl-2 or Epstein-Barr virus infection was involved in the pathogenesis of this neoplasm. Lymphomas in the lung were detected 3 months later. Following neurosurgical excision, radiotherapy, and chemotherapy, the patient had no evidence of Hodgkin’s disease after 13 months of follow-up.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004280050195
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  • 9
    Electronic Resource
    Electronic Resource
    Expression of the epidermal growth factor receptor in astrocytic tumours is specifically associated with glioblastoma multiforme (1992)
    Springer
    Virchows Archiv 420 (1992), S. 321-325 
    Details
    ISSN: 1432-2307
    Keywords: Astrocytoma ; Glioblastoma multiforme ; Oncogenes ; Epidermal growth factor receptor ; Immunohistochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Epidermal growth factor and its receptor (EGFR) constitute an important and well-characterized mitogenic system in various ectodermal tissues including glial cells. Over-expression of the EGFR due to gene amplification has been reported in primary brain tumours of glial origin. Using a monoclonal antibody to the EGFR and immunohistochemical analysis, we examined the expression and distribution of EGFR in 103 astrocytic tumours. In addition, selected tumours were studied by Western blotting using a polyclonal antibody to EGFR and by Southern blot analysis. Glioblastomas (WHO grade IV) showed EGFR expression in 37% of cases, whereas pilocytic (WHO grade I), low-grade (WHO grade II) or anaplastic astrocytoma (WHO grade III) were invariably EGFR negative. Generally, there was a close correlation between the presence of EGFR gene amplification and over-expression of receptor protein. Different patterns of immunoreactive cells and significant intratumour heterogeneity of EGFR expression were observed in glioblastomas. The specific association of EGFR over-expression with glioblastoma may provide a useful diagnostic tool for distinguishing anaplastic astrocytoma (WHO grade III) and glioblastoma multiforme (WHO grade IV).
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01600211
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  • 10
    Electronic Resource
    Electronic Resource
    Perilesional neurochemical changes in focal epilepsies (1996)
    Springer
    Acta neuropathologica 91 (1996), S. 376-384 
    Details
    ISSN: 1432-0533
    Keywords: Key words Epilepsy ; Immunohistochemistry ; Neurotransmitter ; Pathology ; Tumor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Circumscribed cortical lesions are frequently encountered in patients with chronic focal epilepsies. However, the pathogenesis of seizures is poorly understood. To determine whether the perilesional cortex shows evidence for abnormal excitatory or inhibitory neurochemical activity, we immunohistochemically examined the distribution of the α1 subunit of the GABAA receptor (GABAR), the N-methyl-d-aspartate receptor subunit 1 (NR1), and glutamate decarboxylase (GAD) in 30 surgical specimens of neocortical epilepsy-associated lesions. These comprised 7 low-grade gliomas, 2 gangliogliomas, 2 dysembryoplastic neuroepithelial tumors, 4 glioneuronal malformations, 5 vascular malformations, and 10 glial or gliomesodermal scars. All specimens originated from patients with chronic pharmacoresistant epilepsy. In 73% of the cases there was a distinct difference in immunoreactivity for GABAR, GAD or NR1 between the perilesional zone and the normal cortex. With each of the markers there was reduced perilesional immunoreactivity in 30% of the specimens. Increased staining for GAD was seen in 17%, for GABAR in 7%, and for NR1 in 13% of the cases. The age at surgery, onset of seizures, epilepsy duration, and maximal seizure frequency did not differ significantly between patients with normal and those with altered perilesional immunoreactivity patterns. Although the perilesional changes for GAD, GABAR or NR1 were heterogeneous, they suggest a disturbed balance between excitatory and inhibitory synaptic transmission which may contribute to the pathogenesis of focal seizures.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050439
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