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  • 1
    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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  • 2
    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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  • 3
    Electronic Resource
    Electronic Resource
    An experimental model for infiltration of malignant lymphoma to the eye and brain (1997)
    Springer
    Virchows Archiv 431 (1997), S. 459-467 
    Details
    ISSN: 1432-2307
    Keywords: Key words Metastasis ; CNS lymphoma ; Ocular lymphoma ; S49
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Currently there is no adequate experimental model available whereby the lethal infiltration of malignant lymphoma to the eye and CNS can be studied. Variant S49 mouse lymphoma cells that exhibit cell-cell adhesion properties (named Rev-2-T-6) were inoculated intraperitoneally into Balb/C mice at the ages of 6–60 days postnatal. Mice inoculated between days 6–11 postnatal developed signs of eye and CNS involvement with an apparent peak (58% of mice) at day 7. None of the mice inoculated beyond day 11 exhibited such signs. Histological analysis of these sites revealed tumorous infiltrates into a variety of structures in the orbit, intraocular tissues, along the optic nerve and in the brain. Additional analysis of the histopathological data, based on the structures demonstrating the highest frequency of lymphoma infiltration, suggests preferred routes of lymphoma entry to the brain and eye. Thus, entry to the brain can occur mainly through the choroid plexus and cranial nerves or cranial nerve ganglia. Entry to the eye may occur from the brain (along the optic nerve), and through hematogenous infiltration of orbital structures. No data were found that would support retrograde infiltration of the lymphoma from the eye to the brain. These findings present an experimental model for addressing the molecular mechanisms that govern homing of malignant lymphoma to the eye and brain, as well as the development of experimental therapeutic modalities for malignant lymphoma in these organs.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004280050124
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  • 4
    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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  • 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
    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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  • 7
    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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  • 8
    Electronic Resource
    Electronic Resource
    Apoptosis and apoptosis-related gene products in primary non-Hodgkin’s lymphoma of the central nervous system (1998)
    Springer
    Acta neuropathologica 96 (1998), S. 157-162 
    Details
    ISSN: 1432-0533
    Keywords: Key words Central nervous system ; Lymphoma ; B cell ; Apoptosis ; bcl-2
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The incidence of primary lymphomas of the central nervous system (CNS) has significantly increased over the last years. However, the pathogenesis of this serious and fatal disease is still largely unknown. The aim of the present study was to investigate whether impairment of apoptosis is involved in the pathogenesis of primary CNS lymphomas. A series of 35 primary CNS lymphomas was investigated for the presence of apoptotic cells and the expression of apoptosis-inhibiting and proapoptotic gene products of the bcl family by application of the terminal deoxynucleotidyl transferase-mediated dUTP-nick end labeling (TUNEL) technique and immunohistochemistry. The majority (23/35) of the tumors contained no or less than 10% of apoptotic cells. All tumors were MIB-1 positive, and 53% of them showed a high proliferative activity with more than 20% MIB-1-positive cells. The bcl-2 gene was expressed in 54% of the tumors (19/35), whereas bcl-x and bax gene products were present in only a low fraction of these lymphomas (4/35). In contrast, bak and the tumor suppressor gene p53 product were not detectable. These findings indicate that apoptosis is inhibited in the majority of this series of primary CNS lymphomas. Since there was no statistical correlation between the degree of apoptosis and the expression of proteins of the bcl gene family, other apoptosis-inhibiting factors may be involved in the pathogenesis of primary CNS lymphomas.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050876
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  • 9
    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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  • 10
    Electronic Resource
    Electronic Resource
    Altered distribution of the α-amino-3-hydroxy-5-methyl-4-isoxazole propionate receptor subunit GluR2(4) and the N-methyl-d-aspartate receptor subunit NMDAR1 in the hippocampus of patients with temporal lobe epilepsy (1996)
    Springer
    Acta neuropathologica 92 (1996), S. 576-587 
    Details
    ISSN: 1432-0533
    Keywords: Key words Excitatory amino acids ; Therapy-refractory epilepsy ; Ammon’s horn sclerosis ; Quantitative image analysis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In patients with therapy-refractory temporal lobe epilepsy (TLE), alterations of glutamate receptors have been proposed as a mechanism for enhanced excitability. Using commercially available monoclonal antibodies specific for the N-methyl-d-aspartate (NMDA) receptor subunit NMDAR1 and for the α-amino-3-hydroxy-5-methyl-4-isoxazole propionate receptor subunit GluR2(4), we have examined the distribution of these polypeptides in human hippocampal tissue that was surgically removed from patients with intractable TLE. Surgical specimens were classified according to the presence of Ammon’s horn sclerosis (AHS) or a focal lesion in the temporal lobe. Cell counts and a densitometric analysis of the immunoreactivity patterns were carried out for all hippocampal subfields. NMDAR1 and GluR2(4) levels were markedly reduced in patients with AHS, primarily in those subfields with substantial neuronal cell loss (in particular CA1, CA4 and CA3), compared to those seen in patients with focal lesions and in control specimens obtained at autopsy. In contrast, the molecular layer of the dentate gyrus (DG-ML) showed significantly higher levels of GluR2(4) immunoreactivity in AHS compared to control tissue, while NMDAR1 showed no significant up-regulation in this sublayer. When the receptor staining intensity was normalized for alterations in neuronal density, no significant alterations could be detected except for an increase in GluR2(4) in the DG-ML of patients with AHS. These changes may reflect synaptic reorganization observed in the DG-ML of specimens from patients with chronic intractable TLE.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050564
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