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  • 1
    Electronic Resource
    Electronic Resource
    Expression of stem-cell factor and its receptor c-kit protein in normal testicular tissue and malignant germ-cell tumours (1996)
    Springer
    Journal of cancer research and clinical oncology 122 (1996), S. 301-306 
    Details
    ISSN: 1432-1335
    Keywords: Testicular cancer ; Spermatogenesis ; Stem-cell factor (SCF) ; c-kit proto-oncogene ; Growth stimulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The proto-oncogene c-kit and its ligand stemcell factor (SCF) may play an important role in the development of normal and malignant testicular tissue. This study investigates the presence of SCF and c-kit protein in 32 orchiectomy specimens of patients with testicular cancer, in 5 specimens of normal testicular tissue and in three established non-seminomatous germ-cell cancer cell lines (H12.1, H32, 577ML) by an immunohistochemical approach. Out of 9 testicular cancer specimens classified as pure seminomas, 7 (78%) showed a strong immunohistochemical reaction for both SCF and c-kit protein on the surface of the tumour cells. Fourteen non-seminomatous germ-cell tumours composed of embryonal carcinoma were completely negative for both SCF and c-kit protein and only faint positivity was found in 6 tumours (26%). Differentiated teratomatous structures within the specimens of nonseminomatous tumours showed a strong immunohistochemical reaction for SCF and c-kit protein in 8 of 11 (73%) cases. All three testicular cancer cell lines showed only faint staining reactions for c-kit protein and none for SCF. No secretion of SCF by the three lines in vitro was detected. The addition of high concentrations of SCF (100 ng/ml) to the testicular cancer cell lines in culture conditions without fetal calf serum resulted in a 1.4 to 3-fold growth stimulation compared to cell growth in serum-free medium alone. This effect was not detectable when the cells were cultured in serum-containing media. In the normal testicular tissue the germ-cells displayed a strong immunohistochemical reaction for c-kit protein while SCF positivity was found at the tubular membrane and on the surface of Sertoli cells. The SCF/c-kit system may possess a regulatory function in normal testicular tissue by possibly providing the microenvironment necessary for spermatogenesis. With the development of testicular cancer, this regulatory system seems to be lost, particularly in non-seminomatous germ-cell tumours. A growthstimulatory effect of high concentrations of SCF on nonseminomatous testicular cancer cell lines can be detected only in culture conditions with serum-free media. The effects achievable by the combination of SCF with other growth factors need to be further studied, as well as the role of the c-kit/SCF regulatory system for normal spermatogenesis and its possible implications for the understanding and treatment of male infertility.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01261407
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  • 2
    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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  • 3
    Electronic Resource
    Electronic Resource
    Tuberous sclerosis-like lesions in epileptogenic human neocortex lack allelic loss at the TSC1 and TSC2 regions (1996)
    Springer
    Acta neuropathologica 93 (1996), S. 93-96 
    Details
    ISSN: 1432-0533
    Keywords: Key words Chromosome 9 ; Chromosome 16 ; Epilepsy ; Hamartoma ; Pathology
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Glioneuronal malformations with a striking histological resemblance to cortical tubers of tuberous sclerosis, but no extracerebral stigmata of this phacomatosis, are frequently encountered in patients with chronic pharmacoresistant epilepsies. It is controversial as to whether these lesion represent a forme fruste of tuberous sclerosis or a distinct entity. The recently reported loss of heterozygosity (LOH) at the regions of the TSC1 or TSC2 locus in hamartomas obtained from different organs of patients with established tuberous sclerosis, including cortical tubers, stimulated us to examine epilepsy-associated tuberous sclerosis-like glioneuronal malformations with respect to LOH at the TSC1 and TSC2 loci of chromosomes 9q34 and 16p13.3, respectively. The analysis was carried out on DNA derived from paraffin-embedded brain tissues of 11 patients. For 5 patients, peripheral blood leukocytes were also available for DNA extraction. We performed microsatellite analysis with five markers on chromosome 9 and four markers on chromosome 16. In addition, polymerase chain reaction-restriction fragment length polymorphism (RFLP) analysis was performed using a polymorphic EcoRV restriction site in exon 40 of the TSC2 gene. No LOH was identified in any of the cases. These findings do not support a relationship between the epilepsy-associated glioneuronal lesions and tuberous sclerosis. However, tuberous sclerosis is genetically heterogeneous and microsatellite and RFLP analysis cannot exclude small deletions or point mutations. Thus, given the histopathological similarity of glioneuronal malformations in epilepsy patients to cortical tubers, further molecular genetic studies will be needed as our understanding of the molecular basis of tuberous sclerosis increases to completely clarify the relationship of these lesions to tuberous sclerosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050587
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  • 4
    Electronic Resource
    Electronic Resource
    Coexpression of stem cell factor and its receptor c-Kit in human malignant glioma cell lines (1995)
    Springer
    Acta neuropathologica 89 (1995), S. 158-165 
    Details
    ISSN: 1432-0533
    Keywords: Glioma ; Stem cell factor ; Oncogene ; Kit Autocrine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Stem cell factor (SCF), a hematopoietic growth factor, is the ligand of the tyrosine kinase receptor encoded by the c-kit proto-oncogene. Beside the important role of this receptor-ligand complex in hematopoiesis, gametogenesis and melanogenesis, SCF and its receptor have been shown to be expressed in the brain. We have studied the expression of SCF and c-kit in 20 human malignant glioma cell lines at the mRNA as well as at the protein level. In addition, recombinant human (rh) SCF was tested in [3H]thymidine uptake assays for a mitogenic effect on these cells. SCF and c-Kit proteins were detected in the cytoplasm of glioma cells by alkaline phoshatase-monoclonal anti-alkaline phosphatase immunostaining and Western blot analysis. However, neither SCF nor c-Kit were seen on the cell surface by flow cytometry. Furthermore, none of the proliferation assays showed a mitogenic effect for exogenously added rhSCF. Blocking studies using an anti-SCF antibody failed to demonstrate modulating effects on the growth of selected cell lines. These results suggest that SCF and c-Kit may mediate non-proliferative signals or may employ intracellular mechanisms for autocrine growth regulation of glioma cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00296360
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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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  • 6
    Electronic Resource
    Electronic Resource
    Medullomyoblastoma: a histological, immunohistochemical, ultrastructural and molecular genetic study (1998)
    Springer
    Acta neuropathologica 95 (1998), S. 205-212 
    Details
    ISSN: 1432-0533
    Keywords: Key words Medullomyoblastoma ; Medulloblastoma ; c-myc ; c-erb-B2 ; Allelic loss
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Medullomyoblastoma is a rare variant of medulloblastoma containing myoblastic elements. A 9-year-old boy developed a cerebellar syndrome and signs of increased intracranial pressure, the cause of which was a tumor of the cerebellar vermis measuring 7 × 4.5 × 4.5 cm. Morphologically the tumor largely consisted of a medulloblastoma component but displayed glial, myoblastic and ganglionic differentiation on light microscopic, immunohistochemical and ultrastructural examination. The non-enhancing rim of the tumor on magnetic resonance imaging showed extensive ganglionic differentiation. The tumor did not express bcl-2, c-myc, or c-erb-B2 oncoproteins and was negative for the p53 gene product. On molecular genetic studies, the tumor did not show allelic loss on chromosome loci, frequently altered in medulloblastomas, such as 17p, 1q and 9q.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050788
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  • 7
    Electronic Resource
    Electronic Resource
    Neural antigens in oligodendrogliomas and dysembryoplastic neuroepithelial tumors (1997)
    Springer
    Acta neuropathologica 94 (1997), S. 436-443 
    Details
    ISSN: 1432-0533
    Keywords: Key words Epilepsy ; Immunohistochmistry ; Receptor ; Neurotransmitter ; Tumor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Oligodendrogliomas and dysembryoplastic neuroepithelial tumors (DNT) are frequently associated with epilepsies and share the presence of oligodendroglia-like cells with small round nuclei and optically empty perinuclear halos. The two entities may be difficult to discriminate in small surgical specimens and the origin and differentiation of the oligodendroglia-like cells has been controversial. To better characterize and distinguish the two entities we examined 25 oligodendrogliomas and 16 DNT immunohistochemically for the presence of the proliferation–associated Ki-67 antigen and the following neural antigens: the α1 subunit of the GABAA receptor (GABAR), N-methyl-d-aspartate receptor subunit 1 (NR1), glutamate decarboxylase, neuronal nuclei antigen (NeuN), the embryonal form of the neural cell adhesion molecule (E-NCAM), synaptophysin, neurofilament protein (NFP), and glial fibrillary acidic protein (GFAP). Labeling indices for the Ki-67 antigens were generally less than 1% in both entities. In oligodendrogliomas, more than 50% of the tumors contained NR1- or E-NCAM-positive oligodendroglia-like cells, whereas NeuN-positive tumor cells were never observed. In DNT, NeuN- and NR1-positive tumor cells were present in 44% of the cases each; E-NCAM positivity was less frequent (19%). In both entities, immunoreactivity of oligodendroglia-like cells for GABAR and glutamate decarboxylase was rare and positivity for synaptophysin and neurofilament protein was absent. Some GFAP-positive tumor cells were present in approximately 70% of the cases in both entities. Except for the striking difference in NeuN positivity, the immunohistochemical profiles of oligodendroglia-like cells in DNT and oligodendrogliomas largely overlap and the differential diagnosis continues to rest mainly on conventional histopathological features. The NR1 positivity and the recently reported generation of action potentials in oligodendroglioma cells are consistent with neuronal differentiation and may contribute to the high epileptogenic potential of oligodendrogliomas.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050730
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  • 8
    Electronic Resource
    Electronic Resource
    Coexpression of stem cell factor and its receptor c-Kit in human malignant glioma cell lines (1995)
    Springer
    Acta neuropathologica 89 (1995), S. 158-165 
    Details
    ISSN: 1432-0533
    Keywords: Key words Glioma ; Stem cell factor ; Oncogene ; Kit ; Autocrine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Stem cell factor (SCF), a hematopoietic growth factor, is the ligand of the tyrosine kinase receptor encoded by the c-kit proto-oncogene. Beside the important role of this receptor-ligand complex in hematopoiesis, gametogenesis and melanogenesis, SCF and its receptor have been shown to be expressed in the brain. We have studied the expression of SCF and c-kit in 20 human malignant glioma cell lines at the mRNA as well as at the protein level. In addition, recombinant human (rh) SCF was tested in [3H]thymidine uptake assays for a mitogenic effect on these cells. SCF and c-Kit proteins were detected in the cytoplasm of glioma cells by alkaline phoshatase-monoclonal anti-alkaline phosphatase immunostaining and Western blot analysis. However, neither SCF nor c-Kit were seen on the cell surface by flow cytometry. Furthermore, none of the proliferation assays showed a mitogenic effect for exogenously added rhSCF. Blocking studies using an anti-SCF antibody failed to demonstrate modulating effects on the growth of selected cell lines. These results suggest that SCF and c-Kit may mediate non-proliferative signals or may employ intracellular mechanisms for autocrine growth regulation of glioma cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00296360
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  • 9
    Electronic Resource
    Electronic Resource
    Molecular Neuropathology of Astrocytic Brain Tumors (1997)
    Springer
    Journal of neuro-oncology 35 (1997), S. 211-222 
    Details
    ISSN: 1573-7373
    Keywords: angiogenesis ; astrocytoma ; cell cycle ; glioblastoma ; growth factors ; molecular genetics ; neuropathology ; oncogenes ; tumor suppressor genes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Both surgical and molecular neuropathologists have recently achievedremarkable progress in the histogenetic classification and molecularcharacterization of human gliomas. Major histopathological achievements inthe revised WHO classification include the introduction ofimmunohistochemical reagents for glial fibrillary acidic protein andfor the proliferation-associated antigens, the definition of glioblastomamultiforme as an astrocytic neoplasm and the recognitionof the pleomorphic xantho- astrocytomas as a novelclinico-pathological entity.In molecular neuropathology, alterations of oncogenes and tumorsuppressor genes and their potential functions have beenidentified, microsatellite analyses have revealed novel loci forputative tumor suppressor genes and distinct molecular pathwaysfor different tumor entities are beginning to emerge.Mutations in cell cycle regulatory genes are presentin most glioblastomas and may account for theirstriking growth potential. Autocrine and paracrine growth factorsand their respective protein tyrosine kinase receptors appearto contribute both to glial and endothelial cellproliferation.In our contribution, we would like to focuson astrocytic gliomas. Findings with potential diagnostic relevanceinclude changes associated with malignant progression of lowgrade astrocytomas, patterns of genetic alterations which allowto further differentiate histopathological entities such as theglioblastoma multiforme into genetically distinct subsets and mechanismsof tumor angiogenesis in malignant gliomas.One of the major tasks ahead is toestablish correlations and relationships between histopathological, molecular andclinical data. This will require a long-term collaborationbetween molecular neuropathologists, neurosurgeons and clinical neuro-oncologists.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1005843913095
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  • 10
    Electronic Resource
    Electronic Resource
    Expression of Different Extracellular Matrix Components in Human Brain Tumor and Melanoma Cells in Respect to Variant Culture Conditions (1999)
    Springer
    Journal of neuro-oncology 44 (1999), S. 23-33 
    Details
    ISSN: 1573-7373
    Keywords: ECR expression ; glioblastoma ; melanoma ; serum free medium ; migration
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Local tumor invasion into the surrounding brain tissue is a major characteristic of malignant gliomas. These processes critically depend on the interaction of tumor cells with various extracellular matrix (ECM) components. Because only little quantitative information about expression of ECM gene products in general and expression in response to alterations of the surrounding environment is available, the present study was designed. Four human glioblastoma cell lines (U373MG, U138MG, U251MG, GaMG) as well as four human melanoma cell lines (MV3, BLM, 530, IF6) were tested with semiquantitative RT-PCR for their ability to express mRNA of different human ECM components (fibronectin, decorin, tenascin, collagen I, collagen IV, versican). In addition, two human medulloblastoma (MHH-Med 1, MHH-Med 4) and two fibrosarcoma (HT1080, U2OS) cell lines were analyzed. Cells which were grown in DMEM medium containing 10% FCS expressed most of the analyzed protein components. When the same medium, but depleted of ECM proteins by filtrating through a membrane with cut-off at 〉100 kD was used, basal mRNA expression of the ECM proteins was changed in most of the examined cell lines. Using serum free conditions, most of the cell lines again showed a variation in the expression pattern of mRNA encoding for the different ECM proteins compared to the other medium conditions. Comparing different cell lines from one tumor entity or different tumor groups, ECM expression was heterogeneous with regard to the different tumor entities as well as within the entities themselves. Migration assays revealed heterogeneous responses between the different cell lines, ECM components and culture conditions, making it difficult to correlate ECM expression patterns and migratory behavior. Our results revealed that all examined cell lines are able to produce ECM proteins in vitro. This suggests that tumor cells can modulate their microenvironment in vitro which has to be taken into consideration for studies related to migration and invasion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006331416283
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