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  • 1
    ISSN: 1432-0533
    Keywords: Protein kinase C ; Proliferative activity ; Immunohistochemistry ; Human brain neoplasms
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Protein kinase C (PKC), the major receptor for phorbol ester tumor promotors, is a phospholipid- and calcium-dependent phosphorylating enzyme which plays an important role in the intracellular signal transduction necessary for a variety of basic cellular functions including the control of cell proliferation. To determine the expression of PKC in human neurogenic tumors we investigated 121 tumors of the human nervous system by means of immunohistochemistry using the monoclonal antibody C5. The results were compared with immunohistochemical staining for intermediate filament proteins, desmoplakins, and the proliferation-associated nuclear antigen Ki-67. Besides strong staining of normal and reactive astrocytes, C5 immunoreactivity was consistently observed in tumor cells of all types of gliomas. However, the fraction of C5 positive tumor cells varied between the different tumor types with astrocytomas and subependymomas demonstrating the strongest immunoreactivity. In the other gliomas, especially those of higher malignancy, a considerable heterogeneity in C5 expression could be observed. There was a tendency for the percentage of C5 immunostained tumor cells being lower in high-grade gliomas compared to low-grade ones and comparison with Ki-67 staining frequently revealed an inverse relationship between proliferative activity and C5 immunoreactivity. Besides the gliomas we found 3 of 7 neurinomas and 6 of 18 meningiomas which were partially C5 positive. All other tumors investigated including medulloblastomas and metastatic carcinomas were C5 negative. Our results thus indicate that immunohistochemistry for PKC using the monoclonal antibody C5 could be an useful aid for histopathological tumor classification in neurooncology.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0533
    Keywords: Key words Chromosome 1 ; Loss of heterozygosity ; Meningioma ; Progression ; Tumor suppressor gene
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We have studied a series of 63 meningiomas, including 47 benign meningiomas (World Health Organization, WHO, grade I), 13 atypical meningiomas (WHO grade II) and 3 anaplastic meningiomas (WHO grade III), using microsatellite and restriction fragment length polymorphism analysis for loss of heterozygosity (LOH) at 21 polymorphic loci on chromosome 1 (19 loci on 1p and 2 loci on 1q). LOH on 1p was found in 9 of 13 atypical meningiomas (70%) and in 3 of 3 (100%) anaplastic meningiomas, but only in 6 of 47 (13%) benign meningiomas. In 13 tumors allelic loss was observed at all informative loci on 1p. Terminal deletions with retention of heterozygosity at one or more proximal 1p loci were found in 5 tumors. The region commonly deleted in all tumors was located distally to the D1S496 locus, i.e., at cytogenetic bands 1p34 – 1pter, and included the chromosomal segment which is frequently deleted in neuroblastoma, malignant melanoma, and different types of carcinoma.
    Type of Medium: Electronic Resource
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