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      The role of glutamine synthetase in the diagnosis of cerebral tumours.

      Neuropathology and Applied Neurobiology
      Astrocytoma, enzymology, Brain Neoplasms, diagnosis, Diagnosis, Differential, Ependymoma, Glial Fibrillary Acidic Protein, Glioblastoma, Glutamate-Ammonia Ligase, metabolism, Humans, Immunoenzyme Techniques, Intermediate Filament Proteins, Lymphatic Diseases, Lymphoma, Medulloblastoma, Meningeal Neoplasms, Meningioma, Neuroglia, Oligodendroglioma

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          Abstract

          Glutamine synthetase (GS) was studied in a range of human brain tumours and compared with results obtained by staining for glial fibrillary acidic protein (GFAP) using the indirect immunoperoxidase and peroxidase-anti-peroxidase methods. All astrocytomas showed positive staining with GS, the degree of which was related to the extent of differentiation and the amount of cytoplasm of the constituent cells. Ependymomas were only weakly positive, although a dense GFAP reaction was detected around blood vessels; possibly due to the presence of astrocyte foot processes. Medulloblastomas showed signs of astrocytic differentiation by the presence of clusters of positively staining cells amongst undifferentiated neoplastic cells. Oligodendrocytomas and meningiomas were generally negative apart from occasional astrocytes within the former neoplasms. GS and GFAP staining corresponded in virtually all cases; however, GS demonstrated poorly-fibrillated cells better than GFAP, but did not show cell processes so clearly. Although GS appears to be cell-specific in the central nervous system for normal, reactive and neoplastic astrocytes, it is not organ-specific and therefore also stains cells of other tissues, e.g. liver. GS offers a practical alternative to GFAP as an astrocyte specific marker in human cerebral tumours and may be of diagnostic value in cases where poorly-differentiated astrocytic tumours have been found negative to conventional histological stains for glial fibres or demonstrate a weak positive reaction to GFAP.

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