Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017636 (glioblastoma)
 18,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Extraneural metastases from malignant glioma and glioblastoma are believed to be rare. The most common sites of metastases are lung, lymph nodes, bone, and liver. We recently encountered two patients with glioblastoma multiforme who presented with pain and thrombocytopenia caused by diffuse metastasis to bone marrow. A premortem diagnosis was established in the first patient with the aid of peroxidase-antiperoxidase staining of the bone marrow biopsy specimen for glial fibrillary acidic protein, a glial-specific marker. In the second patient glial fibrillary acidic protein staining confirmed the glial nature of the primary brain tumor as well as the metastatic tumor in bone marrow. The first patient also had metastatic nodules on the pleural surface and on the fifth rib. All three metastatic foci had similar cellular morphology, suggesting selection of a population of tumor cells with extraneural metastatic potential.
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PMID:Diffuse bone marrow metastasis by glioblastoma: premortem diagnosis by peroxidase-antiperoxidase staining for glial fibrillary acidic protein. 631 36

The distribution and localization of a glioma-associated antigen defined by monoclonal antibody 81C6 has been examined using human cultured cell lines and tissues. Monoclonal antibody 81C6 was selected from a hybridoma fusion of spleen cells of mice immunized with the glial fibrillary acidic protein-positive human glioma cell line U-251 MG. Results of cell surface radioimmunoassay and absorption analysis demonstrated that 81C6 defined a glioma-mesenchymal extracellular matrix (GMEM) antigen expressed by 14 of 16 gliomas, 1 of 3 neuroblastomas, 1 of 7 melanomas, 2 of 6 sarcoma cell lines, and 8 of 9 cultured fibroblast lines. GMEM was not expressed by carcinoma or by the myeloid-lymphoid cell lines examined. Within the central nervous system, GMEM was expressed in 10 of 11 glioblastomas but was undetected in 5 of 6 astrocytomas and in normal adult and fetal brain by peroxidase-antiperoxidase immunohistology. In glioblastomas, the GMEM antigen was localized to basement membranes of the distinctive glomeruloid endothelial proliferations and hyperplastic blood vessels. The GMEM antigen was also expressed in 3 of 3 glioblastoma cell lines and 6 of 8 glioblastoma biopsy xenografts in athymic nude mice. Among non-central nervous system tissues and tumors, GMEM was found by peroxidase-antiperoxidase immunohistology in normal liver sinusoids, spleen red pulp sinusoids, kidney medullary tubule interstitium, and glomerular mesangium and in association with vascular and stromal elements of several undifferentiated tumors. The GMEM antigen is distinct from previously described forms of fibronectin, laminin, collagen types I to V, hyaluronic acid, chondroitin sulfate, and heparin, as determined by absorption analysis and immunohistological localization in tissues. The expression of GMEM in glioblastoma but not normal brain, association with glioblastoma-proliferative endothelium basement membranes, and expression in glioblastoma cell lines and nude mouse xenografts suggest that GMEM may be a useful marker of gliomas in vivo and in vitro.
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PMID:Human glioma-mesenchymal extracellular matrix antigen defined by monoclonal antibody. 634 60

In 80 specimens of human glioma the production of glial fibrillary acidic protein (GFAP) by tumour cells invading meninges or connective tissue was studied immuno-cytochemically by the PAP technique. In 38 of 55 cases of astrocytoma, glioblastoma, gliosarcoma, and oligoastrocytoma, GFAP immunoreactivity was greater in the invading cells as compared with the main part of the neoplasm. Fifty-eight percent of the astroglial tumours invading the leptomeninges, all astroglial tumours invading connective tissue and all gliosarcomas showed enhanced GFAP immuno-reactivity of tumour cells getting in contact with collagenous tissue, whereas meningeal infiltrates of 25 non-astroglial tumours (oligodendroglioma, ependymoma, medulloblastoma) remained GFAP-negative like the main part of the respective tumours. In the majority of astroglial tumours an increase of GFAP immunoreactivity was found also in perivascular cells of the main part of the tumour. It is concluded that glioma cells are capable of adapting their cytoskeleton to their micro-environment. Contact with dense collagenous tissue appears as an important factor able to induce an increased production of GFAP by adjacent glial cells.
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PMID:Production of glial fibrillary acidic protein (GFAP) by neoplastic cells: adaptation to the microenvironment. 639 Oct 69

GFAP, Factor VIII/RAg, laminin, and fibronectin were immunohistochemically investigated in 15 glioblastomas and 15 gliosarcomas . GFAP was found variably positive in the glial areas. F VIII/RAg characterizes the endothelial cells and in gliosarcomas suggests the origin of the sarcomatous component from the endothelial proliferations. Laminin separates the two components and characterizes the inner and the outer basement membranes in the vessels. It is multiplied and thickened in endothelial proliferations, while it is often fragmented in the larger vessel wall proliferations. Our observations confirm that gliosarcoma represents the last stage of a process which starts with the endothelial hyperplasia of glioblastoma.
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PMID:GFAP, F VIII/RAg, laminin, and fibronectin in gliosarcomas: an immunohistochemical study. 642 54

A 24-year-old female complained of headache and vomiting. The brain-CT scan demonstrated a tumor shadow in the right cerebellar hemisphere. The tumor was partially resected, and irradiation therapy was started. She died of intraventricular hemorrhage about 6 months after the onset of symptoms. Autopsy revealed a recurrent tumor mass in the cerebellum extending to the brain stem. It showed systemic metastases to the leptomeninx, liver, bones and ovaries. Histological examination showed a tumor which was a primarily composed of typical medulloblastoma cells with occasional Homer-Wright type rosettes. It partly showed glioblastoma-like configuration. Some tumor cells were positive for GFAP by the PAP method, suggesting glial differentiation.
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PMID:[Autopsy case of atypical medulloblastoma in an adult]. 666 12

We report two cases of a recently isolated variety of astrocytoma, pleomorphic xanthoastrocytoma, affecting the cerebral cortex and meninges of children and young adults. The first tumor was localized in the left frontal lobe of a 9-year-old girl. The second appeared in the right parietal lobe of a 14-year-old girl. Both tumors displayed a pleomorphic cellular proliferation, with spindle-shaped and bizarre multinucleated giant cells, some positive for neutral lipids, with a prominent reticulin network and areas highly suggestive of malignant fibrohistiocytomas (fibroxanthosarcomas). The glial fibrillary acidic protein was demonstrated by the immunoperoxidase method in the cytoplasm of the giant and the spindle cells. Ultrastructural studies confirmed the glial nature of the tumor. This type of tumor seems to carry a much better prognosis than other tumors from which it has to be separated, e.g., glioblastoma and meningeal sarcomas.
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PMID:Pleomorphic xanthoastrocytoma: a report of two cases. 668 96

The secretion of transforming growth factor-beta (TGF-beta), a growth inhibitory factor with immunosuppressive properties, was investigated in one glioblastoma cell line and seven surgically resected malignant glioma cells. Cultured cells from surgically resected tumors were examined immunohistochemically for glial fibrillary acidic protein (GFAP) and S-100 protein. The levels of TGF-beta 1 and TGF-beta 2 in culture supernatants from malignant glioma cells were determined by a specific bioassay using anti-TGF-beta 1 and anti-TGF-beta 2 antibodies. Two glioblastoma cell lines were cultured in the presence of TGF-beta 1 or TGF-beta 2 to assess the effect of TGF-beta on the growth of glioblastoma cells. Cultured cells from surgically resected tumors were positive for both GFAP and S-100 protein. Both active and latent forms of TGF-beta 1 and TGF-beta 2 were detected in the culture supernatants from malignant gliomas, except in one patient with anaplastic astrocytoma which secreted only latent forms of TGF-beta 1 and TGF-beta 2. There was no statistical difference in the levels of TGF-beta 1 and TGF-beta 2 in glioblastomas and anaplastic astrocytomas. Neither TGF-beta 1 nor TGF-beta 2 affected the growth of glioblastoma cells. These findings suggest that most malignant glioma cells secrete both TGF-beta 1 and TGF-beta 2, can convert TGF-beta from a latent to active form, and may suppress cytokine secretion by activated lymphocytes in vivo as well as in vitro.
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PMID:Secretion of transforming growth factor-beta 1 and -beta 2 by malignant glioma cells. 747 84

Granulocyte-colony-stimulating factor (G-CSF) is a hematopoietic cytokine that regulates the differentiation of myeloid progenitors and the function of mature neutrophils. It is produced in vitro by monocytes/macrophages, mesothelial cells, fibroblasts and endothelial cells after appropriate induction by inflammatory mediators like IL-1 and TNF. Normal as well as tumorous glial cells can also be induced to produce CSFs in vitro. However, little is yet known about the in vivo expression of G-CSF as a mediator in inflammation and malignancy within the human central nervous system. The aim of the present study was to investigate by immunostaining the expression of the G-CSF protein within non-tumorous and tumorous glial tissues, and primitive neuroectodermal tumors. Using the murine monoclonal anti-G-CSF TM 82/60 antibody, we found high G-CSF expression in astrocytoma WHO grades I and II and reactive brain tissue, low expression in astrocytoma WHO grade III, and none in glioblastoma, oligodendroglioma WHO grades II and III, and medulloblastoma. In consecutive sections of the tissue samples, G-CSF protein was localized in GFAP-positive glial cells, but not in macrophages/microglial cells, which expressed HLA-DR, detected by the antibody CR3/43. Computer-assisted microdensitometric evaluation of the intensity of immunostaining for G-CSF and statistic analysis of the data revealed significant differences between the diagnostic entities studied (p < 0.0001). We conclude that in vivo expression of G-CSF is a characteristic of reactive as well as tumorous astrocytes, with the latter losing this feature at higher degrees of dedifferentiation.
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PMID:Immunolocalization of granulocyte-colony-stimulating factor in human glial and primitive neuroectodermal tumors. 751 14

Non-glial intermediate filament (IMF) proteins, as well as glial fibrillary acidic protein (GFAP) and vimentin, were studied by immunohistochemistry in 24 gliomas including low grade astrocytoma, pleomorphic xanthoastrocytoma, anaplastic astrocytoma, glioblastoma, oligodendroglioma, ependymoma and ependymoblastoma, which were fixed in ethanol and embedded in paraffin. Cytoskeletal elements isolated from two glioblastomas were examined with immunoblot analysis. All tumors had GFAP-positive neoplastic cells and vimentin was also found in all the tumors except one oligodendroglioma. Twenty-three gliomas were immunostained with anti-desmin polyclonal antibody (DM-P), but anti-desmin monoclonal antibody reacted to only one glioblastoma. DM-P might crossreact with GFAP and vimentin. Cytokeratin expression was investigated with six antibodies. Twenty gliomas (83%) were positive for the antibody against epidermal keratin (CK-SE), however positive immunoreactivity varied from 58 to 8% with other cytokeratin antibodies. With the Western blot method, CK-SE had protein bands at 53 and 60-66 kDa. Neurofilament was expressed in one pleomorphic xanthoastrocytoma, one anaplastic astrocytoma, one glioblastoma and one ependymoblastoma. Expression of nonglial IMF proteins were observed in 21 tumors (88%), and coexpression of 4 or 5 classes of IMF proteins in 3 tumors (13%). We conclude that, in addition to GFAP and vimentin, gliomas express several types of non-glial IMF proteins.
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PMID:Expression of non-glial intermediate filament proteins in gliomas. 751 71

Possible differentiation mechanisms were investigated in a glioblastoma multiform cell line (GL15) presenting an undifferentiated phenotype with weak glial fibrillary acidic protein (GFAP) and strong vimentin (VIM) expression. Serum-free conditions induced time-dependent increases of GFAP-mRNA and GFAP protein levels, associated with a process-bearing astrocytic morphology. Activation of protein kinase C (PKC) by tumor promoter phorbol 12-myrystate 13-acetate (PMA) induced a rapid morphological differentiation and a decrease in GFAP mRNA, whereas the GFAP level remained unchanged. Such parameters were shown to characterize a physiological differentiation stage in astroglial cultures. Treatment of process-bearing GL15 cells with dibutyryl cyclic AMP (dbcAMP), a protein kinase A (PKA) activator, induced a time-dependent decrease in the GFAP mRNA and GFAP protein levels and reverted morphological changes induced by serum-free conditions. Neither PMA nor dbcAMP influenced the VIM mRNA expression. In GL15 cells, PKC and PKA activation have opposite effects. Understanding the role of these kinases in malignant transformation and in the in vitro differentiation process is of both basic and clinical interest.
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PMID:PKA and PKC activation induces opposite glial fibrillary acidic protein (GFAP) expression and morphology changes in a glioblastoma multiform cell line of clonal origin. 754 74


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