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Query: UMLS:C0017636 (glioblastoma)
 18,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Glioblastoma multiforme, representing about 50% of all gliomas, encompasses a group of intrinsic tumours of the brain in later years (age peak around 50 years), the morphological hallmarks of which are an ensemble of variations in tumour cell and tissue structure featuring its biological malignancy. Glioblastoma, while sometimes appearing as a distinct "primary" tumour type, is usually accepted as an extreme manifestation of anaplasia and dedifferentiation of glia, mostly astrocytic. The astrocytic nature of most glioblastomas has been confirmed by ultrastructural studies and progressive differentiation of tumours maintained in organotypic tissue culture. Reproducible experimental models are particularly induced by oncogenic RNA (oncorna) viruses. The cell kinetic parameters are similar to those of other solid malignant tumours except for a comparatively low growth fraction of glioblastoma. The frequent occurrence of giant cells as well as of regressive changes with necrosis and vascular responses are indirect (secondary) indicators of malignancy which coincide with histochemical (enzymatic anisochronia) and biochemical data (lower level of glia specific S100 protein than in differentiated gliomas). Vascular proliferation, a characteristic feature of glioblastoma, may occasionally progress to sarcomatous transformation with development of gliosarcomas (mixed glial-mesenchymal tumours). While dissemination of glioblastoma through the cerebrospinal pathways is not uncommon, extraneural distant metastatic spread is rare, and usually observed after craniotomy. The results of modern neuro-oncology support the pathogenetic view that glioblastoma results from neoplastic transformation of glial elements with continuing dedifferentiation. This transformation can be experimentally induced by various factors including oncogenic DNA (oncorna) viruses by using a reverse transcriptase, while there is indirect evidence for an oncorna-virus information in human glioblastoma. The significance of immunological factors in the pathogenesis of brain tumours and in the course of neoplastic transformation of glia is not yet understood, but both morphological and immunological data are in favour of a cell mediated immunological reaction against tumour-specific antibodies. Since immunological factors and changes in cytokinetics are apparently active after the transformed tumour cells proliferate, all available therapeutic methods, including radiation, chemotherapy, and immunotherapy of glioblastoma only influence the final stages of neoplastic development with clinical manifestation of the tumour. In spite of modern combination and multimodality therapy schemes the prognosis of glioblastoma is still poor.
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PMID:Glioblastoma multiforme: morphology and biology. 21 8

'Gliosarcomas' have long been considered to be mixed gliomas and sarcomas. The present study failed to define criteria which clearly delineate 'gliosarcomas' from glioblastoma multiforme and suggests that 'gliosarcomas' should be considered as spindle cell glioblastomas. A total of six cases originally diagnosed as 'gliosarcomas' were compared with four cases of glioblastoma multiforme. No clinical or prognostic features were defined which would clearly separate 'gliosarcomas' from glioblastoma multiforme. Macroscopically, biopsies from 'gliosarcomas' ranged from firm, apparently well-circumscribed tumours to poorly circumscribed lesions with a soft consistency resembling glioblastoma multiforme. Histology revealed a continuous spectrum in which 'gliosarcomas' with large reticulin-rich areas of spindle cells merged with typical glioblastomas containing only small islands of spindle cells and reticulin staining. Immunocytochemistry for glial fibrillary acidic protein (GFAP); S100 protein and alpha-smooth muscle actin (ASMA) showed that the majority of cells in reticulin-poor areas of 'gliosarcoma' and glioblastomas expressed S100 protein and GFAP; many expressed ASMA and some expressed both GFAP and ASMA. Spindle cells in reticulin-rich areas of 'gliosarcomas' and glioblastomas most frequently expressed ASMA but many cells also expressed S100 protein and GFAP; some cells expressed both GFAP and ASMA. The results of this study and a review of the literature suggests that there is a clinical, radiological and pathological continuum with glioblastoma and 'gliosarcoma' at different ends of the spectrum. It is suggested, therefore, that most, if not all, 'gliosarcomas' be redesignated as spindle cell glioblastomas and not be considered as a mixture of glioma and sarcoma.
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PMID:Spindle-cell glioblastoma or gliosarcoma? 162 Feb 80

The human glioblastoma-derived cell lines 86HG-39, 87HG-28 and 87HG-31, used for the production of monoclonal antibodies (mAbs) against glioma-associated antigens (GAA), were characterized in terms of morphology, growth behaviour, chromosomes and antigen expression. In the primary tumours, differential expression of glial fibrillary acidic protein, S100 protein, Leu-7 and GAA as defined by mAbs MUC 2-39, MUC 2-63 and MUC 8-22 was demonstrated. Receptors for epidermal growth factor (EGFr) and nerve growth factor (NGFr) were found in many cells in short-term cultures, but the transferrin receptor (Tr) was found in only a few cells of 87HG-28. In permanent cell lines, differentiation antigens and EGFr decreased and Tr increased markedly. NGFr and GAA remained stable. Transplantation tumours of 86HG-39 were partly positive for Tr and GAA. Chromosomal analysis revealed that the 86HG-39 and 87HG-28 cell lines had a hypodiploid or diploid stem line with lines in the hypotetraploid to tetraploid region for 50 in vitro passages. The 87HG-31 cell line had chromosomal patterns in the hypotriploid to triploid region. A gain of chromosomes was seen in the groups C7, C8, C10, D14, F19, F20, G21, G22. The variability of antigens in these tumours and especially during long-term cultivation probably reveals an ability to influence the growth of malignant glioma cells via the respective effector molecules.
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PMID:Morphological, immunocytochemical and growth characteristics of three human glioblastomas established in vitro. 170 26

Antigen expression in a human glioblastoma was investigated by immunochemical methods in the primary tumor, the first and second recurrence, a permanent cell line derived from the first recurrence and in its xenotransplantation tumors. In the primary tumor, GFAP, vimentin, S100, Leu-7 and glioma-associated antigens (GAA) as defined by the monoclonal antibodies (mAbs) MUC 2-39, MUC 8-22 and MUC 2-63 were markedly expressed. In the recurrences, gradual loss of GFAP and Leu-7 could be observed, whereas S100, vimentin and GAA gave similar results to those in the primary tumor. In contrast, fibronectin and collagen IV, which were restricted to the vessel walls in the primary tumor, were represented in sarcomatous areas of the recurrences. In some of these areas, co-expression of glial cell markers was observed. In short-term cell cultures, expression of glia- and glioma-associated antigens as well as fibronectin and collagen IV was comparable to that of the recurrent tumor tissue. In long-term passages, immunoreactivity of GFAP, Leu-7 and S100 decreased, whereas GAA, vimentin and fibronectin increased. Collagen IV positive cells were not visible beyond passage 15. Transplantation tumors were only partly positive for glial cell markers, but revealed strong immunoreactivity for GAA, fibronectin and collagen IV. With these observations we confirm that the phenotypic variability of glioma cells makes it difficult to identify the origin of cells in human glioblastomas from their antigenicity.
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PMID:Antigen variation in a human glioblastoma: from the primary tumor to the second recurrence, permanent cell line and xenotransplantation tumors. 206 11

Three cases of primary intracranial tumours fulfilling the clinical and histological criteria of pleomorphic xanthoastrocytoma are presented. As is typical, they occurred in young people, aged 15, 17, and 22 years, and were composed of lipid-laden pleomorphic cells with frequent bizarre multinucleated forms and a prominent reticulin network. However, subsequent immunohistochemistry, further histological review, and clinical follow-up suggest that these tumours were different entities. In one case the tumour cells were negative for GFAP but positive with a panel of histiocytic markers. The lesion, which extended rapidly and caused death within 6 months, was assumed to be a true meningeal fibrous histiocytoma. The remaining two cases were positive for glial fibrillary acidic protein (GFAP) and S100 protein. One of these was mitotically active, contained areas of necrosis and vascular proliferation, and also led rapidly to death. This, we concluded, was a glioblastoma. The third case showed little mitotic activity and the patient remains well; this is probably a true pleomorphic xanthoastrocytoma. These results indicate that tumours with light-microscopic appearance of pleomorphic xanthoastrocytoma require detailed immunohistochemical investigation. Only those lesions with low mitotic activity and undoubted evidence of glial origin should be accepted as true pleomorphic xanthoastrocytoma. Extensive necrosis in a tumour with GFAP-positive, lipid-rich cells indicates a lipidised glioblastoma, while positive histiocytic immunocytochemistry should suggest a fibrous histiocytoma.
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PMID:Pleomorphic xanthoastrocytoma. Immunohistochemical methods for differentiation from fibrous histiocytomas with similar morphology. 301 Jul 49

The transmission of donor-related malignancies by organ transplantation is a rather rare event. There has only been one report on the development of a brain tumor metastasis in liver transplantation. From September 1988 to January 1993, 342 donor hepatectomies with subsequent transplantation were performed at our center. The main donor diagnoses included subarachnoidal bleeding (n = 128; 37.4%), isolated head injury (n = 114; 33.3%), multiple injuries (n = 55; 16.1%), primary cerebral neoplasia (n = 13; 3.8%), and other (n = 32; 9.4%). Primary cerebral neoplasia included glioblastoma (n = 4), meningioma (n = 3), astrocytoma (n = 2), angioma (n = 2), neurocytoma (n = 1), and ependymoma (n = 1). In the group of donors suffering from primary cerebral neoplasia, procured organs other than the liver included kidneys (n = 20), combined kidneys and pancreata (n = 1), pancreata (n = 2), hearts (n = 8), combined hearts and lungs (n = 1), and single lungs (n = 1). Follow-up of the respective graft recipients ranged from 28 to 68 months (median 43 months). Recurrent malignancy was observed once, in a liver graft recipient. The donor, a 48-year-old female, had undergone surgical resection of an intracerebral multiform glioblastoma and died 4 months later of a relapse in the brain stem. The 28-year-old female recipient had undergone transplantation for an autoimmune-hepatitic cirrhosis. Four months later, histopathological examination of an intraperitoneal and intrahepatic mass revealed a poorly differentiated, small-cell pleomorphic cancer, identified as a glioma metastasis by S100- and glial fibrillary acidic protein immunohistochemical staining. The patient died 6 months post-transplantation. On autopsy, no further neoplastic lesions were detected. Our review adds a second reported case of a liver graft-transmitted brain tumor to the literature and the fourth donor-related malignancy after hepatic transplantation in general.
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PMID:Liver graft-transmitted glioblastoma multiforme. A case report and experience with 13 multiorgan donors suffering from primary cerebral neoplasia. 900 60

We report a new case of melanotic medulloblastoma of the vermis in a 3 1/2 year old boy. This tumor showed a typical histological appearance with pseudoepithelial pigmented structures immunoreactive for S100 protein and vimentin. The tumor did not recur after total surgical removal and post operative radiation. However, after a 10 year follow-up, imaging demonstrated that a second tumor occurred in the left cerebellar hemisphere, which, on histological examination, was a typical glioblastoma. Hypothesis concerning the histogenesis of the second tumor, as well as a causal association with radiation therapy and possible contribution of growth hormone therapy are discussed.
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PMID:[An exceptional variety of medulloblastoma: melanotic medulloblastoma]. 952 28

In order to analyze the steady-state RNA levels of S100A11 in different tissues, a cDNA fragment of human S100A11 was isolated from a cDNA library. The obtained fragment was labeled and hybridized to RNA isolated from various tissues. The Northern blot analysis revealed that S100A11 RNA levels varied from high in placenta, through intermediate in heart, lung, kidney, and most muscle samples, to barely detectable in brain. An efficient purification method for recombinant S100A11 yielding high quantities was developed. Furthermore, to examine the subcellular localization of this protein, the human polypeptide S100A11 antibodies were raised in rabbit. S100A11 was found to have a localization distinct from other S100 proteins examined, and is mostly localized in the nucleus, with slight variations among different glioblastoma cell types.
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PMID:Human S100A11 exhibits differential steady-state RNA levels in various tissues and a distinct subcellular localization. 1048 66

Brain tumors based on their histogenesis, consist of all tumors, derive from the entirely tissue in the intracranial space, both from the neuro-ectodermal/neuro-epithelial tissue and the mesenchymal tissue. By their location they can be divided into infratentorial or supratentorial, and further into deep vs. superficial. The interesting and unique, there are age distribution or location-sex specificity of some brain tumors (BT). WHO Histopathological Typing of Tumors by the CNS, also showing progress on both of their members and new special types of some BT, especially for the meningiomas and neuro-epithelial/neuroglial type. Periodic investigations by the Department of Anatomic Pathology, the Faculty of Medicine, University of Indonesia did not show major changes in their BT types, but there was on their tumors ranging. Astrocytoma (including glioblastoma multiforma) for a while was replaced by meningioma as the most common CNS/Intracranial tumor. There are some techniques for the handling of CNS specimens depending on further purposes through on biomolecular activities or defects. The routine technique using light microscope examination was the most useful one for daily diagnosis for many years. Some immunohistochemistry techniques are needed for difficult cases, e.g., GFAP, NE 14, NSE, S100, and MBP. Diagnostic problems could be caused by tissue- or cell-sampling errors, which are influenced by the tumor location itself. Thus, neurosurgeons encounter problems to pick biopsy intraoperative, or by mishandling by the laboratory of anatomic pathology. Formerly, as final diagnosis, grading of CNS tumors must be put according to the Clinical interest for further management of the patient. CNS grading ranges from grade I (benign looking) to IV (malignant). Morphological grading is based on Kernohan and Adson (1949), or Kernohan and Sayre (1952).
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PMID:Pathological aspects of brain tumors. 1089 65

A cerebral tumour was found in the right frontal lobe of a 7-year-old female mongrel cat. The mass showed infiltrative growth and caused deformation of the corpus callosum. Histopathologically, the tumour cells showed anaplasia, pleomorphism and mitotic figures. Necrosis and vascular proliferation were prominent. The neoplastic cells surrounded areas of necrosis, but as an indistinct pseudopalisade formation. Immunohistochemically, low numbers of tumour cells labelled positively for anti-glial fibrillary acidic protein and anti-S100 protein. Electron microscopically, the majority of tumour cells had no filaments and cytoplasmic processes, but the differentiated cells presented cytoplasmic filaments and glycogen granules. Based on these findings, the tumour was diagnosed as cerebral high-grade astrocytoma, glioblastoma.
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PMID:Cerebral high-grade astrocytoma (glioblastoma) in a cat. 1456 16


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