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)

A human glioblastoma multiforme (M27) tested in early cell cultures by indirect immunofluorescence staining showed SV40-related tumor (T)-antigen, 95% of the cells being positive. SV40-related viral capsid (V)-antigen was absent in all cells tested. Experiments to rescue this virus were performed by fusing M27 cells with CV-I monkey cells, which were permissive for SV40, using polyethylene glycol (PEG) as fusion factor. We succeeded in isolating virus particles SV40-GBM which electron microscopy showed to correspond in size and morphology to papovaviruses. Serological tests (hemagglutination, neutralization, fluorescent antibody) revealed that the virus is indistinguishable from SV40. Despite this apparent antigenic identity SV40-GBM differs slightly from SV40 wild type. This virus can propagate and produce CPE in both CV-I cells and primary fetal human kidney cells. Furthermore digestion of SV40-GBM DNA with the HindII/III restriction endonucleases revealed minor differences compared with the SV40 DNA. Therefore the virus SV40-GBM obtained from glioblastoma cells seems to be closely related to the SV40-PML viruses described earlier.
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PMID:Isolation of a SV40-like Papovavirus from a human glioblastoma. 9 81

Glioblastoma multiforme of the cerebellum is rare. Approximately 33 case of cerebellar glioblastoma have been reported. Two-thirds of the cases occurred in adults and the male to female ratio was 2:1. The mean age was 46.7 years in adults and 10.4 years in children. Most of the tumors were lateral in location. Two of the patients (6%) had multiple glioblastomas. The time from onset of symptoms to death was approximately one year.
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PMID:Gliobastoma multiforme of the cerebellum. 16 63

A 63-year-old man was found to have an intracerebral glioblastoma multiforme and preoperative roentgenographic evidence of a mass in the middle lobe of the right lung. Because of the rarity of extraneural metastases from glioblastoma, especially in the absence of prior surgery, the lesions were considered to be separate neoplasms until death. The histologic appearance of the lung tumor obtained at autopsy was identical to the cerebral tumor. Additional metastases were found to bronchial lymph nodes and a lumbar vertebra. This case demonstrates that a glioblastoma can spontaneously metastasize extraneurally. Invasion of the glioblastoma into the lumen of a blood vessel was demonstrated within the primary tumor. Embolization of cells to the lung and beyond is the suspected mode of spread.
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PMID:Glioblastoma multiforme with extraneural metastases in the absence of previous surgery. 17 71

The Feulgen-DNA cytophotometry was applied for studies of 31 rat cerebellum tumors induced by 9, 10-dimetyl-1,2-bensantracene. Most of these gliomas (22) were astrocytomas of different grades of malignancy. The histological diagnosis of other tumors was: glioblastoma -- 4, oligoastrocytoma -- 2, oligodendroglioma -- 1, gliosarcoma 1. The majority cells of 26 tumors had diploid or paradiploid DNA quantity, 4 tumors (1 astrocytoma, 3 dedifferentiated astroyctomas) had triploid modal classes. The tetraploid modal class and a large number of polyploid cells were found only once for glioblastoma multiforme. A supposition was made that drastic changes of ploidy could arise for the second time during the process of tumor evolution. The authors failed to show any exact differences in the ploidy of gliomas in rats with athyreosis or hyperthyreosis, and in the ploidy of somatic cells in control animals.
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PMID:[Cytophotometric determination of DNA concentration in the cells of experimental brain tumors. II. Primary tumors of rat cerebellum induced by 9, 10-dimethyl-1, 2-benzanthracene]. 18 64

A patient with glioblastoma multiforme survived 18 years after diagnosis and underwent 20 operations for extracranial metastasis. An immunologic survey of the patient was made over a 1-year-period using in vitro tests of lymphocyte responsiveness and skin tests with control and tumor antigens isolated from autologous and allogenic brain cell membranes. Two tissue-associated soluble cell membrane antigens also present in normal white matter, and two tumor-associated antigens (TAA) produce cell-mediated immune responses in patients with brain tumors. One of these tumor-associated antigens predominates in meningioma cells. In addition some low molecular weight components appeared, which seemed to be unique for the glioblastoma cells from the long-surviving patient.
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PMID:Soluble membrane antigens of brain tumors. I. Controlled testing for cell-mediated immune responses in a long surviving glioblastoma multiforme patient. 19 38

Various modes of therapy, alone or in combination, have had little effect in improving the survival of patients with glioblastoma multiforme. Recently, in a pilot study, 34 patients with glioblastoma were treated by fast-neutron-beam irradiation of the whole brain. Following treatment, the patients became steroid-dependent and pursued a gradual downhill course with increasing obtundation. Although there was no improvement in the length or quality of survival of these patients, neuropathological studies in the 13 patients who came to autopsy showed the following: 1) extensive coagulative necrosis of much of the tumor mass; 2) dense infiltration by collagenous connective tissue; 3) minimal phagocytic reaction; 4) marked reduction in the amount of viable tumor; 5) abnormal astrocytic proliferation, which may represent either astrocytoma or a radiation-induced bizarre gliosis, and 6) areas of gliosis and white matter degeneration in the brain stem, remote form the tumor site. These observations suggest that continued efforts to further refine this mode of therapy for glioblastoma are warranted.
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PMID:Fast-neutron irradiation of glioblastoma multiforme. Neuropathological analysis. 20 33

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

The first two instances of mixed sarcoma-glioblastoma with a history of therapeutic irradiation to the head are reported, both occurring within one year of radiation therapy (for pituitary adenoma and residual meningioma). Two novel variants of mixed sarcomas of brain with extreme tumor metaplasia (fibromyxoosteochondrosarcoma and fibrochondroosteosarcoma-glioblastoma multiforme) are documented, and some of the problems concerning the origin of brain tumors with mixed population are discussed.
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PMID:Mixed intracranial sarcomas: rare forms and a new association with previous radiation therapy. 21 26

26 patients, average age of 7.3 years, has biopsies of a brain stem tumor. 62% of the patients presented with hydrocephalus, and ventriculoperitoneal shunts were placed 7-10 days prior to biopsy. The midbrain was biopsied 13 times, the pons 3 and the medulla 12 times. Tissue for histopathologic examination was obtained at each operation and demonstrated astrocytoma in 13 patients, glioblastoma in 6, 'no tumor seen' in 5 and ependymoma in 2. Astrocytomas were usually located in the upper brain stem, and all of the glioblastomas were located in the medulla. The operative mortality was zero, and the morbidity was largely related to increased cranial nerve deficit. All the astrocytoma patients were treated with radiation only; whereas, 4 patients with glioblastoma were treated with vincristine, CCNU and methylprednisone in addition to radiation as described by the Children's Cancer Study Group (CCG-944). 3 patients with 'no tumor' were not treated and are alive and well 15-41 months following operation. 2 patients with no tumor were treated, one as a glioblastoma multiforme, subsequently verified at postmortem examination, and one as a midbrain astrocytoma. 1 patient with astrocytoma died 3 months following operation, all the remainder are living and well 4-51 months following operation. Irrespective of the treatment, all 7 patients with glioblastoma expired within 9 months of diagnosis. The prognosis for survival for patients with brain stem astrocytoma is superior to those with glioblastoma multiforme. Specific histopathologic correlation with clinical management may lead to improved and prolonged survival for patients with brain stem glioma.
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PMID:Biopsy of pediatric brain stem tumors. 45 7

The authors review the clinical and pathological features of 24 patients with gliosarcoma. The study revealed the following findings. Gliosarcoma occurs more frequently than is indicated in the literature, and in our series was present in 8% of all cases of glioblastoma multiforme. The presenting features are not significantly different from those of glioblastoma multiforme. The lesion often presents itself at surgery as a firm, well circumscribed mass within the temporal lobe, and at surgery it is commonly mistaken for a meningioma. There is an increased likelihood of metastasis compared to that of glioblastoma. The prognosis is no worse than that of glioblastoma, in spite of the addition of sarcomatous elements.
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PMID:Clinical and pathological study of 24 cases of gliosarcoma. 95 76


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