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)

The periods of survival which can be obtained on patients with a primary tumor of the brain after an unique or post-operative cobalt-60-irradiation is dependent of the histology: while periods of survival of several years have been obtained in case of medulloblastoma and astrocytoma, the irradiation of the multiform glioblastoma represents only a palliative measure with a temporary amelioration for any months.
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PMID:[Results of cobalt-60-irradiation of brain tumors]. 4 57

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

We report three cases of brain metastases from malignant pleural mesothelioma that were seen at autopsy. We present a summarized review of 15 similar reports that were previously published. Our study included three aged male patients with a long occupational history of heavy asbestos exposure. In two patients, the metastases were discovered incidentally at autopsy, and there were no neurologic symptoms referred to before death. In the other patient, who had clinically occult mesothelioma, the intracranial tumor was discovered ante mortem: in this patient, the clinical features, as well as a computed tomographic scan, suggested a primary tumor of the brain. Interestingly, the histologic features of the latter case that were seen at autopsy depicted a spindle cell tumor that focally exhibited pseudopalisading, necrosis, vascular buds, which deceptively recalled a glioblastoma. All the three cases shared a basic sarcomatous pattern of malignant pleural mesothelioma in both primary and metastatic tumors. The immunohistochemical profile was consistent with such interpretation. It was concluded that metastases to the brain from malignant pleural mesothelioma, although rare, are not exceptional even if their clinical relevance is not prominent. They are seen concomitantly with high-grade tumors, and by mimicking a primary tumor on a clinical, instrumental, and histologic ground, they may occasionally represent a potential source of diagnostic pitfall.
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PMID:Intracranial metastases from malignant pleural mesothelioma. Report of three autopsy cases and review of the literature. 171 Jan 3

Peripheral blood mononuclear cells (PBM) from normal donors and patients with recurrent glioma were activated initially for 48-72 h with phytohemagglutinin-P (PHA) and recombinant human interleukin-2 (IL-2), and then proliferated in vitro for up to 5 months with IL-2. These cells are termed mitogen-stimulated lymphokine-activated T killer (T-LAK) cells. We measured patterns of T-LAK cell growth, in vitro cytolytic activity on a panel of continuous and primary tumor cells, and the phenotypes of the cells in these cultures. Lymphocyte viability declined dramatically over the first 3-5 days; and then the remaining cells in these cultures began to divide and maintained a constant 30-36 h doubling time for long periods in vitro. Phenotyping revealed that cells in the initial few days of culture were heterogeneous, but became almost totally CD3 T cells after 7-10 days in culture. The T-LAK cells from individual normal donors and cancer patients demonstrated a non-genetically restricted cytolytic ability against a panel of both continuous cell lines and primary autologous and allogeneic glioblastoma cells in vitro. This technique provides a method of generating large numbers of autologous cytolytic T cells with non-restricted anti-tumor activity that can be derived from peripheral blood mononuclear cells.
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PMID:Generation of stimulated, lymphokine activated T killer (T-LAK) cells from the peripheral blood of normal donors and adult patients with recurrent glioblastoma. 201 99

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

Reported are three cases of a spinal leptomeningeal dissemination from supratentorial malignant gliomas, in which the recurrence of the primary tumors of the intracranial leptomeningeal involvement was not observed clinicopathologically. All cases complained of spinal cord symptoms such as paraplegia or a sensory disturbance from time to time after the initial operation for their intracranial primary tumors. The duration between the first operation and the appearance of the spinal cord symptoms ranged from 11 to 17 months. In all cases, a computerized tomography scan demonstrated no recurrence of the primary tumor and no findings indicating intracranial leptomeningeal gliomatosis, such as a diffuse contrast enhancement of the ventricular wall or the subarachnoidal space, or hydrocephalus. Myelography showed a block or an irregular filling defect in two cases given immediate operations for spinal mass lesions. In one of these cases, a well-defined extramedullary tumor was removed at the level of the 7th-8th thoracic vertebrae. The pathological diagnosis was a glioblastoma multiforme, which was similar to the primary tumor. The patient survived for 18 months after total removal of the spinal tumor followed by postoperative spinal irradiation. All patients died of recurrent tumors from 3 to 18 months (mean: 8 months) after the appearance of the spinal cord symptoms. In the other case, an intramedullary tumor was found by a laminectomy. These two cases were autopsied. In one, an intramedullary tumor was found to extend from the lower medulla oblongata to the cervical cord, whereas the recurrence of the primary tumor was not seen and there was no intracranial leptomeningeal invasion nor any spinal subarachnoid seeding. The pathological diagnosis of this intramedullary tumor was a glioblastoma. In the other, there was a diffuse leptomeningeal dissemination of glioblastoma multiforme throughout the spinal cord, with an intramedullary invasion to almost all parts. A partial intracranial subarachnoid seeding of a malignant lower grade tumor than seen in the spinal lesion was found, though there was no recurrence of the primary tumor.
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PMID:[A clinicopathological study of the spinal leptomeningeal dissemination from cerebral malignant gliomas without a recurrence of the primary lesions]. 215 48

A 68-year-old male was hospitalized because of headache, nausea, and disturbance of consciousness. Neurological examination on admission disclosed somnolence, disorientation, marked neck stiffness, papilledema, and quadriparesis. Computed tomography (CT) scanning demonstrated a round mass with marked contrast enhancement in the right sylvian fissure and small contrast-enhanced masses in the interpeduncular, quadrigeminal and ambient cisterns. CT also showed marked peritumoral edema, a midline shift, and hydrocephalus. The patient's consciousness level and respiration deteriorated 3 days after admission and a craniotomy was performed. The tumor, which was well demarcated, firmly attached to the sphenoidal ridge, and grossly appeared to be a meningioma, was totally removed. Histologically, the tumor had two well defined components, glioblastoma and fibrosarcoma. The patient underwent ventriculoperitoneal shunting, chemotherapy, and radiotherapy after surgery, but the primary tumor soon recurred, with scalp metastasis, and he died 5 months postoperatively. Autopsy revealed metastases to the liver, spleen, and spinal cord. The histogenesis of this mixed tumor and the mechanism of extracranial metastasis are discussed, and the literature is reviewed.
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PMID:[Gliosarcoma with multiple extracranial metastases. Case report]. 248 46

Twelve cases of malignant gliomas (anaplastic astrocytoma 4, glioblastoma 8, recurrent 3, primary 9) were treated with ACNU and radiation with sensitizing agents after the surgical removal of the tumor. BUdR, Vidarabine (Ara-A), Aciclovir (ACV) were applied for sensitizing agents. BUdR was administrated intraarterially prior to radiation (380 rad, two times a week), and Ara-A and ACV intravenously during and after the radiation. Total dosage of the radiation was 50-60 Grey for each case. All recurrent and eight primary patients died. The mean survival time of the recurrent patients was 17.7 months, while that of the primary patients was 13.4 months. One of the primary patient was glioblastoma and is still surviving more than 24 months by now. The complete response (CR) rate of the primary tumor patients observed by computerized tomography (CT) scan was 5/9. We can expect the availability of this trial for malignant gliomas because of high CR rate in primary tumor cases.
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PMID:[A trial of ACNU and radiation therapy with sensitizing agents for malignant gliomas]. 262 8

Seven human glioblastoma cell lines established in vitro from primary tumor explants were studied. A marked heterogeneity of glial fibrillary acidic protein was observed whereas vimentin was uniformly expressed by all cell lines. Indirect immunofluorescence and flow cytofluorometry revealed a heterogeneous distribution of surface GE 2 and CG 12 tumor-associated antigens (TAA's): three cell lines were positive (greater than 69% TAA-positive cells) and three cell lines were negative (less than 9% TAA-positive cells). One cell line (Hu 228) was moderately positive at early culture passages and subsequently acquired a TAA-negative phenotype. The difference in the relative amounts of surface TAA's of the three positive cell lines was less than twofold. In spite of the heterogeneous distribution of surface TAA's, all cell lines exhibited considerable amounts of intracellular TAA. Treatment with phorbol esters and density-dependent growth arrest decreased the percentage of the TAA-positive cells and the amount of cell-surface TAA's in one cell line (Hu 195). Interferon-gamma treatment in vitro increased the percentage of CG 12-positive cells by 12% and the amount of cell-surface CG 12 antigens by 38% as compared to untreated cells. The percentage of TAA-positive cells among phorbol ester-treated cells of the Hu 195 cell line was lowest 48 hours after treatment, but returned to normal values within the next 48 hours. Reduction of 3H-thymidine incorporation preceded the decrease in number of TAA-positive cells by about 18 hours. Two-color fluorescence analysis performed in positive cell lines for simultaneous determination of surface TAA's and deoxyribonucleic acid content or reactivity with the proliferation-associated Ki67 intracellular marker indicated that GE 2 and CG 12 antigens are expressed preferentially by actively proliferating glioma cells. The results of this study indicate the existence of two different phenotypes in cultured human glioblastoma cells: surface TAA-positive/cytosol TAA-positive and surface TAA-negative/cytosol TAA-positive cell populations. In addition, modulation of TAA expression was dependent on the cell-cycle differentiation stage, culture conditions, and proliferative state of the cells.
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PMID:Heterogeneity and modulation of tumor-associated antigens in human glioblastoma cell lines. 276 91

During the last 17 years, complete autopsies were performed on 51 patients who died of cerebral glioblastoma, and 14 were found to have dissemination by cerebrospinal fluid (CSF). In these 14 cases of glioma, the extent of intraparenchymal invasion by the primary tumor and the degree of seeding were studied in connection with histological findings and immunohistochemical staining for glial fibrillary acidic protein (GFAP) as the most reliable marker of astrocytic differentiation. From the findings obtained, the cases were divided into two groups. In one group, consisting of 7 gliomas, autopsy revealed intense seeding, despite only slight invasion by the primary tumor. Among these 7 extensively disseminated gliomas, 4 expressed almost no GFAP, 2 contained only a few GFAP-positive cells, and only 1 displayed an immunohistochemically high degree of astrocytic differentiation. Clinically, 6 of the 7 affected patients developed symptoms attributable to CSF seeding. In the other group consisting of the remaining 7 gliomas, only slight dissemination was seen, despite extensive infiltration of the primary tumor. Each of these 7 gliomas contained many GFAP-positive cells. None of the affected patients developed symptomatic seeding. This study shows the existence of two clinicopathologically distinct groups of disseminated cerebral glioblastomas and suggests that, regardless of morphological features, glioblastomas showing immunohistochemically poor astrocytic differentiation tend to shed tumor cells more vigorously but are less invasive at the primary site than those with many GFAP-positive cells. It is also suggested that, as a consequence, the former glioma type produces symptomatic seeding more frequently than the latter type.
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PMID:Cerebral glioblastoma with cerebrospinal fluid dissemination: a clinicopathological study of 14 cases examined by complete autopsy. 279 91


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