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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to determine the in vivo immune response in glioblastoma, monoclonal and polyclonal antibodies specific for inflammatory leukocytes and immunoregulatory products were utilized to stain tissue from four surgical specimens. The more activated the inflammatory cells, the more activated the tumors appeared to be. In the tumor with the largest infiltration (Case 3), inflammatory cells were stained for interferon-gamma, interleukin-2, interleukin-1 beta, lymphotoxin, tumor necrosis factor-alpha, and transforming growth factor-beta. The tumor cells also expressed interleukin-1 beta, interleukin-6, transforming growth factor-beta, tumor necrosis factor-alpha, and prostaglandin E. In contrast, in the tumor with the least inflammatory response (Case 1), the tumor cells did not express any cytokines. Expression of cytokines by glioma cells was modest in the two cases with modest inflammatory responses. Cellular inflammation, primarily consisting of T cells and macrophages with few or no B cells or natural killer cells, was two- to 15-fold greater outside the tumor than within. In contrast to leukocytes outside the tumor, which were activated and expressing class II major histocompatibility antigens, leukocytes within the tumor parenchyma or at the tumor's edge were negative for these antigens. In the four specimens studied here, the tumor cells themselves were also negative for class II major histocompatibility antigens. These findings, although preliminary, suggest that inflammatory cells within gliomas are inactivated and that glioma cells may increase the expression of immunosuppressive cytokines in response to an increased lymphocyte infiltrate. This observation, if corroborated by more extensive studies, may help to explain the failure of immune treatments in glioblastoma multiforme.
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PMID:Inflammatory leukocytes associated with increased immunosuppression by glioblastoma. 131 61

In an attempt to improve local control and survival over those achieved with brain implant alone, a Phase I/II study of interstitial thermoradiotherapy was undertaken for recurrent malignant gliomas and recurrent solitary brain metastases. Between June 1987 and September 1990, 49 tumors in 48 patients were treated with thermoradiotherapy, including 26 glioblastoma multiforme (GM), 16 anaplastic astrocytomas (AA), 4 adenocarcinomas, and 3 melanomas. Patient age ranged from 18 to 71 years and Karnofsky Performance Status from 40 to 90. Stereotactically implanted catheters were used for both hyperthermia and brachytherapy. Hyperthermia was administered immediately before and after brachytherapy, heating as much of the tumor as possible to 42.5 degrees C for 30 min using helical coil microwave antennas. High-activity iodine-125 sources delivered tumor doses of 32.6 to 63.3 Gy. Complications included reversible neurologic changes in 13 patients, 9 seizures, 4 infections, 1 deep venous thrombosis with pulmonary embolus, and 1 scalp burn. Eighteen patients underwent reoperation for tumor and/or necrosis. Follow-up ranged from 9 to 166+ weeks. The median follow-up for living patients with GM and AA was 37 weeks and 92 weeks, respectively. Actuarial median survival was 47 weeks for patients with GM. For patients with AA, actuarial survival was 65% at 18 months and median survival has not yet been reached. Multivariate analysis showed a strong correlation between freedom from local tumor progression and "T90" temperature or minimum tumor temperature. Interstitial brain thermoradiotherapy is now being evaluated in a randomized Phase II trial for previously untreated GM.
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PMID:Thermoradiotherapy of recurrent malignant brain tumors. 131 81

We report histologically different gliomas occurring simultaneously in both the cerebrum and cerebellum in a 53-year-old woman. One tumor was a cerebellar astrocytoma, and the second was a temporal glioblastoma multiforme. Two months after the removal of both tumors, the third lesion, located in the basal ganglia, was found on a computed tomographic examination, but it was not verified histologically. We recommend a biopsy of one tumor when a diagnosis of multiple brain tumors is established based on a computed tomographic examination, in order to avoid the misdiagnosis of multicentric gliomas as brain metastases.
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PMID:Cerebral and cerebellar glial tumors in the same individual. 132 Feb 18

We established and characterized two cell lines derived from glioblastoma multiforme. Both cell lines exhibited tumor cell morphology and growth kinetics and showed variable expression of glial fibrillary acidic protein (GFAP), S-100, fibronectin and vimentin. Cytofluorimetrical analysis of tumor samples showed a diploid DNA distribution, whereas permanent culture cells evolved to the hyperdiploid DNA content. Karyotype studies revealed cytogenetical abnormalities described in glial tumors including gain of chromosome 7, loss of chromosome 10 and presence of double minutes (DMs). Enhanced expression of Ha-ras and c-myc genes resulted from high p-21 and p-62 levels. The contemporary presence of TGF-alpha and EGF-Rc transcripts suggested an autocrine mechanism in the cell lines growth.
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PMID:Establishment and characterization of two cell lines derived from human glioblastoma multiforme. 132 Mar 58

Although the loss of tumor suppressor genes and the activation of oncogenes have been established as two of the fundamental mechanisms of tumorigenesis in human cancer, little is known about the possible interactions between these two mechanisms. Loss of genetic material on chromosome 10 and amplification of the epidermal growth factor receptor (EGFR) gene are the most frequently reported genetic abnormalities in glioblastoma multiforme. In order to examine a possible correlation between these two genetic aberrations, the authors studied 106 gliomas (58 glioblastomas, 14 anaplastic astrocytomas, five astrocytomas, nine pilocytic astrocytomas, seven mixed gliomas, six oligodendrogliomas, two ependymomas, one subependymoma, one subependymal giant-cell astrocytoma, and three gangliogliomas) with Southern blot analysis for loss of heterozygosity on both arms of chromosome 10 and for amplification of the EGFR gene. Both the loss of genetic material on chromosome 10 and EGFR gene amplification were restricted to the glioblastomas. Of the 58 glioblastoma patients, 72% showed loss of chromosome 10 and 38% showed EGFR gene amplification. The remaining 28% had neither loss of chromosome 10 nor EGFR gene amplification. Without exception, the glioblastomas that exhibited EGFR gene amplification had also lost genetic material on chromosome 10 (p less than 0.001). This invariable association suggests a relationship between the two genetic events. Moreover, the presence of 15 cases of glioblastoma with loss of chromosome 10 but without EGFR gene amplification may further imply that the loss of a tumor suppressor gene (or genes) on chromosome 10 precedes EGFR gene amplification in glioblastoma tumorigenesis.
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PMID:Association of epidermal growth factor receptor gene amplification with loss of chromosome 10 in human glioblastoma multiforme. 132 Jun 66

Glioblastoma multiforme is an anaplastic neoplasm of glial origin. In spite of the aggressive histologic features and poor prognosis, metastasis outside the cranial vault is distinctly unusual. A patient with glioblastoma multiforme metastatic to the neck is presented. We also review the topic of metastatic intracranial tumors.
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PMID:Cervical metastatic glioblastoma multiforme. 132 Aug 96

The extremely poor prognosis of high-grade brain tumors (glioblastoma multiforme and anaplastic astrocytomas) has been well documented in the literature. Almost 90% of patients die within 18 months after therapy, most commonly because of local persistence of the tumor, which may be controlled if a sufficient amount of irradiation can be delivered. Currently, postoperative radiation therapy offers the best median survival rate. However, the response to external-beam radiation therapy has reached a plateau because of the intolerance of healthy brain tissue to excessive irradiation. To treat these tumors, brachytherapy (interstitial implantation of radioactive sources) can be used with debulking surgery. This therapy is becoming an effective alternative to conventional external-beam radiation therapy, since it allows a higher dose to be delivered to the tumor bed without damaging the surrounding healthy brain tissue. With continual refinements of the technique, brachytherapy, performed by a skilled brachytherapy team, offers an opportunity to improve patient survival.
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PMID:Treatment options in high-grade brain tumors: brain brachytherapy. 132 81

Glioblastoma multiforme, the most common and most lethal primary central nervous system neoplasm, is noted for its phenotypic and biological heterogeneity. This heterogeneity may result from genetic alterations accumulated by a single transformed astrocyte as it evolves into a monoclonal tumor. Alternatively, it may be attributed to the presence of multiple biologically and genetically distinct astrocytic populations within a polyclonal tumor. To address the issue of clonal composition of glioblastoma multiforme the authors used two independent approaches: analysis of X-chromosome inactivation and analysis of chromosomes 10 and 17 for tumor-specific somatic deletions. The analysis included 10 tumors from nine female patients with glioblastoma multiforme (eight primary and two recurrent tumors), who were heterozygous at either of two X-chromosome genes (hypoxanthine phosphoribosyl-transferase or phosphoglycerate kinase). Nine glioblastomas multiforme demonstrated a monoclonal pattern on X-chromosome analysis; contamination with normal tissue obscured the analysis in one tumor. Somatic deletions on chromosomes 10 and/or 17 occurred in nine tumors, supporting a monoclonal composition for these tumors. These data suggest that glioblastoma multiforme is a monoclonal neoplasm, derived from the clonal expansion of a single transformed astrocyte that has, as a fundamental step in tumorigenesis, sustained a critical genetic alteration on chromosome 10 and/or 17.
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PMID:Clonal composition of glioblastoma multiforme. 132 97

The concept of cytoreductive surgery in the treatment of glioblastoma multiforme is controversial. A retrospective study was carried out between 1986 and 1991 to analyze the results of stereotactic biopsy followed by supportive treatment (n = 49), incomplete radiation therapy (less than 40 Gy, n = 26), and complete radiation therapy (greater than or equal to 40 Gy, n = 58) and to compare with those of resection plus irradiation described in the literature. The patients treated with supportive care and an incomplete course of irradiation had a median survival of less than 8 weeks. For the patients who completed the radiation therapy the median survival was 32 weeks. In patients with midline shift the Karnofsky scores worsened more often during the course of radiation therapy, or therapy had to be terminated prematurely. The most important prognostic determinant was the patient's age. A comparison of survival rates in our series with those reported by other authors for patients who received tumor resection with subsequent irradiation yielded no significant difference. This would appear to cast doubt on the concept of cytoreductive surgery. The treatment of choice for patients with glioblastoma multiforme is at present radiation therapy. There is no question about the necessity of decompressive surgery whenever it is required to perform radiation therapy for severe space-occupying lesions and when it can be performed without causing new neurological deficits.
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PMID:[The value of stereotactic biopsy and percutaneous radiation in therapy of glioblastoma multiforme]. 132 87

Several clinical trials have been reported using Fluosol and oxygen breathing as an adjunct to radiation. Theoretical considerations and animal experiments, however, indicate that a combination of perfluorochemicals and hyperbaric oxygen (HBO) increases tumor oxygenation and radiation response to a greater extent than is seen either with a perfluorochemical and normobaric oxygen or with HBO alone. This is the first report of a pilot study of the use of Fluosol and HBO with radiation in humans. Twenty patients with anaplastic astrocytoma or glioblastoma multiforme were treated in a phase I trial of radiation with Fluosol and HBO at three atmospheres. Total Fluosol dose was escalated from 42 ml/kg in six courses to 80 ml/kg in four courses. Patients were irradiated in an HBO chamber with 600 cGy weekly fractions following Fluosol administration. Sixteen patients completed treatment; no interruption was necessitated by treatment toxicity. The addition of Fluosol/HBO did not increase the incidence of HBO related toxicities. No significant chronic toxicities were seen. This pilot study demonstrates that Fluosol and HBO can safely be used as an adjunct to radiation in the treatment of human tumors.
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PMID:Fluosol and hyperbaric oxygen as an adjunct to radiation therapy in the treatment of malignant gliomas: a pilot study. 132 43


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