Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Extracts of glioblastomas and meningiomas were analysed by quantitative immunoelectrophoresis for the presence of foetal brain antigens and tumour-associated antigens, and levels of 2 normal brain-specific proteins were also determined. The following antibodies were used: monospecific anti-S-100 (glia specific); monospecific anti-GFA (glial fibrillary acidic protein), (astroglia specific); polyspecific anti-foetal brain (12-16th week of gestation); a polyspecific anti-glioblastoma antiserum, absorbed with insolubilized serum, haemolysate and normal brain extract; polyspecific anti-alpha-foetoprotein; and monospecific anti-ferritin. Using the antibodies raised against the tumours, several antigens not present in foetal or adult normal brain were found in the glioblastomas and the meningiomas. These antigens cross-reacted with antigens present in normal liver and were therefore not tumour-associated. S-100 was found in glioblastomas in approximately one tenth the amount in whole brain homogenate, whereas GFA was found 2-4 times enriched. The 2 proteins were absent in meningiomas. The possible use of the GFA protein as a marker for astroglial neoplasia is discussed. Five foetal antigens were found in foetal brain, but none in the tumours. alpha-Foetoprotein could only be demonstrated in foetal tissue extracts, including foetal brain, but not in tumours. Ferritin was detected in all tumour extracts, although the amounts determined were unrelated to histological tumour type.
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PMID:Antigens in human glioblastomas and meningiomas: Search for tumour and onco-foetal antigens. Estimation of S-100 and GFA protein. 6 76

Partial biochemical characterization of several neural tissue specific antigens isolated from a murine glioblastoma cell line was accomplished by means of radioiodination of intact cells followed by immunoprecipitation of the cell lysate with a rabbit serum specific for neural tissue antigens. Polyacrylamide gel electrophoresis of the immunoprecipitate in sodium dodecyl sulfate resolved the labeled antigens into several major components: two proteins (or glycoproteins) having apparent m.w.'s of 84,000 and 120,000 and lipid associated components which may be heterogeneous. The protein and lipid associated components apparently possess independent antigenicity because after chloroformmethanol extraction the protein components can be immunoprecipitated from the aqueous phase and the lipid associated component can be immunoprecipitated from the organic phase. Despite their independent antigenicity it is not known whether the components may be noncovalently associated on the cell surface. Although some of these antigens can be isolated from brain or glioma cells (a related tumor), non can be demonstrated in lymphoid tissues or C1300 neuroblastoma cells using identical methods. Therefore, these studies confirm our previous findings concerning the specificity of the anti-NS-2 antiserum by using cytotoxicity tests.
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PMID:Partial characterization of nervous system-specific cell surface antigen(s) NS-2. 6 27

Glial tumors of glioblastoma type, cultured in vitro, have been exposed between the 7th and 14th day of growth to actinomycin C and K in a concentration of 5 x 10(-6) M. The developing degenerative changes in the neoplastic cells were observed after 6, 8, 12 and 24 hours after the addition of actinomycin to the culture of the tumor. It has been found, that the developing degenerative changes in the tumor cells are paralleled by a growing activity of the enzyme tested. The degenerative changes were described in the neoplastic cells, beginning from the accumulation of the enzyme activity in small granules of the cell processes up to very high activity of the enzyme in fragments of the breaking down cells. It is suggested that LDH activity is a good marker of cell form degenerative changes.
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PMID:Lactic dehydrogenase activity in degenerative neoplastic glial cells after actinomycin application in vitro. 8 82

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

Inoculation of 0.02 ml of high-titer Kirsten strain Murine Sarcoma Virus into the brains of 10-day-old Wistar/Furth rats yields, with 100 percent incidence, a uniform glioblastoma-like tumor within 16 days. Light and electronmicroscopy confirmed the neuroectodermal origin of the parenchymal cells. The remarkable vascular component was studied with extracellular tracers. The permeability of the abnormal endothelium to constituents of the blood vascular compartment was confirmed. Accessory vascular channels, and blood channels devoid of endothelium entirely, were observed. This reporducible system should provide a useful model for further studies of the biology of brain tumors.
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PMID:'Glioblastoma'. Induction of a reproducible autochonous tumor in rats with murine sarcoma virus. 17 26

The choice of tumor dose and treatment volume are the two most important radiation factors influencing survival in glioblastomas. Patients treated to their whole brain survive longer than those treated with limited fields. Glioblastomas treated with over 5,000 rads (1,300 rets) survive longer than those treated with smaller doses. Other factors affecting survival are: the pathological grade; age at diagnosis; and surgical treatment performed. Failure patterns in glioblastomas represent intrinsic qualities of the tumor, the host, and the treatment employed. They dictate the strategy to follow. Perhaps some of these are unaffected by irradiation. An increase in dose and the extension of fields in glioblastomas have produced a gain in both the quantity and the quality of survival. The whole brain is treated (5,000-6,000 rads) and the target volume is boosted to 7,000 to 8,000 rads. Grade II astrocytomas perhaps should be treated with whole brain irradiation (4,500 rads) and a boost to the target volume of an additional 1,000 rads.
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PMID:Patterns of failure in intracranial astrocytomas after irradiation: analysis of dose and field factors. 17 98

The quantitative preservation of satellite NA was studied in several central nervous system (CNS) neoplasms; four tumor lines deriveo from 3-methylcholanthrene implantation into the CNS of mice were compared with brain and tissue cultures of normal mouse cells by analytical centrifugation in cesium chlorie. Three tumors showed no detectable difference from normal cells; nuclear and whole cell preparations were comparable. Only a glioblastoma line proucing C-type particles (TC509) revealed a significant difference from normal cells and exhibited a decrease of approximately 20% in satellite DNA or 2% of the total DNA on repeated examination for 1 year. C-type RNA virus may be related to relative decreases in satellite DNA observed in TC509.
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PMID:Amount of satellite DNA in four experimentally induced tumors of the central nervous system. Quantitative changes in a glioblastoma producing C-type particles. 17 80

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

A retrospective study of 127 cases irradiated for glioblastoma was made to assess the role of radiation therapy and to determine the optimal technique of radiation therapy. The over-all survival rates of our series were 52 percent at one year, 19 percent at three years, and twelve percent at five years after radiation therapy. Survival time of the patients is influenced by various factors other than treatment: age, sex, histologic grading, duration of symptoms, and location of tumor. Among these factors, the location of the tumor was the most important in our present series. Surgical treatment can extend the survival time. More extensive resection results in longer survival, provided that the location of the tumor allows such a surgical procedure. Radiation therapy can prolong the survival time of those with glioblastoma, but a high tumor dose of more than 6,000 rads or 1,700 rets is necessary to improve the prognosis significantly. Therefore, irradiation should be administered through generous fields according to the extent of the tumor under precise planning to determine the accurate localization and extent of the tumor.
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PMID:Radiation therapy in the treatment of glioblastoma. 17 94

Penetration of variamycin, a new antitumor antibiotic into the normal and tumor tissues of the brain of rats with multiform glioblastoma was investigated. The content of the C14-labeled antibiotic was determined radiometrically. The radioactive label penetrated into the normal and tumor tissues of the brain during the first hours after the drug administration. The level of the radioactivity in the tumor tissue was higher than that in the normal brain tissue during the whole period of the study. The greatest deviation in the contents of the radioactive label in the tumor and normal tissues was observed 2 and 3 hours after administration of the labeled antibiotic, i. e. 4.3 and 3.6 times respectively.
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PMID:[C14-variamycin content in normal and tumorous brain tissues of white rats]. 17 69


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