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

An account is given of a family from the Canton of Valais suffering from hereditary adenocarcinomatosis. The pedigree extends over four generations; the first three comprised 47 individuals (28 males, 19 females), of whom 21 (16 males and 5 females), i.e. 44.6%, have malignant tumors. Of the 32 people in the fourth generation, only one individual is affected to date (a girl age 21, IV/4). There were 27 tumors in all: 16 adenocarcinomas of the colon, two gastric adenocarcinomas, one duodenal adenocarcinoma, one rectal adenocarcinoma, one papillary carcinoma of the ovary, one osseous sarcoma, one cutaneous fibrosarcoma, a multiform glioblastoma of the basal nuclei of the brain, a basocellular epithelioma, a cerebral metastasis from an adenocarcinoma, the origine of which has not been established, and a tumor invading the biliary tract. Three members of the family had multiple tumors. In three of the patient the colonic adenocarcinoma was accompanied by one or two polyps. The average age at onset for all tumors was 45 years. It was definitely lower in the third than the second generation (anticipation). The transmission was autosomal dominant, with predilection for the male sex (57.1% male and 26.3% female patients). The penetrance was about 80%. Finally, the diagnostic criteria for hereditary adenocarcinoma are discussed and the different familial forms of cancer are reviewed.
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PMID:[Familial cancer syndrome studies in 4 generations of a family]. 19 29

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.
Cancer 1977 Aug
PMID:Soluble membrane antigens of brain tumors. I. Controlled testing for cell-mediated immune responses in a long surviving glioblastoma multiforme patient. 19 38

Autologous leukocytes (10(7) to 10(9)), obtained with the Haemonetic's Leukaphoresis apparatus, were inoculated directly into recurrent glioblastoma tumors via indwelling catheters or by direct intratumoral injection through existing craniotomy openings. The rational use for autologous leukocyte (lymphocyte) infusions was based on in vitro autologous lymphocyte cytotoxicity to glioblastoma cells in the absence of serum inhibitory factors. Seven of 17 patients treated had life expectancy under 1 month; all patients had received definitive surgery, and all but two received radiation, nitrosourea chemotherapy and/or dexamethasone, and showed evidence of clinically recurrent disease. Following autologous leukocyte infusion (lymphocyte/granulocyte ratio 1:1), eight patients sustained clinical improvement and were alive up to 17 months later. No neurotoxicity ascribable to the procedure has been observed. One patient, who was comatose at the time of single leukocyte infusion, returned to full activity and lived for 17 months without an increase in tumor mass by brain scan. These results suggest that infusions of autologous leukocytes (lymphocyte-monocytes) directly into glioblastoma may be a viable additional treatment for glioblastoma and certainly warrants further evaluation.
Cancer 1977 Sep
PMID:Immunotherapy with autologous white cell infusions ("lymphocytes") in the treatment of recurrrent glioblastoma multiforme: a preliminary report. 19 84

We have recently reported that fetal BD IX-rat brain cells (FBC), transferred to long-term culture after a transplacental pulse of EtNU on the 18th day of gestation, undergo neoplastic transformation in vitro ("BT-cell lines"). Tumors developed upon s.c. reimplantation of BT-cells into baby BD IX-rats, appeared histologically as neurinoma-, glioma- or glioblastoma-like, and frequently as pleiomorphic neoplasms. In spite of a more atypic cellular morphology, these tumors grossly resembled the different types of neuroectodermal rat neoplasms induced by EtNU in vivo. Like the neoplastic cell culture lines derived from EtNU-induced, neuroectodermal BD IX-rat tumors ("V-cell lines"), the BT-lines contained multipolar glia-like cells, but also flat cells with fewer and shorter cytoplasmic processes, and occasionally giant cells. Both the V- and BT-lines showed different levels of aneuploidy. They contained multiple subpopulations of cells, as reflected, e.g., by plurimodal pulse-cytophotometric DNA distributions. All lines contained, to varying degrees, the nervous system-specific protein S-100, a "marker" not yet expressed in FBC. There was no indication of more than borderline neurotransmitter activity, suggesting that proliferating (precursor) cells of glial lineages may preferentially undergo malignant transformation after exposure to EtNU during this stage of brain development.
Z Krebsforsch Klin Onkol Cancer Res Clin Oncol 1977 Aug 15
PMID:Phenotypic properties of neoplastic cell lines developed from fetal rat brain cells in culture after exposure to ethylnitrosourea in vivo. 19 83

On the basis of a three stage grading system we report 23 stage one recurrent oligodendrogliomas (O 1), and 29 stage two recurrent oligodendrogliomas (O 2). In the O 1 group after the first interval 15 became O 2 and 2 became glioblastomas. Twenty tumours of the O 2 group after the first interval were not changed, three became oligodendroglioma-astrocytomas stage 2, and six became glioblastomas. The time relation for the recurrent phase in the primary O 1 group is calculated as 42 months, and in the primary O 2 group as 22 months, but this is without significance. For the development of malignancy, especially for the change to glioblastoma, a prominent participation by transformed local astrocytes seems to be essential. Postoperative irradiation most probably does not favour malignant change. A prolongation of the expectation of life by radiotherapy is not noticed.
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PMID:Supratentorial recurrences of gliomas. Morphological studies in relation to time intervals with oligodendrogliomas. 19 51

A pilot clinical trial on radiotherapy of glioblastoma with and without hyperbaric oxygen was performed at the Columbia-Presbyterian Medical Center. Eighty previously untreated patients with histologically proved glioblastoma were evaluated; 38 were irradiated under hyperbaric oxygen and 42 (controls) in atmospheric air. The survival rates were calculated according to the actuarial analysis method. At the end of 18 months, the survival rate appeared considerably higher in the oxygen group (28%) than in the controls (10%). At the end of 36 months, no patients in the control group survived, whereas 2 patients in the oxygen group were alive beyond 45 and 48 months, respectively. The median survival time was 38 weeks for those treated under oxygen and 31 weeks for the air control group. Owing to the small population samples and the pilot nature of this study, the difference in survival rates between the two groups was not statistically significant. The toxicity of hyperbaric oxygen was well tolerated by most patients, and the quality of survival in the hyperbaric oxygen group was equal to or slightly better than that of the control group. This pilot clinical study paved the way for further controlled clinical trials of hyperbaric oxygen and oxygen-mimicking drugs, including the electron-affinic compounds that could have differentially sensitized the hypoxic tumor cells.
Natl Cancer Inst Monogr 1977 Dec
PMID:Hyperbaric oxygen and radiation therapy in the management of glioblastoma. 20 35

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 clinicopathologic features of eight new cases of combined intracranial sarcoma and glioma are described. This type of mixed cerebral tumor is histologically characterized by a peripheral distribution of the gliomatous elements in relation to a more centrally situated meningeal or intracerebral sarcoma, and by the frequent presence of gradual transitions from reactive to frankly neoplastic astrocytes. In six of the eight cases, the additional development of either infiltrating astrocytoma or frank glioblastoma in the adjacent brain was demonstrated; this was interpreted as a further expression of malignant glial reaction. It is suggested that these tumors be termed "sarcogliomas" to distinguish them from the type of mixed glioma and sarcoma that has recently been redesignated "gliosarcoma."
Cancer 1979 Jan
PMID:Reactive glioma in intracranial sarcoma: a form of mixed sarcoma and glioma ("sarcoglioma"): report of eight cases. 21 76

Glial fibrillary acidic protein (GFA) was assayed in nerve-tumour extracts and located in these tumours by indirect immunofluorescence study. We conclude that GFA is a specific marker of both malignant and normal astrocytes. Non-astrocytic tumours (oligodendroglioma, meningioma) do not contain GFA. Tumours with astrocytic differentiation potential (medulloblastoma) may contain GFA. Comparison of microscopic and GFA assays leads us to conclude that GFA concentration is proportional to the amount of malignant astrocytes in the tumour and inversely proportional to the necrotic area of a tumour. Normal tissue GFA and glioblastoma GFA were found to be immunologically identical.
Br J Cancer 1978 Jan
PMID:Glial fibrillary acidic protein in tumours of the nervous system. 33 41

Forty-three patients with inoperable and/or recurring malignant gliomas and 30 patients with multiple recurring brain metastases were treated with a combination of adriamycine (45 mg/m 2 and 4-dimethyl-epipodophyllotoxin D-thenylidene (VM 26) (60 mg/m 2 for 2 days) and 1-(2-chloroethyl)-3-cyclohexyl-1-nitroso-urea (CCNU) (60 mg/m 2 for 2 days). These cycles of treatment were repeated as soon as the hematologic restoration was complete. The treatment was well-tolerated and the clinical condition of 31 out of 43 glioblastoma patients improved during the 2 months after the beginning of the treatment. Six out of eight patients with breast cancer metastases, one out of 13 with bronchial cancer metastases, and three out of nine with other types of cancer metastases also benefitted from the treatment. Examination of the results reveals the following characteristics: 1. A low degree of efficiency of this combination in the treatment of brain metastases, except for breast cancer metastases. 2. Absence of complete correlation between the clinical results observed and the cinegammagraphic developments 3. Similarity of the results independent of the initial localization 4. Establishment of a 6-month median survival period, with ten patients at present in a state of apparently complete remission, 180-506 days after beginning of the treatment.
Recent Results Cancer Res 1977
PMID:Treatment of malignant gliomas and brain metastases in adults using a combination of adriamycine, VM 26, and CCNU. Results of a type II trial. 34 Dec 49


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