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)

Fifteen brain tumor patients were treated with slow neutron. It proved to extend life span of terminal glioblastoma patients irresponsive to Co-60, to 2 years, but quality of survival is poor due to complications of previous treatments. Two glioblastoma patients excluding other treatments, the only genuine Boron-neutron capture therapy cases, have been living for 39+ and 34+ months working full-scale without neurological deficit.
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PMID:A revised boron-neutron capture therapy for malignant brain tumors. II. Interim clinical result with the patients excluding previous treatments. 5 Oct 55

A malignant glioblastoma adherent to the dura mater was removed from the parieto-occipital lobe in a 12-year-old boy. The site of the tumor was subsequently irridiated by 4000 rads of Cobalt-60. Five months later the boy was readmitted complaining of pains in the pelvis an in both thighs. X-ray examination of the pelvis demonstrated multiple metastases. Investigation of bone marrow revealed replacement of normal haematopoiesis by a tumor cell population histologically identical to that of the brain tumor. Reviewing the literature 58 reports on glioblastomas with extracerebrospinal metastases could be found. Metastases were preferably localized in cervical or mediastinal lymph nodes, lungs, bones, liver, dura mater, and operative flap. It is suggested that extracerebrospinal metastases occur most frequently after the tumor has infiltrated the cranium and extracranial soft tissues. In the case reported here it is speculated that the tumor spread to extraneural tissues after invading the dural veins. The possible occurrence of extracerebrospinal metastases in glioblastoma emphasizes the necessity of additional chemotherapy.
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PMID:Extracerebrospinal metastases in glioblastoma. Case report and review of the literature. 18 58

Two brothers developed multiple primary neoplasms in childhood; one had glioblastoma and non-Hodgkin's lymphoma at age 11 years, and the other brain tumor and acute leukemia at six years. A third brother died with myelogenous leukemia at thre years, and a fourth with cyanotic congenital heart disease at 11 weeks. Each child also had at least one hamartomatous lesion of the skin. The clinical features suggested von Recklinghausen's neurofibromatosis or other inherited cancer syndrome, but laboratory studies identified no markers of susceptibility to familial neoplasia.
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PMID:Double primary cancers in 2 young sibs, leukemia in another, and dextrocardia in a fourth. 19 73

The correlation existing in several human malignancies between lymphocytic infiltration and prolonged survival prompted this study. Two hundred selected patients who were operated on for glioblastoma were reviewed to investigate the incidence of the lymphocytic infiltration in the histological slides and its possible relevance to a better clinical course. The group that exhibited a definite lymphocytic infiltration (Group A, 11.5%) had a significantly longer preoperative history and postoperative survival (p less than 0.01) than the other two groups that presented slight or no infiltration (Group B, 23%, and Group C, 65%, respectively). In addition, biopsies of 28 recidivous gliomas were reviewed to study the fate of this lymphocytic infiltration in relation to time and therapy, such as irradiation and steroids which are known to depress the immune response. The authors found that severe lymphocytic infiltration is a rare immunobiological reaction which significantly improves the prognosis of a malignant brain tumor and seems not to be influenced by time, local x-ray therapy, or steroids.
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PMID:Lymphocytic infiltrates in primary glioblastomas and recidivous gliomas. Incidence, fate, and relevance to prognosis in 228 operated cases. 73 2

Normal, viral transformed and tumor-derived cells grown in tissue culture and representing different species were tested for their ability to produce an extracellular tumor angiogenesis factor (TAF). TAF was assayed by measuring the host-mediated vascular response of the chorioallantoic membrane to TAF preparations. All of the viral transformed and tumor-derived cells tested, including SVT2, SVW126, Welker 256 rat carcinoma, B-16 mouse melanoma, human glioblastoma, and human meningioma cells, produced TAF. The potency of the TAF preparations, as measured by the number of cells needed to induce a positive vascular response on the chorioallantoic membrane, varied from cell line to cell line. The most potent cells tested were the glioblastoma and maningioma brain tumor cells. Since these brain tumors are found to be the most highly vascularized tumors in vivo, it was concluded that a correlation exists between the vascularity of a tumor in vivo and the potency of TAF in vitro. There was no detectable angiogenesis activity induced by density-inhibited BALB/c primary mouse embryo or early-passage human skin fibroblasts, even when relatively large numbers of cells were used to make a sample. However, density-inhibited BALB/c 3T3 aan W138 human embryonic lung fibroblasts, two cell lines widely regarded as demonstrating "normal" growth behavior in culture, produced TAF. From these and other observations, it was suggested that BALB/c 3T3 and W138 are not fully "normal" cells. Furthermore, it was suggested that the production of TAF is an early event in the cell transformation process that precedes the loss of density inhibition of growth in vitro.
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PMID:Tumor angiogenesis activity in cells grown in tissue culture. 124 90

Forty-six patients who underwent surgery for brain tumors were studied prospectively with 125I labeled Fibrinogen leg scans to detect postoperative venous thrombosis. The incidence of thrombosis was 72% for meningioma patients, 60% for glioblastoma patients, and 20% for brain metastasis patients. Correlation between the occurrence of venous thrombosis and the various clinical factors thought to be responsible for the high incidence of thrombosis generally failed to show statistical significance. This finding, along with the marked variation in the incidence of venous thrombosis between the different brain tumor groups, strongly suggests that biological factors play a more important role than clinical factors in determining which brain tumor patient will suffer a postoperative thrombotic event.
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PMID:Postoperative venous thromboembolism and brain tumors: Part I. Clinical profile. 133 48

alpha-Difluoromethylornithine (DFMO), an irreversible inhibitor of the polyamine biosynthetic enzyme ornithine decarboxylase, inhibits the growth of brain tumor cell lines and is undergoing clinical trials as a treatment for brain tumors. Platelet-derived growth factor (PDGF) is thought to regulate the growth and development of precursors of both normal and neoplastic astrocytic cells; calcium signaling is thought to play a role in the transduction of PDGF signals. Using laser fluorescence image cytometry, flow cytometry, and spectrofluorometry, we studied the effect of DFMO on the calcium signals induced by PDGF in A172 human glioblastoma cells. Four days of treatment with 5 mM DFMO substantially shortened PDGF-induced calcium signals. The effect was reversed more than 10 h but less than 24 h after putrescine treatment, even though polyamines were repleted 4 h after putrescine and spermidine were added. DFMO did not substantially affect intracellular calcium release or the timing of the opening and closing of plasma membrane calcium channels. These findings support the notion that calcium signaling may be a target for inhibitors of polyamine metabolism.
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PMID:alpha-Difluoromethylornithine alters calcium signaling in platelet-derived growth factor-stimulated A172 brain tumor cells in culture. 145 66

Northern blot analysis with O6-methylguanine-DNA methyltransferase (MGMT) cDNA as a probe was used to analyze the MGMT activity regulating drug resistance of human cells to chloroethylnitrosoureas (CENUs). By this method, the expression levels of MGMT mRNA in six human glioma cell lines and 12 human brain tumor tissues from surgical specimens were determined. These MGMT mRNA levels were compared with the SD10 values of the tumor cells, estimated by cell survival assay, which indicated their resistance to the anticancer drug, 1-(4-amino-2-methyl-5-pyrimidinyl)methyl-3-(2-chloroethyl)-3-nitrosourea (ACNU). Human brain tumors that were highly resistant to ACNU, such as glioblastoma Gbl1 and metastatic brain tumor Col1 with SD10 values (microM) of above 100, expressed markedly increased amounts of 0.95 kb MGMT mRNA. In contrast, tumor cells such as U-87MG, U-251MG, U-343MG, U-373MG and SF-126 with SD10 values of under 14 indicating low resistance to ACNU scarcely synthesized any MGMT mRNA. These results indicated that the level of expression of MGMT mRNA in human brain tumors determined by Northern blot analysis truly reflects their cellular resistance to ACNU. Thus the Northern method with MGMT cDNA probe reported here is a practical and reliable method for estimation of cellular resistance to CENUs such as ACNU and for screening the chemotherapeutic response to CENUs of human brain tumors.
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PMID:Expression of O6-methylguanine-DNA methyltransferase and chloroethylnitrosourea resistance of human brain tumors. 151 62

Brain tumors are the most frequent childhood tumors. There have been few cytogenetic studies published on these tumors in children compared to the numerous studies on adult brain tumors. We examined chromosomes from 45 primary pediatric brain neoplasms including 14 medulloblastomas, 12 astrocytomas, 4 glioblastomas, 7 ependymomas, 5 craniopharyngiomas, 2 meningiomas, and 1 ganglioglioma. Chromosomal abnormalities were found in 10 medulloblastomas out of the 14 analyzed. The most frequently observed abnormalities were the total or partial loss of one chromosome 17: monosomy 17, i(17q), and a monosomy 22 in 4 cases of desmoplastic medulloblastoma. In glioblastoma, we observed the gain of chromosome 7, chromosome 3, a monosomy 10, and hyperdiploidy. The loss of chromosome X was observed in 2 cases of ependymoma as was a monosomy 22. Our observations show that from the cytogenetic point of view childhood brain tumors differ from adult brain tumors.
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PMID:Cytogenetic studies in 45 pediatric brain tumors. 152 1

Frozen tissue sections obtained from human glioblastomas, brain tumor metastases and normal brain were examined for the expression of molecules known to be involved in lymphocyte activation and/or adhesion and migration. The molecules studied included CD3, CD45R, UCHL-1 (CD45RO), lymphocyte function-associated antigen 1 (LFA-1) (CD11a, CD18), intercellular adhesion molecule 1 (ICAM-1) (CD54), 4B4 (CD29), CD44, CD2, and LFA-3 (CD58). CD3+ lymphocytes infiltrating human glioblastomas and brain tumor metastases expressed LFA-1 alpha and beta. Many cells were also UCHL-1+ whereas only a small percentage were CD45R+. CD2+ lymphocytes were also present. Tumor-infiltrating lymphocytes (TIL) were found to be negative for CD29, which was, however, expressed on intratumoral vessels in addition to vessels found in normal brain. Glioblastoma cells and intratumoral vessels expressed ICAM-1 whereas no ICAM-1 was found on TIL or on normal brain. Glioblastoma cells also expressed high levels of both CD44 and LFA-3 whereas TIL were negative for these antigens. CD44 was also expressed on certain regions of normal brain. Antibodies to LFA-1 alpha and -beta and ICAM-1 could significantly block the binding of lymphokine-activated killer (LAK) cells or TIL to human glioblastoma cells suggesting that these molecules play a role in the binding and subsequent migration of lymphocytes into brain tumor tissue.
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PMID:Activation and adhesion molecule expression on lymphoid infiltrates in human glioblastomas. 169 16


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