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)

A number of cases of multiple primary intracranial neoplasms have been reported, including tumors of neuroepithelial and mesenchymal origin. The presence of meniogioma has been reported in association with glioblastoma, oligodendroglioma, astrocytoma, and eosinophilic adenoma. This case represents a unique example of adjacent chromophobe adenoma and meningioma. The usefulness of computed tomography in the diagnosis of concomitant lesions with different density attenuations is discussed.
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PMID:Case report. Tandem lesions: chromophobe adenoma and meningioma. 61 35

In this investigation, the lipid composition of a number of human brain tumors was determined and compared to that of normal adult brain. Glioblastomas (11 samples), astrocytomas (4 samples), an acoustic neurinoma, an oligodendroglioma, and a meningioma were analyzed. All of the tumors had substantial levels (0.8-3.4% of total phospholipids) of choline plasmalogen which was present in only trace amounts in normal brain. With the exceptions of the acoustic neurinoma and the meningioma, the concentration of alkylacylglycerophosphorylcholine was also higher in the tumors than in normal brain. Neutral lipids of brain tumors also contained high concentrations of both alkyl (1.6-4.8% of total neutral gsults from this investigation indicate that increases in ether-linked glycerolipids may be characteristic of human brain tumors.
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PMID:Ether-linked glycerolipids in human brain tumors. 84 2

The familial occurrence of brain tumors are exceedingly rare except in cases with phacomatosis. We encountered pituitary adenomas in two sisters of a family, so far presenting no evidence of multiple endocrine adenomatosis (MEA). Case 1, K. O. a 26-year-old woman was admitted to our Hospital on September 10, 1970 with visual acuity and field disturbance, irregular menstruation and acromegaly. Neurological examination: Her visual acuity was Vd 0.6 and Vs 0.3, visual field was bitemporal hemianopsia, and ther was papilledema bilaterally. She had left exophthalmos and left abducens palsy. Roentgenogram of the skull, brain scanning, cerebral angiogram, pneumoencephalogram suggested the presence of a pituitary tumor. On Sep. 17, 1970, through a left frontotemporal craniotomy the tumor was removed subtotally. The pathological diagnosis was pituitary adenoma (chromophobe). Case 2, M. T. a 31-year-old woman, sister of case 1, was admitted to the Hospital on September 19, 1973, with mild headache, left visual field disturbance and amenorrhea. She had a child, and a past history of pulmonary tbc. Neurological examination: Her visual acuity was Vd 1.2 and Vs 0.03, and visual field of the right eye was temporal lower quandrant anopsia. There was optic nerve atrophy in the left eye. Plain X-ray craniogram, brain scanning, cerebral angiogram and pheumoencephalogram suggested the presence of a pituitary tumor. On Sep. 28, 1973, a right frontal craniotomy was performed. The tumor tissue with capsule was removed subtotally. The pathological diagnosis was pituitary adenoma (mixed type). In the literatures about familial brain tumors with histological diagnosis, glioma and glioblastoma are common, meningioma is relatively rare. Pituitary adenoma with no evidence of MEA is exceedingly rare. The two sisters presented in this paper, have no evidence of hyperparathyroidism, pancreas adenoma and peptic ulcer. So, we consider, at present, these cases should not be field in MEA.
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PMID:[Familial occurrence of pituitary adenoma (author's transl)]. 94 79

The authors review the clinical and pathological features of 24 patients with gliosarcoma. The study revealed the following findings. Gliosarcoma occurs more frequently than is indicated in the literature, and in our series was present in 8% of all cases of glioblastoma multiforme. The presenting features are not significantly different from those of glioblastoma multiforme. The lesion often presents itself at surgery as a firm, well circumscribed mass within the temporal lobe, and at surgery it is commonly mistaken for a meningioma. There is an increased likelihood of metastasis compared to that of glioblastoma. The prognosis is no worse than that of glioblastoma, in spite of the addition of sarcomatous elements.
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PMID:Clinical and pathological study of 24 cases of gliosarcoma. 95 76

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

All primary intracranial neoplasms diagnosed between 1935 and 1964, inclusive, in the well-defined populations of children under age 15 residing in the state of Connecticut and the city of Rochester, Minnesota, formed the basis for this study. The tumors occurring in this group were characterized by histologic type and by the patient's sex and the age when the tumor occurred. In Connecticut, over the 30-year period, a primary intracranial neoplasm was diagnosed in 380 patients in a mean population of 582,286 children, yielding an average annual incidence rate of 2.17 cases/100,000 population per year. Of the microscopically confirmed tumors, the most common, in order, were medulloblastoma (24.2%), astrocytoma (20.6%), glioblastoma (20.3%), ependymoma (6.5%), craniopharyngioma (5.6%) and meningioma (4.6%). These figures contrast sharply with the corresponding frequency of these tumors in the adult Connecticut population. In Rochester during the same years, 12 primary intracranial neoplasms occurred in a mean population of 7,981 children, yielding an average annual incidence rate of 5.01 cases/100,000 population per year.
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PMID:The epidemiology of primary intracranial neoplasms of childhood. A population study. 124 98

Cell-mediated cytotoxicity (CTX) of meningioma patients was assessed postoperatively by a [3H]proline microcytotoxicity test. Autologous and allogeneic tumour cells were used for prelabelling with isotope and peripheral blood lymphocytes added in a ratio of 200:1. After 60 hg the plates were washed and residual CMP counted. Control target cells consisted of normal skin fibroblasts. CTX was calculated in percentage reduction compared to cultures incubated with control lymphocytes. Specific CTX on meningioma cells (i.e. not destroying control cells) greater than 20% was considered 'positive' if significant at P less than 0-05. Fifteen of twenty-three meningiomas showed specific CTX (65%). Among eight CNS tumours of different type and thirteen non-malignant diseases and normals only three (14%) were specifically cytotoxic for meningioma cells. A cross-reaction could be demonstrated between autologous and allogeneic meningioma target cells. However, no activity of lymphocytes from patients with meningiomas on glioblastoma cells and foetal brain tissue could be found at the ratio used for evaluation. Evidence is presented indicating that a cellular immune response as measured in the microcytotoxic test may be dependent on a residual or recurrent tumour in the body.
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PMID:Cell-mediated immune response of patients with meningiomas defined in vitro by a [3H]proline microcytotoxicity test. 127 80

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

Cytogenic and molecular genetic analyses of the major histological subtypes of nervous system tumors, gliomas, meningiomas, and neurinomas, have provided interesting information on the mechanisms responsible for or contributing to their origin and development. Regarding malignant gliomas, a complex pattern of chromosomal involvement has been documented at the cytogenetic level: gains of chromosome 7 and losses of chromosome 10, 9p, 17p, and 22; further molecular characterization of these abnormalities has shown that mutational alterations of the p53 gene, together with the loss of alleles at 17p, seem to be the earliest abnormalities occurring during the genesis and progression of these neoplasms. The losses of regions on chromosomes 22 and 13 might also be relatively early events, perhaps characterizing subgroups of low grade gliomas. The mutations of the p53 gene in low grade tumors leads to a selective advantage in vivo and seems to be a critical step in the transformation from low grade to high grade gliomas. The loss of sequences on chromosome 10 and the deletions of 9p (that is loss of tumor suppressor genes on these locations), and epidermal growth factor receptor gene amplification, have been proposed as sequential abnormalities participating in glioblastoma tumorigenesis. The available data on meningiomas and neurinomas show that loss of regions on chromosome 22 is the main characteristic feature. Thus, tumor suppressor genes located in this chromosome are non-randomly involved in both neoplasms, and may present as solitary, sporadic tumors or as multiple associated lesions in neurofibromatosis type 2 (NF-2). The molecular analysis of a large series of meningiomas to determine the common chromosome 22 region lost has revealed that a putative meningioma tumor suppressor gene should be located at the distal 22q12.3-qter region. In parallel, the linkage data on the mapping of the NF-2 gene suggest that the NF-2 and meningioma loci are separate entities. However, some evidence exists on a possible participation of the NF-2 locus in the genesis of some meningiomas. The efforts to identify and isolate the genes involved, as well as their functional analysis, will contribute to a better understanding of the mechanisms of oncogenesis in these neoplasms and will doubtless have a clinical impact in the diagnosis, treatment and prognosis of nervous system tumors in patients.
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PMID:Cytogenetics and molecular genetics of nervous system tumors. 133 85

Glutathione (GSH) and Glutathione S-transferase (GST) plays an important role in the protection of cells against damage from free radicals and also influences cytotoxicity to some kinds of chemotherapeutic agents. GST comprises a group of abundant and widely distributed catalytic and binding proteins that facilitate the conjugation of GSH with the electrophilic center of a large spectrum of hydrophilic molecules. Multiple GST isozymes in mammalian tissues arise from dimeric combination of a number of distinct subunits grouped into three major classes: alpha (alpha), mu (mu), and pi (p). We report the total GST, GST-p activity and GSH content of human brain tumors, C6 rat glioma cells and drug resistant C6 cells. The values of total GST activity in 42 normal brain and brain tumors were quantitatively analyzed. Total GST activity was 92.6 +/- 25.1 units (mean +/- standard deviation) in 8 samples of normal brain tissues, 126 +/- 58.8 units in five grade II or III astrocytomas (154 +/- 63.3 units in grade II astrocytomas, 84.4 +/- 2.7 units in 2 grade III astrocytoma), 66.2 +/- 29.3 in 5 glioblastoma cases, 94.7 +/- 47.7 units in 3 metastatic tumors, 302 +/- 114 unit in 8 meningiomas and 213 +/- 90.4 units in 3 neurinomas. Differences of GST activity between glioblastomas and meningiomas, grade II or III astrocytomas and meningioma, in normal brain tissues and meningioma were statistically significant (p < 0.01). The difference between normal brain tissues and benign tumors (meningiomas and neurinomas), gliomas and benign tumors were also statistically significant (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Quantitative analysis of glutathione and glutathione S-transferase in human brain tumors, C6 rat glioma cells and drug resistant C6 cells]. 140 41


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