Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017638 (glioma)
 30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a series of 26 consecutive autopsy cases of intracranial tumors of neuroectodermal origin, tumor seeding on the ventricular surface and in the subarachnoid space was studied. Five cases of glioblastoma multiforme, six of malignant astrocytoma, six of medulloblastoma, one mixed glioblastoma-fibrosarcoma, one unclassified glioma, and one ependymoma showed ventricular and/or subarachnoid seeding of tumor. The incidence of tumor seeding in our series (76.9%) is much higher than in other series. This discrepancy is probably due to the inclusion of a large number of very small tumor metastases that may have been overlooked in other series. In all cases where metastases were observed the primary tumor extended into the cerebrospinal fluid (CSF). Tumor seeding via the cerebrospinal pathway was more frequently associated with malignant tumors. The distribution of tumor metastases correlated with CSF flow and with the site of focal ependymal defects, which were present in normal brains but occurred more frequently and widely in hydrocephalus.
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PMID:Ventricular and subarachnoid seeding of intracranial tumors of neuroectodermal origin--a study of 26 consecutive autopsy cases with reference to focal ependymal defect. 630 22

Ten (23%) patients out of 43 with malignant glioma developed meningeal gliomatosis during the follow up period of at least one year. The duration between the first surgery and diagnosis of meningeal gliomatosis ranged from one to 78 weeks (median 45 weeks). In younger age group less than 20 years old, 5 (56%) out of 9 patients had meningeal gliomatosis, and on the contrary the incidence was lower in older age group above 20 years old (5 of 34, 15%). Seven (22%) out of 32 male and 3 (27%) out of 11 female patients developed meningeal gliomatosis. The primary tumor location were frontal lobe in 4 cases (including one bifrontal tumor), temporal in 2, parieto-occipital in 1, thalamus in 1, midbrain in 1, and cerebellar hemisphere in 1, respectively. Histologically, 7 tumors were anaplastic astrocytoma, and 3 were glioblastoma. The characteristic neurological findings observed during the course of meningeal gliomatosis were abnormal mental status (80%), cranial nerve palsies (50%), paraplegia (60%), stiff neck (80%), seizure (50%), and respiratory disturbance (80%), CSF cytology was positive in all 9 patients tested. CT scan demonstrated hydrocephalus (70%), and diffuse contrast enhancement of ventricular wall (60%) and basal cistern (10%). In 2 cases, block and irregular filling defect were seen by myelography. Six patients were treated by irradiation to the whole brain and/or spine, and 5, by intrathecal chemotherapy with methotrexate, cytosine arabinoside and bleomycin. However, all patients died of the tumor one to 46 weeks (median 18 weeks) after the diagnosis of meningeal gliomatosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical studies of meningeal gliomatosis]. 649 23

Regional blood flow was measured in experimental brain tumors using iodoantipyrine labeled with carbon 14 and quantitative autoradiography. A total of fifteen oligodendrogliomas, sixteen mixed gliomas, one astrocytoma, one ependymoma, and three malignant schwannomas were studied in 9 rats. The mean tumor blood flows for all glioma classifications were similar, averaging 45 +/- 3 (standard error of the mean) ml . hg-1 . min-1. Flow was fairly uniform within individual oligodendrogliomas and there was no apparent correlation between blood flow and tumor size or location. The mixed gliomas were larger than the oligodendrogliomas and had a wider range of blood flow. Small focal areas of necrosis were observed in 7 mixed gliomas, and low flows were usually measured in these regions; these flows were not always the lowest regional values measured within the mixed gliomas or total group of tumors, however. Small tumor regions with increased vascularity, frequently with endothelial cell proliferation, were observed in oligodendrogliomas and to a greater extent in mixed gliomas; these regions were correlated with small elevations in blood flow (10 to 15 ml . hg-1 . min-1) in comparison with surrounding tumor tissue. Brain adjacent to tumor usually had higher blood flows than that in tumor periphery. Hemispheric differences in blood flow related to the site of primary tumor growth were not observed.
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PMID:Regional blood flow in ethylnitrosourea-induced brain tumors. 662 36

In order to better understand the cellular mechanism of glioma invasion, we investigated migratory responses and adhesiveness of human malignant glioma cells to fibronectin (FN) or vitronectin (VN). In addition, an expression of integrin subunits for FN and VN was analyzed by flow cytometry. All glioma cells tested migrated to both FN and VN to a various degree. Glioma cells which strongly migrated to FN or VN showed an intense expression of alpha 5 or alpha v, respectively, while there was no correlation between cell adhesiveness to FN or VN and intensity of the integrin expression. Studies using primary tumor cells from surgical specimen revealed that only an intensity of cell adhesiveness to FN was negatively correlated well with the degree of clinical invasion of gliomas. That is, the more glioma cells adhered to FN, the less the original tumor tissues showed tumor invasion.
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PMID:[Migration and adhesiveness of malignant glioma cells to fibronectin or vitronectin and their expression of integrin subunits]. 754 63

A 63-year-old female presented with recurrent glioblastoma at the site of a right parietal glioblastoma which was diagnosed 1 year before. She was treated at that time by total removal of the tumor, irradiation, and chemotherapy. Four months after the initial treatment, serial thallium-201 single photon emission computed tomography (201Tl SPECT) showed increased uptake at the edge of the original tumor site. The index, the ratio of 201Tl uptake in the lesion to the normal brain, was 2.9 which suggested a recurrent tumor. Magnetic resonance images with gadolinium over the next 7 months demonstrated an enhanced mass lesion at the site of primary tumor resection and a new enhanced mass in the right temporal lobe. The lesion in the right parietal lobe had a 201Tl uptake index of 2.5, while the lesion in the right temporal lobe had an index of 1.5. Re-craniotomy and total resection of the tumors in the right parietal and temporal lobes were performed. The histological diagnosis of both tumors was glioblastoma. The proposed use of 201Tl SPECT for the differential diagnosis of recurrent glioma and radiation necrosis should be carefully considered because the 201Tl uptake index can vary in tumor with the same malignancy grade.
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PMID:Variation in appearance of glioma on serial thallium-201 single photon emission computed tomography--case report. 762 55

The p16/CDKN2 gene has many features of a growth suppressor gene: it maps to 9p21, a frequent region of loss of heterozygozity in a variety of tumor types; it encodes an inhibitor of cyclin-dependent kinase 4; and its homozygous deletion is common in tumor-derived cell lines. However, the lower frequency of alteration of the gene in primary tumor tissue as compared to the cognate tumor cell lines has brought this interpretation into question. We have assessed the growth suppressive function of p16/CDKN2 by gene transfer. The introduction of full-length p16/CDKN2 cDNA caused marked growth suppression in p16/CDKN2-null human glioma cells, but was without significant effect in those cells with endogenous wild-type p16/CDKN2 alleles. These results provide functional evidence in support of the hypothesis that the p16/CDKN2 gene is a functional growth suppressor gene, at least in gliomas.
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PMID:Replacement of the p16/CDKN2 gene suppresses human glioma cell growth. 788 35

The authors report a series of 31 children under 17 years of age with primary spinal cord tumors who underwent radiation treatment following decompression laminectomy with or without tumor resection between 1959 and 1990. The tumors consisted of 15 astrocytomas, 11 ependymomas, one mixed glioma, one gangliolioma, and three of unknown histology. Ten- and 20-year survival rates and 10- and 20-year relapse-free survival rates for the 28 patients with known histology were 80% and 53%, and 73% and 67%, respectively. Eleven patients (35%) had no resection, 14 (45%) had a partial resection, and six (19%) had a grossly complete resection. Eight patients (26%) are dead: five due to recurrent tumor, two due to a second malignant tumor, and one due to intercurrent disease. primary tumor relapse or progression occurred in nine patients (29%), four of whom were salvaged. A second malignant tumor developed in four patients (13%), two of whom died. Local control of the tumor was finally achieved in 26 cases (84%), despite either grossly incomplete or no resection in 25 of these cases (81%). These statistics suggest that radiation treatment without resection may achieve long-term control in children with astrocytoma or ependymoma of the spinal cord.
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PMID:Spinal cord tumors in children: long-term results of combined surgical and radiation treatment. 786 Dec 37

Mutations in, and aberrant expression of, the p53 tumor suppressor gene were assessed in 17 cell lines derived from human malignant brain tumors (glioblastoma multiforme). Exons 5 through 8 were screened by single strand conformational polymorphism analysis (SSCP), followed by direct DNA sequencing. Mutations were found in 6 of 17 glioma cell lines, i.e., at a frequency similar to that found in primary malignant gliomas. Loss of the wild type allele was observed in 4 of the mutated cell lines. Two cell lines had the same mutation (CGG-->TGG; Arg-->Trp) in codon 248. Five of 6 mutations were transitions, 4 of which occurred at CpG dinucleotides. In one cell line a 10-bp deletion at the intron 4/exon 5 junction was found. Five of 6 glioma cell lines contained a mutation identical to that in the respective primary tumor despite prolonged in vitro culture (140-221 passages). Thus, the acquisition of p53 mutations during culture appears to be infrequent. Two cell lines derived from heterozygous tumors maintained the wild type p53 allele during long term culture. p53 protein levels were assessed by immunofluorescence cytochemistry and immunoprecipitation followed by Western blot analysis and revealed elevated levels of the p53 protein, although to a variable extent, in all cell lines with p53 mutations. A marked p53 protein accumulation was also observed in two cell lines lacking p53 mutations in exons 5 through 8, indicating that a prolonged half life of the gene product is not solely dependent on an aberrant coding sequence. The remaining cell lines had either low levels or no detectable p53 protein; one of the latter contained a gross rearrangement of the p53 gene. Our results suggest that with respect to p53 gene status, glioma cell lines usually resemble the original tumors and may, therefore, be suitable for studying the biological changes associated with p53 mutations in glial tumors.
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PMID:p53 protein accumulation and gene mutations in human glioma cell lines. 825 36

Astrocytic neoplasms show a high incidence of elevated or mutated epidermal growth factor receptor (EGFR) expression. Although proliferative effects from EGFR activation are well described, the role that changes in this receptor play in glioma growth and migration remain poorly addressed. This report characterizes changes in the levels of EGFR expression in three glial tumors at initial presentation (resection) and at the time of recurrence. By quantitative flow cytometry the mean level of EGFR expression increased, decreased, or remained the same in different recurrent astrocytomas relative to their primary tumor cells. Immunocytochemistry for EGFR on monolayer cells corroborated the level of expression in the recurrent tumors relative to their matched primary specimen. Immunoprecipitation indicated that 170 kd EGFR was expressed in each of the tumors, and showed normal down regulation following treatment with EGF. Proliferation response to EGF was seen in only 1/6 instances, but was concentration-dependent when observed. Stimulated migration of the cells was frequently seen and was also concentration-dependent on EGF; the magnitude of response was related to the relative level of 170 kd EGFR expression in the cells. EGFR immunostaining of tissue sections from the tumors confirmed the levels of EGFR expressed in primary and recurrent astrocytomas as was seen in the cultured cells. These results indicate that the relative levels of EGFR in early passage cell cultures from glioma specimens concurs with the measured tissue levels of expression. Human glioma cells are more responsive to migration induction than proliferation induction by EGF.
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PMID:Proliferation and motility responses of primary and recurrent gliomas related to changes in epidermal growth factor receptor expression. 869 21

Cancer has been proposed to develop by a process of stepwise accumulation of growth-advantageous genetic alterations which result in the evolution of clones which are outgrowths of such rare cells [1]. This model has recently been extensively tested in human gliomas, the most common primary tumor of the adult central nervous system. Temporal disease progression involves an interplay between growth-suppressing and growth-promoting genes. Specifically for gliomas, genetic studies have indicated loss of germline heterozygosity for chromosome 17p; mutation of the p53 gene; overexpression of the platelet-derived growth factor-alpha receptor; allelic losses of chromosomes 22q, 13q, and 19q; deletion of the interferon-alpha and beta and CDKN2 loci on chromosome 9p; amplification and rearrangement of the epidermal growth factor receptor gene, and monosomy of chromosome 10. The following discussion details these genetic alterations and their consequences for the biology of glioma progression with the ultimate aim of providing new avenues for clinical intervention.
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PMID:Molecular biology of malignant degeneration of astrocytoma. 881 14


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