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)

Non-glial intermediate filament (IMF) proteins, as well as glial fibrillary acidic protein (GFAP) and vimentin, were studied by immunohistochemistry in 24 gliomas including low grade astrocytoma, pleomorphic xanthoastrocytoma, anaplastic astrocytoma, glioblastoma, oligodendroglioma, ependymoma and ependymoblastoma, which were fixed in ethanol and embedded in paraffin. Cytoskeletal elements isolated from two glioblastomas were examined with immunoblot analysis. All tumors had GFAP-positive neoplastic cells and vimentin was also found in all the tumors except one oligodendroglioma. Twenty-three gliomas were immunostained with anti-desmin polyclonal antibody (DM-P), but anti-desmin monoclonal antibody reacted to only one glioblastoma. DM-P might crossreact with GFAP and vimentin. Cytokeratin expression was investigated with six antibodies. Twenty gliomas (83%) were positive for the antibody against epidermal keratin (CK-SE), however positive immunoreactivity varied from 58 to 8% with other cytokeratin antibodies. With the Western blot method, CK-SE had protein bands at 53 and 60-66 kDa. Neurofilament was expressed in one pleomorphic xanthoastrocytoma, one anaplastic astrocytoma, one glioblastoma and one ependymoblastoma. Expression of nonglial IMF proteins were observed in 21 tumors (88%), and coexpression of 4 or 5 classes of IMF proteins in 3 tumors (13%). We conclude that, in addition to GFAP and vimentin, gliomas express several types of non-glial IMF proteins.
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PMID:Expression of non-glial intermediate filament proteins in gliomas. 751 71

Tenascin, an extracellular matrix glycoprotein, has been reported to be expressed predominantly on glioma tissue in the CNS, both in a cell associated and an excreted form. Recently, a highly sensitive sandwich type enzyme immunoassay for quantitative determination of tenascin was developed. In the present study, the amount of tenascin in CSF was measured. An increase of tenascin in CSF (> 100 ng/ml) was found in patients with an astrocytic tumour. The concentration was significantly higher (> 300 ng/ml) in high grade astrocytoma (anaplastic astrocytoma and glioblastoma) and a further increase (> 1000 ng/ml) was found in cases of CSF dissemination of high grade astrocytoma. On the other hand, tenascin concentrations were less than 100 ng/ml in non-astrocytic tumours and non-neoplastic neurological diseases, except meningeal dissemination of tumour cells, meningeal stimulation by infection, and subarachnoid haemorrhage. In cases of treated astrocytomas in remission, tenascin was negligible (< 100 ng/ml) in the CSF. The measurement of tenascin in CSF is useful for differential diagnosis of brain tumours and monitoring of astrocytic tumours.
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PMID:Tenascin in cerebrospinal fluid is a useful biomarker for the diagnosis of brain tumour. 752 4

The treatment and prognosis of patients with cerebral astrocytic tumours are currently guided by histopathological classification. This study evaluates immunohistochemistry using Ki-67, an antibody to a nuclear protein expressed in proliferating cells, and DO-7, an antibody to the product of the tumour suppressor gene p53, as prognostic indicators for these tumours. Immunohistochemistry with Ki-67 has been correlated with the behaviour of many different tumours, but its value as a prognostic indicator in astrocytic tumours is diminished by the conflicting results of previous studies. Immunohistochemistry with antibodies to the p53 protein has been used as a prognostic indicator in melanomas and some carcinomas, but the relation between prognosis and accumulation of this protein in astrocytic tumours has not been clarified. We have tested the hypothesis that survival is correlated with Ki-67 immunolabelling indices (LIs) and patterns of p53 immunolabelling in the cerebral astrocytic tumours of a large cohort of patients (n = 123) for whom clinical indices were well documented. Astrocytic tumours were divided into three histological types: fibrillary astrocytoma (n = 24), anaplastic astrocytoma (n = 31), and glioblastoma (n = 68). Histological type and patient age were independent predictors of survival. Median Ki-67 LIs differed significantly (P < 0.0001) between the types of astrocytic tumour, and tumours with a Ki-67 LI < 2% had a significantly (P < 0.0001) better prognosis. Ki-67 LI as a continuous variable carried a significant (P = 0.0043) unadjusted hazard to survival which was lost when adjusted for other variables, notably histological type. By contrast, no relation was found between survival and three categories of p53 labeling (p53-negative, p53 LI < 40%, and p53 LI > 60%). The results indicate that, whereas Ki-67 immunohistochemistry predicts survival in patients with astrocytic tumours, conventional histological appraisal remains the best guide to prognosis, and immunohistochemistry for p53 has no value in the assessment of these tumours.
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PMID:Prognostic indicators in a range of astrocytic tumours: an immunohistochemical study with Ki-67 and p53 antibodies. 756 22

We investigated the frequency of p53 mutations in 47 pediatric brain tumors of various histologic subtypes that were collected over a period of 5 years. The specimens included 15 primitive neuroectodermal tumors (PNETs), 17 low grade astrocytomas, one anaplastic astrocytoma, three glioblastomas (GBMs), one mixed glial tumor, eight ependymomas, one choroid plexus carcinoma, and one gangliocytoma/ganglioneuroma. Mutations were identified by single strand conformation polymorphism analysis of exons 4-8 and verified by sequencing. Mutations were present in 2 of 3 cases of GBM, but not in 17 low grade astrocytomas (P = 0.02, Fisher's exact test). One GBM demonstrated a germline GGC to AGC transition (gly to ser) at codon 245 with loss of the wild-type allele. A second GBM contained a CGG to TGG transition (arg to trp) at codon 248, also with loss of the wild-type allele, but normal tissue was not available for comparison. In addition, one of 15 PNETs retained heterozygosity but demonstrated a somatic CGT to TGT transition (arg to cys) at codon 273. p53 mutations were absent in other histologic subtypes and in two cases with multiple primary cancers. These data are consistent with earlier findings that p53 mutations are rare in PNETs, which are primarily pediatric tumors. In contrast to adult gliomas, p53 mutations in pediatric gliomas appear restricted to the GBMs. The lack of p53 mutations in pediatric low grade astrocytomas suggests not only histological differences, but also a different molecular pathogenesis in adult and pediatric patients.
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PMID:p53 gene mutations in pediatric brain tumors. 756 4

Diffusely infiltrating low-grade astrocytomas (WHO grade II) have an intrinsic tendency for progression to anaplastic astrocytoma (WHO grade III) and glioblastoma (WHO grade IV). This change is due to the sequential acquisition of genetic alterations, several of which have recently been identified. In low-grade astrocytomas, p53 mutations with or without loss of heterozygosity on chromosome 17p are the principal detectable change. Anaplastic astrocytomas contain p53 mutations at an overall incidence of 34% and, in addition, loss of heterozygosity on chromosome 19q and frequent homozygous deletion of the p16 tumor suppressor (MTS-1) gene. The most malignant astrocytic neoplasms, the glioblastoma, further shows loss of chromosome 10 and amplification of the epidermal growth factor receptor (EGF-R) gene at overall incidences of 66% and 34%, respectively. The type and distribution of p53 mutations in astrocytic brain tumours are not suggestive of specific environmental carcinogens operative in their aetiology. Analysis of 91 families with p53 germline mutations reported to date show that tumours of the nervous system account to 12% of all neoplasms. Of a total of 57 brain tumours reported, 30 were classified histologically and of these, 73% were of astrocytic origin. The observation that somatic p53 mutations in sporadic brain tumours are largely restricted to those of astrocytic origin and that astrocytomas also prevail among CNS neoplasms associated with p53 germline mutation strongly suggests, that p53 mutations are capable of initiating neoplastic transformation in astrocytes of the human nervous system.
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PMID:Genetic alterations associated with the evolution and progression of astrocytic brain tumours. 758 39

In 1955, Collins made the observation that tumor recurrence in children with Wilms' tumor was correlated with the child's age plus 9 months. This concept of a period of risk for recurrence was later applied to a variety of tumors in children and became known as Collins' Law (CL). The law has been a successful predictor of survival for some children with neural tumors within the central nervous system and a poor predictor for others. We tested Collins' concept of a period of risk for recurrence and extended it to survival for 14 childhood neural tumors described in the Childhood Brain Tumor Consortium (CBTC) database. The CBTC data describe clinical, surgical, and histological details (over a 49-year period in 10 institutions) from 3921 patients under the age of 21 years at the time of their first surgical procedure for a brain tumor. CL was considered to be a good predictor of survival if fewer than 10% of patients who die survive beyond the expiration of the period of risk for that child. We found that CL applied to tumors such as anaplastic astrocytoma, glioblastoma, pineoblastoma, medulloblastoma or "primitive neuroectodermal tumor," teratoma, and germinoma, as well as ependymoma, papilloma, and tumors that could not be classified; it had no predictive value in craniopharyngioma, oligodendroglioma, or plain, fibrillary, pilocytic, or protoplasmic astrocytoma. We had sufficient follow-up data to determine adherence to CL when the child's age at diagnosis was less than 8 years; it is likely that CL applies to older children with these tumors, but we did not have the data to show this unequivocally.
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PMID:The applicability of Collins' Law to childhood brain tumors and its usefulness as a predictor of survival. 764 86

Eighteen patients have been treated for gliomas with fractionated stereotactic linear accelerator (LINAC) irradiation. A plastic halo ring secured with skull pins allows daily attachment of the patient to the stereotactic frame mounted on the linear accelerator. The patients received 9-31 fractions of 1.8-3 Gy/fraction over periods of 20-49 days. Total doses delivered stereotactically where 16-60 Gy (90% isodose) delivered to 3-7 cm diameter tumors. The six patients with glioblastoma had a median survival of 16 months (range 7-60 months). The two patients with anaplastic astrocytoma survived 7 and 78 months. Most of the patients with high grade tumors also received other adjuant treatments. Of the ten patients with low grade gliomas, one expired 66 months after treatment, and the remainder are alive 22-82 months after treatment. One pediatric patient displayed evidence of focal radiation injury with visual loss. No patient developed initial recurrence of tumor outside the focally irradiated field. Stereotactic localization of irradiation protects surrounding brain tissue; fractionation improves the therapeutic ratio. These extended follow-up data indicate that stereotactic restriction of radiation fields in treatment of gliomas does not result in deterioration of survival results. Further investigation is warranted into the use of higher focal fractionated radiation doses to attempt to improve local control and survival.
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PMID:Long-term follow-up of gliomas treated with fractionated stereotactic irradiation. 771 40

MRI provides additional information about tumor location, extent, and margins. MRI was used in 158 patients with CNS tumors for treatment planning from 1985-89 and they were studied in a prospective manner. The most common site was cerebrum (73 pts), then extradural spinal axis (21 pts) posterior fossa (17 pts), brain stem (14 pts) and pituitary (13 pts), etc. The most common histological primary tumor was glioblastoma multiform (25 pts), then low grade astrocytoma (22 pts), anaplastic astrocytoma (14 pts), pituitary tumor (13 pts), medulloblastoma (9 pts), ependymoma (7 pts), and germ cell tumors (6 pts). Twenty-nine patients had metastasis to the brain. A majority of the patients with CNS tumors had the studies using Gadolinium-DTPA. Of the patients with CNS tumors, 120 (76%) had better information based on the MRI, which improved the treatment planning (using the three dimensional images) and field arrangement. In 89 patients (56%) the MRI was very decisive in the treatment volume and field arrangement. In 31 patients (20%) the MRI was beneficial and confirmed the treatment plan. MRI provides important additional information for radiation therapy planning.
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PMID:Use of magnetic resonance imaging in central nervous system tumors. 773 Jul 30

Between July 1989 and July 1992, 58 patients with newly diagnosed, histologically confirmed malignant gliomas (40 anaplastic astrocytomas, 18 glioblastoma multiforme) underwent implantation with low-activity iodine-125 sources. Patients were considered appropriate candidates for brachytherapy if their Karnofsky scores were > or = 70 and their contrast-enhancing tumors were < 6 cm in maximum diameter. Tumor volumes ranged from 0.1 to 90 ml. Ten patients had implants only. The other 48 patients received additional external beam radiation; 38 patients received radiation 1 to 2 weeks after the implant, and 10 patients received radiation preceding the implant. Median survival has not been reached but is currently greater than 31 months for patients with anaplastic astrocytoma and greater than 23 months for patients with glioblastoma. The rate of second operation for this group of patients was 45% (26 patients). Brain necrosis requiring resection occurred in 11 patients (19%). Although further follow-up is required, we conclude that low-activity permanent iodine-125 implants provide patients who have newly diagnosed malignant gliomas long-term survival with an acceptable risk of late complications.
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PMID:Permanent iodine-125 implants in the up-front treatment of malignant gliomas. 775 45

In the present study, an analysis was made of chromosomal aberrations in brain tumors using the fluorescence in situ hybridization (FISH) technique. At the same time DNA histograms were obtained by flow cytometry (FCM) to make a comparative study of histological malignancy and prognosis. The subjects included 30 gliomas (7 of astrocytoma grade II, 15 of anaplastic astrocytoma (grade III), 8 of glioblastoma (grade IV)) and 26 meningiomas. In the study of FISH, DNA probes for chromosomes No. 7, 9, 10, and 17, were used to cause a reaction with chromosome No. 22 added for meningiomas. In the study with FCM, DNA index from DNA histogram was calculated using lymphocytes as the internal standard. In gliomas as a whole, chromosomes No. 7 and 17 showed high values, whereas, chromosomes No. 9 and 10 low values. Analysis by the grades of glioma showed that compared with gliomas of other grades, grade IV gliomas were higher for chromosome No. 17 and lower for chromosome No. 10. In meningiomas, while many cases showed a low value for chromosome No. 22, most cases of recurrent and atypical meningiomas showed a high value for chromosome No. 17. In gliomas, DNA index showed a correlation with the grade, and a positive correlation particularly with chromosome No. 17 in FISH. Recurrent and atypical meningiomas had a high DNA index.
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PMID:Cytogenical analysis of brain tumors by FISH (fluorescence in situ hybridization) and FCM (flow cytometry). 779 34


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