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)

Cytoplasmic estrogen receptor (ER) and progesterone receptor (PR) proteins were measured by a dextran-coated charcoal absorption technique in 19 intracranial tumors (10 meningiomas, two acoustic neurinomas, two glioblastomas, one primary tumor of neuroectodermal origin, one hemangioblastoma, one metastasis of carcinoma, one chordoma, and one pituitary adenoma). Positive PR values (greater than or equal to 10 fmol/mg of protein) were found in nine meningiomas (90% of these tumors), in the chordoma, in one glioblastoma, and in the hemangioblastoma, whereas positive ER values were recorded only in the pituitary adenoma and in one glioblastoma. Evidence of PR in meningiomas might explain their predominance in women. A possible pharmacological therapy, based on these findings, is discussed.
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PMID:Estrogen and progesterone receptors in intracranial tumors. 650 43

A series of 16 cases of intracerebral hemorrhage associated with brain tumors are described. The literature is reviewed and the incidence of these cases is reported to be low, but we had clinically encountered these cases more commonly than reported, since CT was introduced to the neurosurgical field as a diagnostic aid. The presenting symptoms were those of spontaneous intracerebral hemorrhage or brain tumor. The intracerebral hemorrhage associated with brain tumor may mask the cause of bleeding and confuse the diagnosis. The majority of the tumor causing the intracerebral hemorrhage are highly malignant as glioblastoma or metastatic brain tumor, but there are some benign tumors such as pituitary adenoma, hemangioblastoma, benign astrocytoma and meningioma, which would have good survival rates if discovered early. The mechanisms of massive hemorrhage with brain tumor are not clear. From pathological findings of our cases and other reports, the mechanism seems to be due to the vascular endothelial proliferation with subsequent obliteration of the lung of the vessel. Thin walled, poorly formed vessels in tumor may also become distorted with growth of the tumor and these may easily rupture and bleed. Necrosis with subsequent loss of vessel support may be a factor in production of hemorrhage. Radiation therapy may be a predisposing factor. Children are rarely involved in these cases. The prognosis in the majority of cases would seen to be poor, since the majority of the tumor are highly malignant and most such patients are seen by the neurosurgeon some time after the hemorrhage has accomplished its fatal mischief.
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PMID:[Intracerebral hemorrhage in brain tumors (author's transl)]. 744 24

The distribution of type VII collagen was examined in the normal human nervous system, in brain tumour biopsies and in glioma cell lines by immunohistochemistry and western blotting. In normal tissue, positivity was observed beneath choroid plexus epithelial cells and around pineal gland and pituitary gland cell nests, while other brain regions and peripheral nerves were negative. Expression was preserved in most related tumours (choroid plexus papilloma, pineoblastoma, pituitary adenoma). Scattered abnormal vessels showed neo-expression of type VII collagen in about half of the astrocytic and ependymal tumours. Glioma cells in situ were consistently negative for type VII collagen, whereas the glioblastoma cell lines were positive. Our results suggest that anchoring fibrils or at least epitopes of their major structural component are present in normal and pathological cerebral structures, indicating a unique distribution of type VII collagen in the nervous system.
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PMID:Expression of type VII collagen, the major anchoring fibril component, in normal and neoplastic human nervous system. 775 91

Epidermal growth factor (EGF) and transforming growth factor alpha (TGF alpha) are potent mitogens for normal cells of ectodermal and mesodermal origin. Evidence is accumulating that suggests that EGF, TGF alpha and their common receptor (EGF/TGF alpha-R) influence development and functioning of tissues of the central nervous system (CNS). To further investigate the possible roles of EGF, TGF alpha and their receptor in autocrine/paracrine regulation of tumor growth in the CNS, a series of tumors of the CNS were analyzed for the presence of specific, high affinity EGF/TGF alpha receptors and for the presence of immunoreactive TGF alpha protein. Binding of 125I-EGF to crude membranes from a pool of meningiomas was competed for equally well by low concentrations of unlabeled EGF or TGF alpha, but not by high concentrations of other protein hormones, demonstrating the high degree of specificity of the EGF/TGF alpha receptor. Specific binding of 125I-EGF was dependent upon time and temperature, with maximum specific binding achieved after two hours at 22 degrees C. Scatchard analysis of six tumors of the CNS large enough to permit titration analysis generated linear plots with an average kilodalton of 1.1 +/- 0.1 nanometer (+/- standard error of the mean), suggesting the presence of a single class of EGF/TGF alpha-R with high affinity. EGF also stimulated phosphorylation of a 170 kilodalton protein in membrane fraction of a meningioma, demonstrating that the EGF/TGF alpha-R in this tumor retained EGF-stimulated kinase autophosphorylating activity. Membranes for 17 additional smaller tumors of the CNS were analyzed for specific binding of 125I-EGF by single, high concentration method, and all 17 tumors were found to contain specific binding of 125I-EGF. The average level of 125I-EGF for all 23 tumors of the CNS was 46 +/- 27 femtomoles per milligram protein with a range of 1 femtomoles per milligram for both a pituitary adenoma and meningioma to 638 femtomoles per milligram for a glioblastoma. A series of 13 tumors of the CNS were analyzed for EGF alpha with use of a specific radioimmunoassay. TGF alpha immunoreactive protein was detected in all four malignant tumors of the CNS assayed at an average level of 2.6 +/- 1.1 nanograms per milligram soluble protein, whereas TGF alpha immunoreactive protein was detected in only two of nine benign tumors of the CNS. These results add support to the hypothesis that TGF alpha and its receptor may act by autocrine/paracrine mechanisms to influence growth of tumors of the CNS in vivo.
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PMID:Detection of epidermal growth factor and transforming growth factor alpha protein in meningiomas and other tumors of the central nervous system in human beings. 821 1

We studied the immunohistochemical expression of integrin alpha and beta chains in the normal and neoplastic human brain. Normal astrocytes expressed alpha 2, alpha 3, alpha 6, beta 1, and beta 4 chains in some areas facing major interstitial tissues, but they were consistently negative for the other integrins examined (alpha 4, alpha 5, alpha V, alpha L, alpha M, alpha X, beta 2, beta 3). Neoplastic astrocytes in vivo and in vitro showed increased expression of alpha 3 and beta 1, and some also of alpha 5, alpha V, beta 3, and beta 4. Neoexpression of alpha 4 and reduced levels of beta 4 were detected in glioblastoma vascular proliferations compared with normal endothelial cells. Oligodendroglioma, ependymoma, choroid plexus papilloma, pituitary adenoma, and meningioma cells showed the same integrin pattern as their normal counterparts. Adhesion assays using the astrocytoma cell lines U-138 MG and U-373 MG revealed strong attachment to collagen types I to VI and undulin, which was inhibited by antibodies to beta 1, but not by those to alpha 2, alpha 3, alpha 6, and alpha V. We conclude that astrocytomas show increased levels or neoexpression of various integrins and strong attachment to various extracellular matrix components, which appears to be almost exclusively mediated by beta 1-integrins.
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PMID:Characterization of integrin receptors in normal and neoplastic human brain. 831 46

In our retrospective analysis of 305 patients with primary brain tumors, treated and followed at Rambam Medical Center between 1983-1990, 56% were males; mean age was 43; 47% were Ashkenazi Jews, 22% Sephardi Jews, 22% Arabs and 9% were Jews of unspecified origin. 3-year actuarial survival for all patients was 33.5%, Arabs 51%, Sephardi Jews 40%, Ashkenazi Jews 20%; for those younger than 20, it was 57%, and older than 20, 26%. Diagnoses were: astrocytoma grades I-II, 68%; astrocytoma grade III, 24%; glioblastoma multiforme, 5.5%; medulloblastoma 73%; ependymoma, 75%; oligodendroglioma, 85%; meningioma, 100%; pituitary adenoma, 100%. Survival probability of those with glioblastoma multiforme treated by combined surgery and radiotherapy was superior to that of those treated by surgery alone. In low-grade astrocytoma there was no difference in survival probability between those with combined therapy and those treated by surgery alone. Survival when the diagnosis was based on imaging studies alone without histological confirmation of malignancy, was similar to that of those with glioblastoma: only 3.0% at 3 years. Prognostic factors identified by univariate analysis were histology, age of patient and ethnic origin, and type of treatment.
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PMID:[Primary brain tumors]. 898 15

In the last decade, the prognosis of brain tumor patients has dramatically improved due to recent advances in microsurgical techniques and the development of functioning neuroimaging, computer-assisted neuronavigation, endoscopic surgery, intravascular surgery and radiosurgery. According to a report by the Committee of Brain Tumor Registry of Japan, the ten year survival rate of patients with benign brain tumors (meningioma, neurinoma and pituitary adenoma) is more than 95%. In contrast, patients with glioma (which constitute 33% of primary brain tumor cases) still have a poor prognosis, especially in the case of malignant (anaplastic astrocytoma and glioblastoma). This poor prognosis is related to the fact that malignant glioma cells aggressively infiltrate into normal brain tissues, making total removal of the tumor impossible. The median survival time of glioblastoma patients is less than 2 years, despite multimodality treatment with extensive surgical resection and adjuvant therapies using radiation and immunochemotherapy. In order to overcome this formidable neoplasm, the effectiveness of molecular neurosurgery using gene therapy has been investigated since 1992. In this paper, molecular genetic studies and the current state of gene therapy for malignant brain tumors are described, and the future direction of this fascinating approach is discussed.
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PMID:Molecular neurosurgery using gene therapy to treat malignant glioma. 921 35

Water-soluble metabolites extracted from 60 surgically excised samples of various brain tumors and four nontumorous lobectomized brains were measured quantitatively using in vitro high-resolution magnetic resonance spectroscopy. A detailed MR spectrum-histology correlation study in a glioblastoma was made, to reveal MR spectral changes in accordance with the density of glioma cells. Furthermore, three cases that had difficult preoperative diagnoses are discussed. MR spectra from gliomas exhibited characteristic patterns according to malignancy, presumably reflecting its metabolic effects. Concentrations of choline-containing compounds, inositol, alanine, glycine and phosphorylethanolamine (PEA) increased according to the degree of malignancy, but it was noteworthy that in glioblastoma the choline-containing compounds, inositol, alanine, glycine and phosphorylethanolamine increased according to the degree of malignancy. In particular, the glycine concentration was very high in glioblastoma. We also detected a large amount of taurine in medulloblastoma. Although the total creatine concentrations decreased according to the malignancy, the concentration of total creatine was relatively preserved in neuroectodermal tumors but was low in nonneuroectodermal tumors. N-acetyl-aspartate was unequivocally demonstrated in normal tissues, but could not be detected in nonneuroectodermal brain tumors such as metastatic brain tumor, meningioma, neurinoma and chordoma. In meningioma, although a high peak of choline-containing compounds has been reported uniquely by in vitro and in vivo 1H-MRS, we demonstrated that its concentration was not increased in meningioma; instead, there was an increased alanine content. 1H-MRS of neurinoma demonstrated high inositol peaks, and a large amount of inositol. The reason for the high inositol content in neurinoma is unknown, but the prominent peak of inositol on MR spectra should be useful for the differential diagnosis of neurinoma from meningioma. PEA concentration was increased four to five times in pituitary adenoma, malignant lymphoma, and medulloblastoma as compared with normal brain. Thus 1H-MRS might provide clinically useful information on tumor malignancy and characteristic tumor metabolism. Although excellent anatomical information of tumors can be readily obtained by magnetic resonance imaging. MRS provides metabolic information. MRS may provide additional information in cases in which the differential diagnosis of tumors by neuroimaging is difficult.
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PMID:Absolute concentrations of metabolites in human brain tumors using in vitro proton magnetic resonance spectroscopy. 925 Nov 9

Cadherins are a family of glycoproteins that are associated with cell adhesion mechanisms. They are divided into subclasses. The E- and P-cadherins are regarded as the epithelial subtype. Their expression has been demonstrated in many different carcinoma types. Using immunomorphological techniques, we studied the expression of E-cadherin in a series of 145 human brain tumours with the monoclonal antibody 5H9. Western blot analysis was used to confirm the immunohistochemical data. The tumour types represented were astrocytoma WHO I (n = 7), astrocytoma WHO II (n = 6), astrocytoma WHO III (n = 14), glioblastoma WHO IV (n = 8), oligodendroglioma WHO II (n = 5), ependymoma WHO II (n = 5), choroid plexus papilloma WHO I (n = 5), pineoblastoma WHO IV (n = 5), medulloblastoma WHO IV (n = 5), neurinoma WHO I (n = 5), meningioma WHO I and WHO III (n = 75) and pituitary adenoma WHO I (n = 5). Only choroid plexus papillomas (5/5) and meningiomas showed E-cadherin expression. In benign meningiomas (n = 45; 100%), positive E-cadherin immunoreactivity was found regardless of the histomorphological subtype. E-Cadherin was also expressed in 21 WHO I meningiomas (100%) invading dura, bone, brain, and muscle. In contrast, E-cadherin was absent from the majority of morphologically malignant meningiomas (6/9, 66.6%). In addition, in recurrent meningiomas (n = 9), E-cadherin expression in the recurrent tumours was identical to that in the primary neoplasm except in cases with malignant progression, where the malignant recurrent tumour was E-cadherin negative. In 2 cases of metastasizing meningiomas, no E-cadherin immunoreactivity was found in the primary tumours or their metastases.
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PMID:E-Cadherin in human brain tumours: loss of immunoreactivity in malignant meningiomas. 950 62

We discussed usefulness of cytology for rapid intraoperative diagnosis of intracranial tumors using frozen section. Twenty five cases of intracranial tumors (6 cases of astrocytoma, 6 cases of glioblastoma multiforme, 4 cases of meningioma, 2 cases of pituitary adenoma, 1 case of ependymoma and 6 cases of metastatic carcinoma) were observed by cytological specimen, frozen section and formalin fixed-paraffin embedded section. When only frozen section were used for histopathological diagnosis, it was difficult to diagnose in a few case of astrocytic tumors by artifact in freezing process. When only cytological specimen were used for diagnosis, histological findings, for example pseudopalisading around necrosis in glioblastoma or rosette formation in ependymoma, were not identified. However, diagnostic accuracy were improved when both cytological and frozen specimen were used if adequate material were obtained for diagnosis. In conclusion, cytological approach used in addition to frozen section was useful for rapid intraoperative diagnosis.
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PMID:[Usefulness of cytology applied simultaneously to frozen section at rapid intraoperative diagnosis of intracranial tumors]. 980 Apr 83


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