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)

Although scientific advances have recognised the prognostic power of telomerase activity in different cancers, as yet there has been no investigation regarding the expression variation of telomerase subunits in glioma tissues and cell lines. In this study, a recurrent anaplastic ependymoma and seven glioblastoma biopsy samples, four cell lines and four controls including two normal brain tissues were analysed for telomerase subunit expression profiles together with telomerase activity. Since telomerase activity is linked to tumourgenesis, the genes were analysed with respect to their expression variation. TEP1 was expressed in all glioma cell lines and 70% of glioblastoma tissues, in addition to the control brain tissues. Tankyrase was expressed in 85% of the glioblastoma tissues and was down-regulated in the recurrent anaplastic ependymoma tissue control cell lines. However, it was expressed in the control tissues. Dyskerin was expressed in all cell lines and tissues apart from U87-MG and NHA cells and the recurrent anaplastic ependymoma tissue. As expected, PARP1 and GAPDH showed constitutive expression throughout all cell lines and tissues since both are known to be housekeeping genes. hTERT was expressed in all glioma cell lines and tissues but was absent in the control cells and tissues. Telomerase activity was absent in IPDDC-A2 cells and 57% of the glioblastoma tissues. These results suggest that hTERT expression and not telomerase activity possibly represents a simple and reliable biological diagnostic tool.
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PMID:Telomerase subunits expression variation between biopsy samples and cell lines derived from malignant glioma. 1719 47

Enzyme activity changes in reagent and neoplastic glia are examined. In the case of reagent glia, considerably increased ADPase, ATPase and AMPase values have been observed in experimental elective parenchymal necrosis in the rat, in hypertrophic astrocytes from recent plaques in multiple necrosis, in demyelinisation associated with cyanide encephalopathy, and in reagent astrocytes surrounding tumours and arteriosclerosis sites. Depressed ATPase values have been observed in experimental oedema, as compared with increased TPPase in human oedema. BuChE and ChE activity disappears in both oligodendro- and astroglia near old cerebral infarct sites, whereas there is marked BuChE activity peripherally to multiple sclerosis plaques and in areas of phenylpyruvic oligophrenia demyelinisation. In neoplastic glia, ADPase is clearly evident in malignant gliomas, ATPase is related to the extent of the cell body, AMPase is positive in medulloblastoma cell cytoplasm and beta-glucuronidase increases in anaplasia. Above-normal ChE activity has been observed in astrocyte tumors, while BuChE is greater than that of AChE. Phosphorylase reaction is intense in astrocytoma and in glioblastoma giant cells. Phosphoglucomutase values are below-normal in tumours, except in the case of ependymoma, while both phosphohexoisomerase and hexokinase display increased activity in atypical forms.
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PMID:[Histochemical demonstration of glial enzyme activity. II. Reagent and neoplastic glia]. 1734 Aug 8

5-Aza-2'-deoxycytidine (5azadC) inhibits DNA methyltransferase and subsequently induces the expression of genes silenced by methylation. While treatment with 5azadC downregulated hTERT and upregulated MGMT expression in two glioma cell lines, there was no change in the expression of these two genes in the normal cell line. However, cell viability was reduced as a result of 5azadC treatment in all three cell lines. 5azadC treatment reduced telomerase expression and activity and subsequently enhanced chemosensitivity towards cisplatin, taxol and tamoxifen but not with the alkylating agents temozolomide (TMZ), carmustine and chlorambucil. To further evaluate the effect of these findings, the level of hTERT and MGMT expression was measured in a recurrent anaplastic ependymoma, seven glioblastoma and two normal brain tissues. While four of eight gliomas and one of the normal tissues expressed MGMT, hTERT was expressed in all gliomas but not in the normal brain tissue. Results of this study suggest that taxol together with 5azadC may be a good therapeutic combination for glioma. In addition, the work on cell lines can be repeated on tissues utilizing hTERT as the therapeutic target for demethylation using 5azadC in glioma.
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PMID:Epigenetic silencing of telomerase and a non-alkylating agent as a novel therapeutic approach for glioma. 1802 53

Pleomorphic xanthoastrocytoma (PXA) has been considered an astrocytic tumor with a relatively favorable prognosis. However, PXA cases having several recurrent patterns with poor prognosis have been reported in recent years, and a new concept of anaplastic PXA has been proposed. The present case was a 59-year-old woman who presented with tumor bleeding onset and cerebrospinal fluid dissemination. The patient had sudden-onset right hemiparesis, aphasia, and consciousness disturbance and was admitted to a local area hospital. After emergency surgery had removed the hematoma, postoperative contrast-enhanced CT scan revealed a left temporal tumor. A second surgery was therefore performed for initial tumor removal 2 months later. Histopathological findings showed that the tumor was typical PXA with strong pleomorphism and xanthomatous changes and contained an ependymoma-like component in the center area. However, endothelial proliferation and mitosis were more remarkable compared to ordinary PXA. The MIB-1 labeling index was 9.8% high. From these findings, the histopathological diagnosis was anaplastic PXA. The patient underwent surgery to remove recurrent tumors 5 and 16 months later. The patient died 36 months after the first onset, and CT revealed glioblastoma-like findings and cerebrospinal fluid dissemination. This case report is the first case in which PXA presented with tumor bleeding onset. Histopathological findings suggested anaplastic PXA from the first surgical specimens, and PXA recurred many times. We thus believe that the patient displayed primary anaplastic PXA rather than secondary anaplastic PXA that results in malignant transformation.
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PMID:A case of anaplastic pleomorphic xanthoastrocytoma presenting with tumor bleeding and cerebrospinal fluid dissemination. 1809 20

We report here a rare case of supratentorial ectopic cortical ependymoma. This tumor was localized in the left angular gyrus, occurred with intratumoral hemorrhage, was attached to the dura mater, exhibited no continuity with the ventricular system, showed distinctive pathological features (perivascular pseudo-rosette formations and firework-like giant rosette formations), and finally transformed to a glioblastoma-like high-grade lesion. A cortical ependymoma should be considered in the differential diagnosis of supratentorial cortical tumors with intraparenchymal hemorrhage and high vascularity, even if not in contact with the ventricular system. Although malignant transformation is unusual in cortical ependymoma, close observation and adjunctive radiotherapy are strongly recommended after the excision.
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PMID:Supratentorial ectopic cortical ependymoma occurring with intratumoral hemorrhage. 1809 43

Olig2, a member of the group of basic helix-loop-helix transcription factors, is innately expressed in oligodendrocytes. In the neoplastic condition, Olig2 is widely expressed in astrocytomas and oligodendrogliomas, but its expression in ependymomas remains poorly documented. A total of 59 brain tumors including 16 ependymomas, 32 astrocytomas, and 11 oligodendrogliomas were immunohistochemically studied for the expression of Olig2 as well as other markers including epithelial membrane antigen (EMA) and CD99. In general, the Olig2-positive nuclei were only sparsely distributed in ependymomas; in contrast, they were very numerous in astrocytomas and oligodendrogliomas. Particularly in cases of glioblastoma or pilocytic astrocytoma that histologically mimicked ependymoma, the Olig2-positive nuclei were numerous as in conventional astrocytomas, which helped to differentiate them from ependymomas. The EMA-positive structures were helpful for the diagnosis of ependymoma, however, they were occasionally very modest and sparse on immunostained sections. A quantitative study showed that the Olig2-positive nuclei were much fewer in ependymomas than in astrocytomas and oligodendrogliomas. These results indicate that the Olig2-immunohistochemistry is useful and potentially more reliable than the EMA-immunohistochemistry for the diagnosis ofependymoma. CD99 is a cell surface antigen expressed in some tumors, most notably in Ewing's sarcomas. In our preliminary experiment, we noted the absence of CD99-immunoreactivity in a fraction of brain tumors with clear cell morphology, including oligodendroglioma, clear cell ependymoma, and pilocytic astrocytoma (the oligodendroglioma-like component). Thus, we investigated the expression of CD99 in an additional series of brain tumors with clear cell morphology, including oligoastrocytoma (7 cases), central neurocytoma (6), and dysembryoplastic neuroepithelial tumor (9). We found that the absence of CD99-immunoreactivity was dependent on clear cell morphology rather than on tumor entities. The CD99-immunohistochemistry is unique in that it is helpful for the diagnosis of clear cell brain tumors through the visualization of CD99-negative clear cells.
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PMID:Olig2 and CD99 are useful negative markers for the diagnosis of brain tumors. 1855 83

One of the specific forms of progression of malignant tumors of the central nervous system is meningeal dissemination. Meningeal dissemination is a condition in which tumor cells migrate to the brain surface and sub arachnoid space via cerebrospinal fluid and then infiltrate there. This condition can arise from both primary and metastatic brain tumors, with reported incidences of 4.2% for primary tumors and 5.1% for metastatic tumors. Meningeal dissemination frequently arises from germinoma, medulloblastoma, ependymoma and glioblastoma in cases of primary brain tumors and frequently arises from breast cancer, lung cancer and gastric cancer in cases of metastatic brain tumors, known as meningeal carcinomatosis. The prognosis of meningeal dissemination is poor, and conventional treatments such as systemic chemotherapy and radiation therapy are ineffective. Intrathecal infusion of anti neoplastic agents is one of the options for treatment of meningeal dissemination. The advantage of intrathecal chemotherapy is that the anti neoplastic agent is rapidly diffused in the sub arachnoid space, and its duration of activity is long due to its slow clearance and metabolism. Routes of administration include infusion into the lateral ventricle by puncture of the Ommaya reservoir, infusion into the sub arachnoid space by lumbar puncture, or both of these procedures performed alternately or simultaneously, and methods of infusion include bolus injection and ventriculo lumbar perfusion. Commonly used drugs include methotrexate (MTX), cytarabine (Ara-C), and 3-[(4-amino-2-methyl-5-pyrimidinyl)methyl]-1-(2-chloroethyl)- 1-nitrosourea hydrochloride (ACNU), and some new drugs have also begun to be used clinically. Although there are differences depending on the histological type of the tumor, the anti neoplastic agent administered and the method of administration, the response rate is about 40-80% and mean survival time is about 4-25 months. Although side effects of the anti neoplastic agents are not as severe as with agents used for systemic chemotherapy, specific side effects include nonspecific drug-induced meningitis or ventriculitis, transient or permanent paralysis and leukoencephalopathy. These side effects can be alleviated by reducing the dose or discontinuing the anti neoplastic agents, and a small dose of an adrenocorticosteroid is sometimes administered simultaneously. Bacterial meningitis is another complication and requires discontinuation of anti neoplastic agents, removal of the Ommaya reservoir, or systemic or intrathecal administration of antibiotic agents. Although meningeal dissemination is a rare metastatic condition with a poor prognosis, there have been some reports of successful treatment using this method, which is expected to be widely used in the future.
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PMID:[Intrathecal infusion of the antineoplastic agents for meningeal dissemination]. 1863 17

Recurrence of clear cell ependymoma is not a rare condition, but malignant transformation of clear cell ependymoma has not yet been well presented. The authors report a 44-year-old man who presented with progressive right hemiparesis. A brain tumor in the left frontal premotor area was removed and an initial pathological diagnosis of oligodendroglioma was made. The tumor recurred 4 months later, and reoperation of the tumor and adjuvant local radiotherapy were performed. The patient subsequently underwent surgical removal of recurrent tumors on another four occasions (6 times in total) during a period of 11 years and finally died of the original disease. Histopathological studies of all surgical and autopsy specimens were carried out. The first and second surgical specimens did not contain any ependymal rosettes or pseudorosettes, and thus a diagnosis of oligodendroglioma was made. However, the third surgical specimen showed pseudorosettes. At this time, the tumor had an ultrastructural appearance compatible with ependymoma. Thereafter, the recurrent tumors showed anaplastic features such as nuclear pleomorphisms and necrosis with pseudopallisading. The autopsy specimens resembled a feature of glioblastoma but the tumor was sharply demarcated from the surrounding parenchyma.
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PMID:Malignant transformation of supratentorial clear cell ependymoma. 1864 67

The World Health Organization recently updated its classification of central nervous system tumors, adding 8 entities, as well as defining new variants and morphologic patterns of existing entities. Despite the continued refinement of brain tumor histologic classification and grading, there remain some diagnostic "gray zones" that challenge general surgical pathologists and neuropathologists alike. These include the presence of oligodendroglial features in (mixed) oligoastrocytomas and glioblastomas (GBMs), GBM variants (such as small cell GBM), meningioma classification and grading, medulloblastoma variants, ependymoma grading, the presence of "neuronal features" in otherwise morphologically classic gliomas, and low-grade gliomas with high Ki-67 labeling indices. In the current review, we discuss these issues and offer some practical guidelines for dealing with problematic cases.
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PMID:Gray zones in brain tumor classification: evolving concepts. 1872 2

Glioma includes astrocytoma, oligodendroglioma, ependymoma and glioblastoma. We previously reported the epigenetic silencing of paternally expressed gene 3 (PEG3) in glioma cell lines. In this study, we investigated methylation of an exonic CpG island in the promoter region and the expression of PEG3 gene in 20 glioma and 5 non-tumor tissue samples. We found wide variations in the methylation level. Hypomethylaiton and hypermethylation was found in 3 and 4 glioma tissue samples, respectively. Monoallelic expression, which is an evidence of an imprinted gene, was maintained in eight out of nine informative cases which have T/C polymorphisms in PEG3. The lower gene expression, which suggested epigenetic silencing of PEG3, was confirmed statistically in glioblastoma using quantitative reverse-transcription polymerase chain reaction. Interestingly, we found higher expression of PEG3 in two out of three oligodendrogliomas. A negative correlation between the methylation level and gene expression was shown by regression analysis. These results suggest that the abnormal regulation of PEG3 is associated with several glioma subtypes and that it plays an important role in tumorigenesis.
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PMID:Aberrant promoter methylation and expression of the imprinted PEG3 gene in glioma. 1936 87


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