Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 68-year-old male presented with an anaplastic astrocytoma deep in the sensorimotor cortex manifesting as acute pure motor hemiparesis suggestive of a vascular mechanism rather than tumor mass effect. Perfusion-weighted magnetic resonance (MR) imaging showed a significant decrease of blood flow in the sensorimotor area, where fluid-attenuated inversion recovery imaging demonstrated a prominently edematous area. Angiography also suggested ischemia with poor visualization of the precentral and central arteries. Diffusion-weighted MR imaging failed to identify the edema as cytotoxic or vasogenic due to technical problems. Brain tumors may manifest through impairment of peritumoral blood supply, which can be clarified by recent MR methods.
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PMID:Supratentorial glioma manifesting as acute onset of pure motor hemiparesis--case report. 918 43

CD95 (Fas/APO-1) and its ligand (CD95L) belong to a growing cytokine and cytokine receptor family that includes nerve growth factor (NGF) and tumor necrosis factor (TNF) and their corresponding receptors. CD95 expression increases during malignant progression from low-grade to anaplastic astrocytoma and is most prominent in perinecrotic areas of glioblastoma. There is, however, no evidence that CD95 expression in malignant gliomas is triggered by hypoxia or ischemia. Agonistic antibodies to CD95, or the natural ligand, CD95L, induce apoptosis in human malignant glioma cells in vitro. Glioma cell sensitivity to CD95-mediated apoptosis is regulated by CD95 expression at the cell surface and by the levels of intracellular apoptosis-regulatory proteins, including bcl-2 family members. Several cytotoxic drugs synergize with CD95L to kill glioma cells. For as yet unknown reasons, glioma cells may co-express CD95 and CD95L in vitro without undergoing suicide or fratricide. Yet, they kill T cells via CD95/CD95L interactions and are sensitive to exogenously added CD95L. Since CD95L is expressed in gliomas in vivo, too, forced induction of CD95 expression might promote therapeutic apoptosis in these tumors. That glioma cells differ from nontransformed T cells in their sensitivity to CD95 antibodies or recombinant ligand, may allow the development of selective CD95 agonists with high antitumor activity that spare normal brain tissue. A family of death ligand/receptor pairs related to CD95L/CD95, including APO2L (TRAIL) and its multiple receptors is beginning to emerge. Although several issues regarding glioma cell sensitivity to CD95L/CD95-mediated apoptosis await elucidation, CD95 is a promising target for the treatment of malignant glioma.
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PMID:CD95 ligand: lethal weapon against malignant glioma? 954 87

Glioblastomas may develop rapidly without clinical and histopathological evidence of a less malignant precursor lesion (de novo or primary glioblastoma) or through progression from low-grade or anaplastic astrocytoma (secondary glioblastoma). Primary glioblastomas typically show overexpression of EGFR, but rarely p53 mutations, while secondary glioblastomas frequently carry a p53 mutation, but usually lack overexpression of EGFR, suggesting that these glioblastoma subtypes develop through distinct genetic pathways. In the present study, we assessed the expression of Fas/APO-1 (CD95), an apoptosis-mediating cell membrane protein, and its relation to necrosis phenotype in primary and secondary glioblastomas. Large areas of ischemic necroses were observed in all 18 primary glioblastomas, but were significantly less frequent in secondary glioblastomas (10 of 19, 53%; p = 0.0004). Fas expression was predominantly observed in glioma cells surrounding large areas of necrosis and was thus significantly more frequent in primary glioblastomas (18 of 18, 100%) than in secondary glioblastomas (4 of 19, 21%; p < 0.0001), suggesting that these clinically and genetically defined subtypes of glioblastoma differ in the extent and mechanism of necrogenesis. Necrosis and microvascular proliferation are histologic hallmarks of the glioblastoma. Following incubation of glioblastoma cell lines under hypoxic/anoxic conditions for 24-48 hours, Fas mRNA levels remained unchanged, whereas VEGF expression was markedly upregulated. This suggests that in contrast to VEGF Fas expression is not induced by ischemia/hypoxia. Analysis of Fas mRNA levels in a glioblastoma cell line containing a p53 mutation and an inducible wild-type p53 gene showed little difference under induced and noninduced conditions, suggesting that in glioblastomas, Fas expression is not directly linked to the p53 status.
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PMID:Necrogenesis and Fas/APO-1 (CD95) expression in primary (de novo) and secondary glioblastomas. 960 Feb 16

In the last 11 years we operated on 20 patients (1.03% of all operated brain tumors) with lateral ventricular masses. Anamnesis lasted from 6 months in the case of epileptic seizures to 6 years when headache was the main symptom of disease only. Tumor was located in the anterior cornu and pars centralis in 15, in the trigonum of lateral ventricle in 2, and in the posterior cornu of the lateral ventricle in 3 cases. 13 tumors were large and in MRI the largest diameter was above 5 cm. Tumors located in the anterior cornu and pars centralis were removed using transcortical (10 cases) or transcallosal approaches (5 times). The tumor of the trigonum of ventricle was removed twice through superior parietal lobulus. Tumors of the posterior cornu were operated on via precuneus in order to save visual fields or through the occipital cortex. In 4 cases after removal of tumor the orifice in the frontal lobe was closed with fibrine glue. We totally removed tumors from lateral ventricles in 85% and subtotally in 15% of all cases. Histopathological examination revealed: astrocytoma anaplasticum in 5 cases, astrocytoma pilocyticum 4, oligodendroglioma 2, oligodendroglioma mixtum 1, papilloma plexus chorioidei 2, cystis epidermalis 2, subependymoma 1, ependymoma 1, pineocytoma 1 and haemangiona arterio-venosum 1. Two patients (10%) with diagnosis of anaplastic astrocytoma died after the operation as a result of ischemia and edema cerebri. During the follow-up examination, where the average time of observation was 3.7 years, 15 patients were found to be in a good condition (GR+MD), 1 patient was severely disabled (SD), 2 patients with anaplastic astrocytoma and pineocytoma died because of enlargement of the remnants of tumors left at first operation in spite of reoperation. Tumors of the lateral ventricle grow slowly and often achieve a large size before their clinical appearance. Most of tumors are accessible for a total or subtotal removal with acceptable morbidity and mortality rate after the operation. Long-term results depend on the size of resection and histopathological investigation.
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PMID:[Surgical treatment of intraventricular tumors]. 1535 29

Peritumoral regional cortical blood flow (rCoBF) was studied intraoperatively using thermal diffusion flowmetry. Histology included glioblastomas (n=5), anaplastic astrocytoma (n=1), pilocytic astrocytomas (n=2), metastatic melanoma (n=1), and trigeminal schwannoma (n=1). Pre-resection rCoBF values were low in all but two tumors where perfusion was in the low normal range. Post-resection rCoBF values were either low or normalized. Seizure activity was documented in a pilocytic astrocytoma with a significant rCoBF increase during resection. Our findings indicate that hypoperfusion in the cortex adjacent to malignant brain tumors is the result of primary metabolic failure and tumor pressure ischemia.
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PMID:Intraoperative measurement of peritumoral regional cortical cerebral blood flow. 2159 20