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)

Chordoid gliomas are rare, slow-growing neoplasms of the anterior third ventricle. We reported a case of chordoid glioma in a 41-year-old man with obstructive hydrocephalus. Histologically, the tumor consisted of polygonal epithelioid cells admixed with elongated cells in a myxoid stroma. A prominent lymphoplasmacytic infiltrate was present. The tumor cells expressed glial fibrillary acidic protein (GFAP), epithelial membrane antigen (EMA), vimentin, CD31, CD34, epidermal growth factor receptor (EGFR) and S100 but were negative for pankeratin and E-cadherin. The percentage of Ki67 positive cells was approximately 3%. Weak p53 immunoreactivity was seen in less than 10% of the cells. Array comparative genomic hybridization performed on this case, as well as on four other archived cases, showed losses at several loci. Fluorescence in situ hybridization (FISH) confirmed consistent genetic alterations at 9p21 and 11q13. These are the fifth through ninth reported cases of chordoid gliomas with molecular characterization suggesting a distinct genetic origin from other gliomas.
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PMID:Chordoid glioma: a case report and molecular characterization of five cases. 1865 91

Pleomorphic xanthoastrocytoma (PXA) is a rare superficial glioma that predominates in the young and has good prognosis. A long history of repeated seizures is commonly associated with PXA, which is frequently observed in neuroimaging scans as a solid-cystic, contrast-enhancing lesion. We report a case in which PXA diagnosis was favored by its histological features, such as pleomorphic multinucleated giant cells, with disproportionately few mitoses and necrotic areas. An eye-catching feature was widespread, pale-staining, circumscribed deposits in the cytoplasm of tumor cells, which turned out to be glycogen upon histochemical and electron-microscopical examination. The stored material was strongly PAS-positive and digested by diastase, and had a finely granular ultrastructural appearance. No evidence of lipid droplets was found on oil-red-O staining. The tumor was immunoreactive for glial fibrillary acidic protein and vimentin. Many cells were positive for CD34 on the external membrane, a feature which has been described in chronic CNS lesions associated with epilepsy. Intracytoplasmic immunostaining for EGFR was observed in most tumor cells, which might have favored neoplastic proliferation. Nuclear immunolabeling for p53 protein was rare and does not support a major role for p53 mutation in PXA tumorigenesis. Intracellular accumulation of glycogen in glial tumors is uncommon and may originate from abnormalities in carbohydrate metabolic pathways.
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PMID:Temporal pleomorphic xanthoastrocytoma with glycogen accumulation--case report. 1866 39

We evaluate the effects of adjuvant treatment with the angiogenesis inhibitor Avastin (bevacizumab) on pathological tissue specimens of high-grade glioma. Tissue from five patients before and after treatment with Avastin was subjected to histological evaluation and compared to four control cases of glioma before and after similar treatment protocols not including bevacizumab. Clinical and radiographic data were reviewed. Histological analysis focused on microvessel density and vascular morphology, and expression patterns of vascular endothelial growth factor-A (VEGF-A) and the hematopoietic stem cell, mesenchymal, and cell motility markers CD34, smooth muscle actin, D2-40, and fascin. All patients with a decrease in microvessel density had a radiographic response, whereas no response was seen in the patients with increased microvessel density. Vascular morphology showed apparent "normalization" after Avastin treatment in two cases, with thin-walled and evenly distributed vessels. VEGF-A expression in tumor cells was increased in two cases and decreased in three and did not correlate with treatment response. There was a trend toward a relative increase of CD34, smooth muscle actin, D2-40, and fascin immunostaining following treatment with Avastin. Specimens from four patients with recurrent malignant gliomas before and after adjuvant treatment (not including bevacizumab) had features dissimilar from our study cases. We conclude that a change in vascular morphology can be observed following antiangiogenic treatment. There seems to be no correlation between VEGF-A expression and clinical parameters. While the phenomena we describe may not be specific to Avastin, they demonstrate the potential of tissue-based analysis for the discovery of clinically relevant treatment response biomarkers.
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PMID:High-grade glioma before and after treatment with radiation and Avastin: initial observations. 1877 28

Endothelial progenitor cells (EPCs) are important initiators of vasculogenesis in the process of tumor neovascularization. However, it is unclear how circulating EPCs contribute to the formation of tumor microvessels. In this study, we isolated CD34(+)/CD133(+) cells from human umbilical cord blood (HUCB) and obtained EPCs with the capacities of forming colonies, uptaking acetylated low-density lipoprotein (ac-LDL), binding lectins and expressing vascular endothelial growth factor (VEGF) receptor 2 (VEGFR-2, KDR), CD31 and von Willebrand factor (vWF). These EPCs were actively proliferative and migratory, and could formed capillary-like tubules in response to VEGF. When injected into mice bearing subcutaneously implanted human malignant glioma, EPCs specifically accumulated at the sites of tumors and differentiated into mature endothelial cells (ECs), which accounted for 18% ECs of the tumor microvessels. The incorporation of circulating EPCs into tumor vessel walls significantly affected the morphology and structure of the vasculature. Our results suggest that circulating EPCs constitute important components of tumor microvessel network and contribute to tumor microvascular architecture phenotype heterogeneity.
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PMID:Incorporation of endothelial progenitor cells into the neovasculature of malignant glioma xenograft. 1905 96

Malignant astrocytomas are highly vascular neoplasms with potent angiogenic activity. The present study aimed to investigate peripheral and local expression of interleukin (IL)-8 in astrocytomas with possible associations to IL-6, cyclooxygenase-2 (COX-2), vascular endothelial growth factor (VEGF) expression, and microvessel morphometry. IL-6- and IL-8-secreting peripheral blood monocytes (PBMCs) were evaluated in 17 glioblastoma (WHO grade IV), 5 anaplastic astrocytoma (WHO grade III), and 6 diffuse astrocytoma patients (WHO grade II), in parallel with 23 healthy controls using enzyme-linked immunosorbent spot (ELISPOT) assay. The IL-8 expression was assessed immunohistochemically in patients' tumor tissue sections and correlated with the expression of COX-2, VEGF, IL-6, and microvessel morphometry (assessed using CD34 antibody). Eighteen cases were also stained for CD31 and used as an additional vessel marker to validate our results regarding microvessel morphometry. IL-6 and IL-8 were highly secreted in the PBMCs of glioma patients compared with controls (p = 0.0001, p < 0.0001, respectively), with a positive correlation between IL-8 expression and secretion levels (p = 0.001). IL-8 immunoreactivity was detected in malignant cells or macrophages in perivascular areas and in pseudopalisading cells around necrosis and was positively correlated with histological grade (p = 0.0175) and tumor necrosis (p = 0.0793). IL-6 and IL-8 expression levels were positively correlated (p = 0.0036) and associated with COX-2 and VEGF expression (IL-6: p = 0.0133, p = 0.065; IL-8: p = 0.0139, p = 0.0101), but not with microvessel morphometry, by either CD31 or CD34. The coordinate expression and topographical relationship of IL-6, IL-8, COX-2, and VEGF in the same tumor areas (e.g., perinecrotic areas) attest to their intimate liaison in terms of cancer-induced angiogenesis, which is probably secondary to the induction of multiple interdependent molecular pathways. Moreover, our study seems to be the first attempt to link IL-8 expression by tumor cells with histological grade, implicating its potent role in gliomagenesis.
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PMID:Analysis of interleukin (IL)-8 expression in human astrocytomas: associations with IL-6, cyclooxygenase-2, vascular endothelial growth factor, and microvessel morphometry. 1933 96

L-type amino acid transporter 1 (LAT1) is a neutral amino acid transport system and is a major route for the transport of large neutral amino acids, including methionine, through the plasma membrane. LAT1 requires the heavy chain of 4F2 cell surface antigen (4F2hc) for its functional expression. Positron emission tomography (PET) with L-[methyl-(11)C] methionine (MET) provides information about amino acid metabolism in brain tumors. We conducted a clinicopathologic study to elucidate the correlation of LAT1 and 4F2hc expression with MET uptake in patients with newly diagnosed human gliomas. Thirty-three newly diagnosed glioma patients were enrolled in this study. Uptake of MET in the tumor was evaluated with the maximum standardized uptake value (SUVmax). Expression of the LAT1, 4F2hc, and CD34, and Ki-67 labeling index of the tumor were analyzed by immunohistochemical staining, and the correlation with the SUVmax in the tumors was examined. Expression of LAT1 and 4F2hc was higher in high-grade gliomas than in low-grade gliomas. The grade of LAT1 immunostaining increased with glioma grade. LAT1 was mainly expressed in the tumor cytoplasm and vascular endothelium and 4F2hc was mainly expressed in the tumor cytoplasm and plasma membrane. Expression of LAT1 but not 4F2hc was significantly correlated with MET SUVmax. Expression of LAT1 in the tumor vascular endothelium is significantly correlated with CD34 positive microvessel density. In conclusion, MET SUVmax correlates with LAT1 expression in the tumor in newly diagnosed gliomas. MET transport may be increased by an increased number of microvessels combined with a higher density or activity of LAT1 in the tumor endothelial cells in high-grade gliomas. Use of MET-PET as a molecular target combined with anti-angiogenesis in glioma therapy should be addressed in future studies.
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PMID:Correlation of L-methyl-11C-methionine (MET) uptake with L-type amino acid transporter 1 in human gliomas. 2009 33

The transdifferentiation of normal stem cells in many kinds of tissues or organs has been studied. However, whether glioma stem cells can transdifferentiate is seldom reported. Meanwhile, the mechanism of angiogenesis in tumors is in disputations, and it is still unknown that whether glioma stem/progenitor cells (GSPCs) participate into angiogenesis in glioma. In this study, we cultivated GSPCs in endothelial differentiation medium for 10 days and found they present to be the typical "flagstone" appearance of vascular endothelial cell (VEC); when cultured on Matrigel, GSPCs gradually formed tubular-like structures in vitro, and cells, which formed the tubular-like structures, showed similar ultrastructural characteristics of VEC under a transmission electron microscope. Furthermore, when cultured in hypoxia or oxygen-glucose deprivation for 4h, GSPCs transcribed and expressed molecular markers of VEC, including CD31, CD34 and vWF. These results indicated that GSPCs could participate into angiogenesis of glioma by transdifferentiating into VEC-like cells.
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PMID:Endothelial cell transdifferentiation of human glioma stem progenitor cells in vitro. 2059 93

This study tried to use CD133 positive U251 glioblastoma stem cells to establish nude mice model of transplanted tumor. CD133 positive U251 stem cells were isolated and identified. Twenty-five male nude mice were divided into three groups: U251 cell group, U251 stem cell group and normal control group. U251 cells and stem cells were respectively inoculated into mouse brain to establish model of transplanted tumor. Mice growing condition and behavior were observed. Magnetic resonance imaging (MRI) was performed to detect tumor growth in brain. HE staining assay, immunohistochemical assay and CD34 marked microvascular density (MVD) test were performed. As a result, the successful rates of both model groups were 100%. Growing condition and behavior in U251 stem cell group was more significantly exaggerated and tumor growth and image in magnetic resonance in U251 stem cell group was more significantly malignant than that in U251 cell group. It could be found that models in U251 stem cell group showed stronger pathogolical malignance features than that in U251 cell group. Glial fibrillary acidic protein (GFAP) expression in U251 cell and stem cell group showed the transplanted tumor originated from astrocytes. CD34 in U251 stem cell group was highest and significantly higher than that in the other two groups. In conclusion, use of U251 stem cells to establish transplanted tumor model in nude mice is an excellent method and the model is more likely and malignant than the one established by cancer cells, which showed a new animal model to research glioma.
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PMID:Using CD133 positive U251 glioblastoma stem cells to establish nude mice model of transplanted tumor. 2097 Oct 95

We report a rare case of epileptogenic glioma composed of glial progenitor cells that differentiated into an astrocytic and oligodendrocytic tumor. This 4-year-old girl presented with a 1-year history of complex partial seizure. MR scan showed a mass in the left temporal lobe with a cyst and a contrast-enhanced component. Subtotal resection of the tumor was achieved. Histological examination revealed that the tumor exhibited low cellularity composed of astrocytic and oligodendrocytic components, as well as low mitotic activity (MIB-1 = 1%). Immunohistochemical examination revealed GFAP positivity within the astrocytic cells, olig2 positivity within the oligodendrocytic cells, and S100 positivity in both cell types. MAP2 and CD34 were negative, and neurofilament was only positive in preexisting neurons. The pathological diagnosis was epileptogenic glioma (grade I) composed of glial progenitor cells. The postoperative course has been uneventful with good seizure control for 3 years.
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PMID:Epileptogenic glioma in a 4-year-old child: a case report. 2104 16

FAK (focal adhesion kinase), which plays a pivotal role in mediating cell proliferation, survival and migration, is frequently overexpressed in human malignant glioma. The expression of FAK increases with the advance of tumour grade and stage. Based on these observations, we hypothesized that attenuation of FAK expression may have inhibitory effects on the growth of malignant glioma. In the present study, human glioma cell line U251 was transfected with plasmids containing U6 promoter-driven shRNAs (small-hairpin RNAs) against human FAK using cationic liposome. The effects of FAK knockdown in U251 cells in vitro were analysed by using flow cytometry and PI (propidium iodide)-staining assays. Based on the encouraging in vitro results with FAK silencing, plasmids encoding FAK-targeted shRNA were encapsulated by DOTAP (dioleoyltrimethylammonium propane):Chol (cholesterol) cationic liposome and injected via tail vein to evaluate its therapeutic efficiency on suppressing tumour growth in a human glioma xenograft model. PCNA (proliferating-cell nuclear antigen), CD34 immunostaining and TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling) assay were used to assess the changes in tumour angiogenesis, apoptosis and proliferation respectively. The results indicated that DOTAP:Chol cationic liposome could deliver therapeutic plasmids systemically to tumour xenografts, resulting in suppression of tumour growth. Treatment with plasmid encoding FAK-targeted shRNA reduced mean tumour volume by approx. 70% compared with control groups (P<0.05), accompanied with angiogenesis inhibition (P<0.05), tumour cell proliferation suppression (P<0.05) and apoptosis induction (P<0.05). Taken together, our results demonstrated that shRNA-mediated silencing of FAK might be a potential therapeutic approach against human malignant glioma.
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PMID:RNA interference-mediated silencing of focal adhesion kinase inhibits growth of human malignant glioma xenograft in nude mice. 2124 11


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