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oligodendroglioma/hypoxia

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Page 1 from 27 results

Expression of hypoxia-inducible factor-1 alpha in oligodendrogliomas: its impact on prognosis and on neoangiogenesis.

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BACKGROUND Hypoxia-inducible factor (HIF)1 alpha is considered to play a key role in the adaptation of cells to hypoxia by stimulating angiogenesis via regulation of vascular endothelial growth factor and by metabolic adaptation to O(2) deprivation. METHODS Expression of HIF-1 alpha protein and p53

Hypoxia specifically and reversibly induces the synthesis of ferritin in oligodendrocytes and human oligodendrogliomas.

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Neonatal (3 day old) rat oligodendrocytes grown in monolayer culture and exposed to increasingly hypoxic culture conditions showed increased Tran35S-label incorporation into a 22-kDa protein. Reoxygenation of cultures reversed the synthesis of the protein. Amino acid sequencing of a peptide derived

Expression of hypoxia-related tissue factors correlates with diminished survival of adjuvantly treated patients with chromosome 1p aberrant oligodendroglial neoplasms and therapeutic implications.

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OBJECTIVE Oligodendroglial neoplasms with chromosome 1p deletion are chemosensitive, and stratified adjuvant therapies have been proposed on the basis of 1p status. In this study, we evaluated expression of hypoxia-related factors and its influence on survival in oligodendroglial brain tumors with

Hypoxia-inducible factor-1-regulated protein expression and oligodendroglioma patient outcome: comparison with established biomarkers and preoperative UCSF low-grade scoring system.

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Methods for predicting outcome for patients with oligodendrogliomas and anaplastic oligodendrogliomas (AOs) are limited. Hypoxia-inducible factor-1α (HIF-1α) controls many proteins involved in glycolysis and angiogenesis including VEGF, Glut-1, and CA-IX. We examined whether expression of HIF-1α and

Expression of hypoxia-inducible factor-1alpha in oligodendrogliomas: its impact on prognosis and on neoangiogenesis.

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Toward improved grading of malignancy in oligodendrogliomas using metabolomics.

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In spite of having been the object of considerable attention, the histopathological grading of oligodendrogliomas is still controversial. The determination of reliable biomarkers capable of improving the malignancy grading remains an essential step in working toward better therapeutic management of

Heme oxygenase (HO)-1 expressing macrophages/microglial cells accumulate during oligodendroglioma progression.

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Heme oxygenase (HO-1, HSP32) catalyzes the oxidation of heme to biliverdin and carbon monoxide, a putative neurotransmitter. In the brain, HO-1 expression has been associated with neuroprotection during oxidative stress and hypoxia. However, consecutive downstream mediation is involved in

Vascular endothelial growth factor expression in oligodendrogliomas: a correlative study with Sainte-Anne malignancy grade, growth fraction and patient survival.

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Microangiogenesis is a delayed but crucial event in the malignant progression of oligodendrogliomas. Accord-ingly, in the new Sainte-Anne grading system of oligodendrogliomas, endothelial hyperplasia and contrast enhancement, both being indicators of microangiogenesis, are key criteria for the

Expression of vascular endothelial growth factor and its receptors in the anaplastic progression of astrocytoma, oligodendroglioma, and ependymoma.

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Vascular endothelial growth factor (VEGF) is a hypoxia-inducible angiogenic factor, which is known to be upregulated in most cases of glioblastoma multiforme (GBM). The expression of VEGF and its receptors in ependymomas, oligodendrogliomas, and particularly the expression during anaplastic

DEC1 expression in 1p-aberrant oligodendroglial neoplasms.

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Expression of hypoxia-related tissue factors in 1p-aberrant oligodendroglial neoplasms diminishes patient outcome. Differentiated embryo-chondrocyte expressed gene 1 (DEC1) has been described as novel hypoxia-related tissue factor. In our study, we assessed the expression of DEC1 in 1p aberrant

High Carbonic Anhydrase-9 Expression Identifies a Subset of 1p/19q Co-Deletion and Favorable Prognosis in Oligodendroglioma.

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OBJECTIVE To investigate the relationship between 3 hypoxic markers, carbonic anhydrase-9 (CA-9), hypoxia-inducible factor (HIF)-1α, and HIF-2α and the traditional genetic markers, deletions of chromosomes 1p and 19q and Isocitrate dehydrogenase 1 (IDH1) R132H mutation in

The Dilemma of Cure and Damage in Oligodendroglioma: Ways to Tip the Balance Away from the Damage.

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Current treatments for oligodendrogliomas are powerful but have a negative impact on the rest of the body. The bone marrow is damaged by the chemotherapeutics, but other parts of the body are also affected. In this paper, the current treatment method and its collateral damage is described.

Hypoxia alters iron homeostasis and induces ferritin synthesis in oligodendrocytes.

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Both iron and the major iron-binding protein ferritin are enriched in oligodendrocytes compared with astrocytes and neurons, but their functional role remains to be determined. Progressive hypoxia dramatically induces the synthesis of ferritin in both neonatal rat oligodendrocytes and a human

ISL2 modulates angiogenesis through transcriptional regulation of ANGPT2 to promote cell proliferation and malignant transformation in oligodendroglioma

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Oligodendroglioma is an important type of lower-grade glioma (LGG), which is a slowly progressing brain tumor. Many LGGs eventually transform into a more aggressive or malignant type. Enhanced angiogenesis is a characteristic of malignantly transformed oligodendroglioma (m-oligodendroglioma).

Mechanisms of action of rapamycin in gliomas.

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Rapamycin has previously been shown to be efficacious against intracerebral glioma xenografts and to act in a cytostatic manner against gliomas. However, very little is known about the mechanism of action of rapamycin. The purpose of our study was to further investigate the in vitro and in vivo
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