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Query: UMLS:C0017638 (glioma)
30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The harmonious development of the central nervous system depends on the interactions of the neuronal and glial cells. Extracellular matrix elements play important roles in these interactions, especially laminin produced by astrocytes, which has been shown to be a good substrate for neuron growth and axonal guidance. Glioblastomas are the most common subtypes of primary brain tumors and may be astrocytes in origin. As normal laminin-producing glial cells are the preferential substrate for neurons, and glial tumors have been shown to produce laminin, we questioned whether glioblastoma retained the same normal glial-neuron interactive properties with respect to neuronal growth and differentiation. Then, rat neurons were co-cultured onto rat normal astrocytes or onto three human glioblastoma cell lines obtained from neurosurgery. The co-culture confirmed that human glioblastoma cells as well as astrocytes maintained the ability to support neuritogenesis, but non-neural normal or tumoral cells failed to do so. However, glioblastoma cells did not distinguish embryonic from post-natal neurons in relation to neurite pattern in the co-cultures, as normal astrocytes did. Further, the laminin organization on both normal and tumoral glial cells was altered from a filamentous arrangement to a mixed punctuate/filamentous pattern when in co-culture with neurons. Together, these results suggest that glioblastoma cells could identify neuronal cells as partners, to support their growth and induce complex neurites, but they lost the normal glia property to distinguish neuronal age. In addition, our results show for the first time that neurons modulate the organization of astrocytes and glioblastoma laminin on the extracellular matrix.
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PMID:Interactive properties of human glioblastoma cells with brain neurons in culture and neuronal modulation of glial laminin organization. 1717 53

Diazinon and cypermethrin are pesticides extensively used in sheep dipping. Diazinon is a known anti-cholinesterase, but there is limited information regarding its molecular mechanism of action. This paper describes the effects of diazinon and cypermethrin at a morphological and molecular level on differentiating mouse N2a neuroblastoma and rat C6 glioma cell lines. Concentrations up to 10 microM of both compounds and their mixture had no effect on the viability of either cell line, as determined by methyl blue tetrazolium reduction and total protein assays. Microscopic analysis revealed that 1 microM and 10 microM diazinon but not cypermethrin inhibited the outgrowth of axon-like processes in N2a cells after a 24-h exposure but neither compound affected process outgrowth by differentiating C6 cells at these concentrations. Under these conditions, 10 microM diazinon inhibited AChE slightly compared to the control after a 4-h exposure but not after 24 h. Western blotting analysis showed that morphological changes were associated with reduced cross-reactivity with antibodies that recognize the neurofilament heavy chain (NFH), microtubule associated protein MAP 1B and HSP-70 compared to control cell extracts, whereas reactivity with anti-alpha-tubulin antibodies was unchanged. Aggregation of NFH was observed in cell bodies of diazinon-treated N2a cells, as determined by indirect immunofluorescence staining. These data demonstrate that diazinon specifically targets neurite outgrowth in neuronal cells and that this effect is associated with disruption of axonal cytoskeleton proteins, whereas cypermethrin has no effect on the same parameters.
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PMID:The effects of diazinon and cypermethrin on the differentiation of neuronal and glial cell lines. 1723 17

Diffusion tensor imaging and multiple voxel magnetic resonance spectroscopy were performed in the MRI follow-up of a patient with a glioma treated with temozolomide chemotherapy. Tumor shrinkage was paralleled by reductions in choline level and by increases in apparent diffusion coefficient indicating decreased cellularity. Within the tumor, choline level and apparent diffusion coefficient showed a significant inverse correlation (P < 0.01). Fractional anisotropy distribution in the tumor correlated positively with N-acetyl aspartate level (P < 0.001), indicating that these parameters reflect (remaining) axonal structure. Tumor lactate level, also found to decrease under therapy, did not correlate with any other parameter.
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PMID:Diffusion tensor imaging and chemical shift imaging assessment of heterogeneity in low grade glioma under temozolomide chemotherapy. 1805 66

Magnetic resonance microscopy (microMRI) is becoming an important tool for non-destructive analysis of fixed brain tissue. However, unlike MRI, X-ray computed tomography (CT) scans show little native soft tissue contrast. In this paper, we explored the use of contrast enhanced (brains immersion stained in iodinated CT contrast media) micro-CT (microCT) for high resolution 3D imaging of fixed normal and pathological brains, compared to microMRI and standard histopathology. An optimum iodine concentration of 0.27 M resulted in excellent contrast between gray and white matter in normal brain and a wide range of anatomical structures were identified. In glioma bearing mouse brains, there was clear deliniation of tumor margin which closely matched that seen on histopathology sections. microCT tumor volume was strongly correlated with histopathology volume. Our data suggests that microCT image contrast in the immersion-stained brains is related to axonal density and myelin content. Compared to traditional histopathology, our microCT approach is relatively rapid and less labor intensive. In addition, compared to microMRI, microCT is robust and requires much lower equipment and maintenance costs. For simple measurements, such as tumor volume and non-destructive postmortem brain screening, microCT may prove to be a valuable alternative to standard histopathology or microMRI.
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PMID:3D micro-CT imaging of the postmortem brain. 1846 2

Ependymomas are generally considered to be noninfiltrative tumors that have discrete borders with adjacent brain tissue. Most occur in the posterior fossa or spinal cord. Supratentorial ependymal tumors arise near the ventricular system or, more rarely, within the cerebral white matter or cortex. Presented here are 6 supratentorial ependymal tumors, 3 that primarily involve the cerebral cortex and 3 that extend into the cortex from the underlying white matter. By microscopy, all of these tumors locally infiltrate the cortex and/or white matter along small blood vessels and axonal fiber tracts. They also form other glioma secondary structures including perineuronal tumor cell satellitosis and subpial tumor cell mounds. The 3 cortical ependymal tumors show a spectrum of features ranging from conventional and clear-cell ependymoma-like patterns to more angiocentric glioma-like histology. Because ependymal tumors generally have a significantly better prognosis than other infiltrating gliomas, recognition of their capacity to infiltrate adjacent cortex and white matter is important to prevent the misdiagnosis of oligodendroglioma, astrocytoma, or infiltrating glioma, not otherwise specified. Cortical ependymomas and angiocentric gliomas may comprise a group of locally infiltrative ependymal tumors that are associated with an excellent prognosis after gross total surgical resection.
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PMID:Patterns of brain infiltration and secondary structure formation in supratentorial ependymal tumors. 1871 54

In the developing brain, cell migration is a crucial process for structural organization, and is therefore highly regulated to allow the correct formation of complex networks, wiring neurons, and glia. In the early postnatal brain, late developmental processes such as the production and migration of astrocyte and oligodendrocyte progenitors still occur. Although the brain is completely formed and structured few weeks after birth, it maintains a degree of plasticity throughout life, including axonal remodeling, synaptogenesis, but also neural cell birth, migration and integration. The subventricular zone (SVZ) and the dentate gyrus (DG) of the hippocampus are the two main neurogenic niches in the adult brain. Neural stem cells reside in these structures and produce progenitors that migrate toward their ultimate location: the olfactory bulb and granular cell layer of the DG respectively. The aim of this review is to synthesize the increasing information concerning the organization, regulation and function of cell migration in a mature brain. In a normal brain, proteins involved in cell-cell or cell-matrix interactions together with secreted proteins acting as chemoattractant or chemorepellant play key roles in the regulation of neural progenitor cell migration. In addition, recent data suggest that gliomas arise from the transformation of neural stem cells or progenitor cells and that glioma cell infiltration recapitulates key aspects of glial progenitor migration. Thus, we will consider glioma migration in the context of progenitor migration. Finally, many observations show that brain lesions and neurological diseases trigger neural stem/progenitor cell activation and migration toward altered structures. The factors involved in such cell migration/recruitment are just beginning to be understood. Inflammation which has long been considered as thoroughly disastrous for brain repair is now known to produce some positive effects on stem/progenitor cell recruitment via the regulation of growth factor signaling and the secretion of a number of chemoattractant cytokines. This knowledge is crucial for the development of new therapeutic strategies. One of these strategies could consist in increasing the mobilization of endogenous progenitor cells that could replace lost cells and improve functional recovery.
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PMID:Cell migration in the normal and pathological postnatal mammalian brain. 1942 61

Individuals with neurofibromatosis type 1 (NF1) are prone to develop optic pathway gliomas that can result in significant visual impairment. To explore the cellular basis for the reduced visual function resulting from optic glioma formation, we used a genetically engineered mouse model of Nf1 optic glioma (Nf1+/-(GFAP)CKO mice). We performed multimodal functional and structural analyses both before and after the appearance of macroscopic tumors. At 6 weeks of age, before obvious glioma formation, Nf1+/-(GFAP)CKO mice had decreased visual-evoked potential amplitudes and increased optic nerve axon calibers. By 3 months of age, Nf1+/-(GFAP)CKO mice exhibited pronounced optic nerve axonopathy and apoptosis of neurons in the retinal ganglion cell layer. Magnetic resonance diffusion tensor imaging showed a progressive increase in radial diffusivity between 6 weeks and 6 months of age in the optic nerve proximal to the tumor indicating ongoing deterioration of axons. These data suggest that optic glioma formation results in early axonal disorganization and damage, which culminates in retinal ganglion cell death. Collectively, this study shows that Nf1+/-(GFAP)CKO mice can provide a useful model for defining mechanisms of visual abnormalities in children with NF1 and lay the foundations for future interventional studies aimed at reducing visual loss.
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PMID:Optic nerve dysfunction in a mouse model of neurofibromatosis-1 optic glioma. 1952 1

The Lgi1 protein is involved in the pathogenesis of autosomal dominant lateral temporal epilepsy because mutations in the leucine-rich, glioma-inactivated 1 (LGI1) gene have been found in affected subjects and families; however, the function of Lgi1 is still unclear. Definition of the fine intracellular distribution of Lgi1 in normal cortical tissue would add in understanding its role and envisage pathogenetic mechanisms. Therefore, we analyzed normal rat cortex for Lgi1 by combining biochemistry, immunohistochemistry and immunoelectron microscopy. Our results demonstrate that Lgi1 is a cytoplasmic protein distributed both in the soma and in the processes of neurons: it occurs on the rough endoplasmic reticulum, the site of synthesis, in the Golgi complex, where it undergoes glycosylation, and in close proximity to neurotubules and neurofilaments, especially in the axons, but it is scarce at synapses and the neurilemma. Lgi1 association with axonal cytoskeletal structures would imply Lgi1 is either transported along axons by motor proteins, or playing some role as a carrier in the axonal Xux, or it could be involved in the regulation of cytoskeletal organization.
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PMID:Distribution of the epilepsy-related Lgi1 protein in rat cortical neurons. 1975 93

There is increasing evidence that the extent of tumor removal in low-grade glioma surgery is related to patient survival time. Thus, the goal of resecting the largest amount of tumor possible without leading to permanent neurological sequelae is a challenge for the neurosurgeon. Electrical stimulation of the brain to detect cortical and axonal areas involved in motor, language, and cognitive function and located within the tumor or along its boundaries has become an essential tool in combination with awake craniotomy. Based on a literature review, discussions within the European Low-Grade Glioma Group, and illustrative clinical experience, the authors of this paper provide an overview for neurosurgeons, neurophysiologists, linguists, and anesthesiologists as well as those new to the field about the stimulation techniques currently being used for mapping sensorimotor, language, and cognitive function in awake surgery for low-grade glioma. The paper is intended to help the understanding of these techniques and facilitate a comparison of results between users.
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PMID:Intraoperative electrical stimulation in awake craniotomy: methodological aspects of current practice. 2012 42

The segregation and myelination of axons in the developing PNS, results from a complex series of cellular and molecular interactions between Schwann cells and axons. Previously we identified the Lgi4 gene (leucine-rich glioma-inactivated4) as an important regulator of myelination in the PNS, and its dysfunction results in arthrogryposis as observed in claw paw mice. Lgi4 is a secreted protein and a member of a small family of proteins that are predominantly expressed in the nervous system. Their mechanism of action is unknown but may involve binding to members of the Adam (A disintegrin and metalloprotease) family of transmembrane proteins, in particular Adam22. We found that Lgi4 and Adam22 are both expressed in Schwann cells as well as in sensory neurons and that Lgi4 binds directly to Adam22 without a requirement for additional membrane associated factors. To determine whether Lgi4-Adam22 function involves a paracrine and/or an autocrine mechanism of action we performed heterotypic Schwann cell sensory neuron cultures and cell type-specific ablation of Lgi4 and Adam22 in mice. We show that Schwann cells are the principal cellular source of Lgi4 in the developing nerve and that Adam22 is required on axons. Our results thus reveal a novel paracrine signaling axis in peripheral nerve myelination in which Schwann cell secreted Lgi4 functions through binding of axonal Adam22 to drive the differentiation of Schwann cells.
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PMID:Adam22 is a major neuronal receptor for Lgi4-mediated Schwann cell signaling. 2022 21


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