A 31-Year-Old Woman With a Transformed Low-grade Glioma [Clinical Crossroads]
Low-grade gliomas in adults have an incidence of 0.8 to 1.2 per 100 000, and their causes are unknown. Despite their histological classification as low-grade, they cannot be cured by any current treatment mode, and no class I evidence exists to guide initial treatment of these tumors. Median survival ranges between 7.5 years and 10 years, with a 5-year survival probability between 55% and 86%. The prognosis depends on age, World Health Organization (WHO) tumor grade, Karnofsky performance score, cytological type (oligodendroglioma vs astrocytoma), and, potentially, the extent of resection. Oligodendrogliomas with loss of heterozygosity on chromosomes 1p and 19q have a distinctly more favorable prognosis and therapeutic response rate. Low-grade tumors progress to high-grade gliomas wit......
POSTED 03/09/2010 at 02:50 PM --
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Gliomas [JAMA Patient Page]
(Source: JAMA)...
POSTED 03/09/2010 at 02:50 PM --
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Lycopene in treatment of high-grade gliomas: A pilot study
Conclusions : Addition of nutrition supplements such as lycopene may have potential therapeutic benefit in the adjuvant management of high-grade gliomas. (Source: Neurology India)...
POSTED 03/09/2010 at 09:01 AM --
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Optimization of magnetosonoporation for stem cell labeling
This study demonstrated that the optimized MSP cell labeling technique can achieve both high cell viability and intracellular uptake of MR contrast agents, and has the potential to be a useful cell labeling technique to facilitate future clinical translation of MRI-integrated cell therapy. Copyright © 2010 John Wiley & Sons, Ltd. (Source: NMR in Biomedicine)...
POSTED 03/08/2010 at 06:00 PM --
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New Insights Into Susceptibility to Glioma [Neurological Review]
The study of inherited susceptibility to cancer has been one of the most informative areas of research in the past decade. Most of the cancer genetics studies have been focused on the common tumors such as breast and colorectal cancers. As the allelic architecture of these tumors is unraveled, research attention is turning to other rare cancers such as glioma, which are also likely to have a major genetic component as the basis of their development. In this brief review we discuss emerging data on glioma whole genome–association searches to identify risk loci. Two glioma genome-wide association studies have so far been reported. Our group identified 5 risk loci for glioma susceptibility (TERT rs2736100, CCDC26 rs4295627, CDKN2A/CDKN2B rs4977756, RTEL1 rs6010620, and PHLDB1 rs498872).......
POSTED 03/08/2010 at 02:50 PM --
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Bevacizumab for Malignant Gliomas [Neurological Review]
Malignant gliomas are the most common and aggressive primary brain tumors in adults. Despite optimal treatment with surgery, radiotherapy, and temozolomide, tumor recurrences are frequent and patients with malignant gliomas continue to have poor prognoses. Malignant gliomas are often highly vascularized, and significant advances have been made in the last few decades in our understanding of the mechanisms of tumor angiogenesis. Recently, bevacizumab, an antibody against vascular endothelial growth factor, has demonstrated significant activity in recurrent glioblastomas, resulting in US Food and Drug Administration approval and raising the prospect for other antiangiogenic drugs now entering clinical trials. (Source: Archives of Neurology)...
POSTED 03/08/2010 at 02:50 PM --
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Morphological Characteristics of Brain Tumors Causing Seizures [Original Contribution]
Conclusions The influence of size and location of the tumors on their propensity to cause seizures varies with the grade of the tumor. In high-grade gliomas, rapidly growing tumors, particularly those situated in deeper structures, present with non–seizure-related symptoms. In low-grade gliomas, lesions in the temporal lobe or the insula grow large without other symptoms and eventually cause seizures. Quantitative image analysis allows for the mapping of regions in each group that are more or less susceptible to seizures. (Source: Archives of Neurology)...
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Efficacy and Safety of Levetiracetam in Patients With Glioma: A Clinical Prospective Study [Original Contribution]
Conclusion The results of this study provide good evidence that levetiracetam is efficacious and safe in patients with epilepsy due to glioma. (Source: Archives of Neurology)...
POSTED 03/08/2010 at 02:50 PM --
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Evaluation of O-(2-[18F]-Fluoroethyl)-L-Tyrosine in the Diagnosis of Glioblastoma [Observation]
Conclusion The initial results are promising and indicate that FET PET is a valuable and applicable tool for the imaging of high-grade glioma. (Source: Archives of Neurology)...
POSTED 03/08/2010 at 02:50 PM --
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Tat-BMPs-PAMAM Conjugates Enhance Therapeutic Effect of Small Interference RNA on U251 Glioma Cells in Vitro and in Vivo
Human Gene Therapy , Vol. 0, No. 0. (Source: Human Gene Therapy)...
POSTED 03/08/2010 at 07:07 AM --
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Improved Killing of Human High-Grade Glioma Cells by Combining Ionizing Radiation with Oncolytic Parvovirus H-1 Infection
Conclusion. This study demonstrates intact
susceptibility of previously irradiated glioma-cells for H-1PV
induced oncolysis. The combination of ionizing radiation followed
by H-1PV infection increased viral cytotoxicity, especially in
radioresistant gliomas. These findings support the ongoing
development of a clinical trial of H-1PV in patients with
recurrent glioblastomas. (Source: Journal of Biomedicine and Biotechnology)...
POSTED 03/07/2010 at 10:09 AM --
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Mechanisms of tumor necrosis factor-alpha-induced interleukin-6 synthesis in glioma cells
Conclusion:
These results strongly suggest that TNF-alpha induces IL-6 synthesis through the JAK/STAT3 pathway in addition to p38 MAP kinase and SAPK/JNK in C6 glioma cells, and that phosphorylation of NFkB at Ser 536 and Ser 468, and NADPH oxidase are involved in TNF-alpha-stimulated IL-6 synthesis. (Source: BioMed Central)...
POSTED 03/05/2010 at 06:00 PM --
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Accumulation of CD133-positive glioma cells after high-dose irradiation by Gamma Knife surgery plus external beam radiation.
Conclusions The results indicate that CD133-positive glioma stemlike cells can survive high-dose irradiation, leading to recurrence, despite prolonged damage to tumor blood vessels. This could be an essential factor limiting the effectiveness of GKS plus EBRT for malignant gliomas.
PMID: 20205512 [PubMed - as supplied by publisher] (Source: Journal of Neurosurgery)...
POSTED 03/04/2010 at 06:00 PM --
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Carvedilol in glioma treatment alone and with imatinib in vitro.
Authors: Erguven M, Yazihan N, Aktas E, Sabanci A, Li CJ, Oktem G, Bilir A
The purpose of the study was to investigate whether carvedilol has an antiproliferative effect alone and whether carvedilol provides an additive, synergistic or antagonistic effect on imatinib mesylate-induced cytotoxicity in both C6 glioma monolayer and spheroid culture. The C6 rat glioma chemoresistant experimental brain tumour cell line, that is notoriously difficult to treat with combination chemotherapy, was used both in monolayer and spheroid cultures. We treated C6 glioma cells with carvedilol alone and a combination of carvedilol and imatinib mesylate at a concentration of 10 microM. Following treatment, we evaluated cell proliferation index, bromodeoxyuridine labelling index (BrDU-LI), cell cycle distri......
POSTED 03/04/2010 at 04:59 PM --
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miR-221/222 promote malignant progression of glioma through activation of the Akt pathway.
In this study, we aimed to explore the coordinated function of miR-221/222 in glioma by bioinformatics and experiment methods. Bioinformatics analysis revealed that miR-221/222 had the potential to regulate about 70 common target genes and may exert a cooperative effect on regulation and function via Akt signaling pathway. Overexpression of miR-221/222 increased glioma cell proliferation and invasion in vitro and induced glioma growth in a subcutaneous mouse model. Furthermore, miR-221/222 overexpression resulted in an obvious activation of p-Akt and significant changes of Akt-related gene expression in glioma cells. Our results suggest that miR-221/222 co-enhance the glioma malignant phenotype via activation of the Akt pathway mediated by regulation of common gene expression.
PMID: 20......
POSTED 03/04/2010 at 04:58 PM --
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Gene expression profile in a glioma cell line resistant to cell death induced by a the chimeric tumor suppressor-1 (CTS-1), a dominant-positive variant of p53--the role of NF{kappa}B
The identification of genes involved in carcinogenesis and tumor progression is of great interest since these genes might be feasible as candidates for new tumor-targeted therapy strategies. Chimeric tumor suppressor-1 (CTS-1), an artificial synthetic variant of p53, resists common p53 inactivation and could therefore be defined as a dominant-positive p53 variant. Overexpression of CTS-1 induces caspase-independent cell death. We used whole-genome microarray expression analysis in a parental (229P) and a CTS-1-resistant glioma cell line (229Res) to analyze alterations in gene expression in Ad-CTS-1-infected and in uninfected parental and resistant cells. In total, 700 genes were differentially expressed in infected and 313 genes in uninfected 229Res versus 229P cells. Ingenuity Pathway Ana......
POSTED 03/04/2010 at 09:26 AM --
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Low field intraoperative MRI-guided surgery of gliomas: A single center experience
Conclusion: Low field iMRI is a helpful tool in modern neurosurgery and facilitates brain tumor resection to a maximum safe extent. Its use translates into a better prognosis for these patients with devastating tumors. Future studies covering the use of iMRI will need to be conducted in a prospective, randomized fashion to prove the true benefit of iMRI in glioma surgery. (Source: Clinical Neurology and Neurosurgery)...
POSTED 03/02/2010 at 11:56 AM --
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Resisting arrest: a switch from angiogenesis to vasculogenesis in recurrent malignant gliomas
The cellular and molecular events that initiate and promote malignant glioma development are not completely understood. The treatment modalities designed to promote its demise are all ultimately ineffective, leading to disease progression. In this issue of the JCI, Kioi et al. demonstrate that vasculogenesis and angiogenesis potentially play distinct roles in the etiology of primary and recurrent malignant gliomas, suggesting that patient therapy should perhaps be tailored specifically against the predominant vasculature pathway at a given specific stage of gliomagenesis. (Source: Journal of Clinical Investigation)...
POSTED 03/02/2010 at 11:25 AM --
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The striate sign: peritumoural perfusion pattern of infiltrative primary and recurrent gliomas
Abstract MR perfusion depicts angiogenesis as a key factor for growth and malignancy in gliomas by means of increased regional cerebral
blood volume (rCBV). The rCBV increase is not limited to the tumour area, but may also produce a stripe-like pattern of peritumoural
rCBV increase that we defined as the “striate sign”. We evaluated if prior radiochemotherapy influences perfusion values and
pattern in and adjacent to malignant gliomas comparing rCBV of treated recurrent gliomas with untreated gliomas. Ninety-three
patients with primary or recurrent WHO grades II–IV glial tumours underwent T2*-weighted dynamic susceptibility-weighted contrast-enhanced
(DSC)-MRI. Differences of normalised rCBV and rCBVmax were evaluated using Kruskal−Wallis analysis with post hoc test......
POSTED 03/02/2010 at 04:03 AM --
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Response to article "Proton magnetic resonance spectroscopy in the distinction of high-grade cerebral gliomas from single metastatic brain tumors"
Authors: Sijens PE
PMID: 20192894 [PubMed - as supplied by publisher] (Source: Acta Radiologica)...
POSTED 03/01/2010 at 06:00 PM --
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