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2,292 results for “glioma”
Safety and Tolerability of Carboxyamidotriazole Orotate (CTO) in Solid Tumors or With Temodar® in Glioblastoma or Other Recurrent Malignant Gliomas or in Combination With Temodar® and Radiation Therap
ClinicalTrials.gov study NCT01107522. IPD Sharing: Not stated. Countries: 1. Publications: 1.
How the Precise Habitats Can Predict the IDH Mutation Status and Prognosis of the Patients With High-grade Gliomas
ClinicalTrials.gov study NCT04908267. IPD Sharing: NO. Countries: 1. Publications: 1.
A Study of the Drugs Selumetinib vs. Carboplatin and Vincristine in Patients With Low-Grade Glioma
ClinicalTrials.gov study NCT04166409. IPD Sharing: YES. Countries: 3. Publications: 2.
Early noninvasive metabolic biomarkers of mutant IDH inhibition in glioma
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Data from: Post-operative follow-up for selected diffuse low-grade gliomas with WHO grade III/IV foci
Objective: Diffuse low-grade gliomas (DLGG) are defined by a continuous growth and an almost unavoidable malignant transformation. Foci of malignant glioma can be found within DLGG samples obtained from surgical resections. As the medical management of patients is classically based on the higher tumor grade, an immediate adjuvant treatment is usually proposed. To determine whether postponing the medical treatment in selected patients is feasible, we conducted a single-center retrospective study. Methods: Single-center retrospective analysis of a consecutive series of DLGG managed with this conservative strategy. Inclusion criteria were: at least one focus of malignant tumor (grade III-IV, WHO 2016), no previous chemotherapy or radiotherapy, no less than a subtotal resection of the FLAIR tumor volume, no intention of treating with immediate adjuvant therapy, minimum two years of follow-up. The time interval to the following oncological medical treatment was analyzed, as well as the functional and survival results. Results: 45 patients met the inclusion criteria (median age 36.5, median time interval from diagnosis: 7.3 months). Most tumors (86.7%) were IDH-mutant and 1p19q intact (60.0%); 10 presented with grade IV foci. With a median follow-up of 6.3 years, 75.5% of patients received a subsequent medical treatment, after a median time of 3.7 years since surgery. At the time of analysis, 9 patients (20.0%) had died (5-years and 7-years survival rates: 95.2% and 67.0%). Most surviving patients were still active professionally, without seizures. Conclusions: Postponing the medical treatment in DLGG with foci of malignant tumor following total or subtotal resection should be considered in selected patients.
Fiber-tract localized diffusion coefficients highlight patterns of white matter disruption induced by proximity to glioma
Gliomas account for 26.5% of all primary central nervous system tumors. Recent studies have used diffusion tensor imaging (DTI) to extract white matter fibers and the diffusion coefficients derived from MR processing to provide useful, non-invasive insights into the extent of tumor invasion, axonal integrity, and gross differentiation of glioma from metastasis. Here, we extend this work by examining whether a tract-based analysis can improve non-invasive localization of tumor impact on white matter integrity. This study retrospectively analyzed preoperative magnetic resonance sequences highlighting contrast enhancement and DTI scans of 13 subjects that were biopsy confirmed to have either high or low-grade glioma. We reconstructed the corticospinal tract and superior longitudinal fasciculus by applying atlas-based regions of interest to fibers derived from whole-brain deterministic streamline tractography. Within-subject comparison of hemispheric diffusion coefficients (e.g., fractional anisotropy and mean diffusivity) indicated higher levels of white matter degradation in the ipsilesional hemisphere. Novel application of along-tract analyses revealed that tracts traversing the tumor region showed significant white matter degradation compared to the contralesional hemisphere and ipsilesional tracts displaced by the tumor.
Data from: A systematic review and meta-analysis of gene therapy in animal models of cerebral glioma: why did promise not translate to human therapy?
Background: The development of therapeutics is often characterized by promising animal research that fails to translate into clinical efficacy; this holds for the development of gene therapy in glioma. We tested the hypothesis that this is because of limitations in the internal and external validity of studies reporting the use of gene therapy in experimental glioma. Method: We systematically identified studies testing gene therapy in rodent glioma models by searching three online databases. The number of animals treated and median survival were extracted and studies graded using a quality checklist. We calculated median survival ratios and used random effects meta-analysis to estimate efficacy. We explored effects of study design and quality and searched for evidence of publication bias. Results: We identified 193 publications using gene therapy in experimental glioma, including 6,366 animals. Overall, gene therapy improved median survival by a factor of 1.60 (95% CI 1.53–1.67). Study quality was low and the type of gene therapy did not account for differences in outcome. Study design characteristics accounted for a significant proportion of between-study heterogeneity. We observed similar findings in a data subset limited to the most common gene therapy. Conclusion: As the dysregulation of key molecular pathways is characteristic of gliomas, gene therapy remains a promising treatment for glioma. Nevertheless, we have identified areas for improvement in conduct and reporting of studies, and we provide a basis for sample size calculations. Further work should focus on genes of interest in paradigms recapitulating human disease. This might improve the translation of such therapies into the clinic.
Data from: Comparative dynamics of microglialand glioma cell motility at the infiltrative margin of brain tumours
Microglia are a major cellular component of gliomas, and abundant in the centre of the tumour and at the infiltrative margins. While glioma is a notoriously infiltrative disease, the dynamics of microglia and glioma migratory patterns have not been well characterized. To investigate the migratory behaviour of microglia and glioma cells at the infiltrative edge, we performed two-colour time-lapse fluorescence microscopy of brain slices generated from a platelet-derived growth factor-B (PDGFB)-driven rat model of glioma, in which glioma cells and microglia were each labelled with one of two different fluorescent markers. We used mathematical techniques to analyse glioma cells and microglia motility with both single cell tracking and particle image velocimetry (PIV). Our results show microglia motility is strongly correlated with the presence of glioma, while the correlation of the speeds of glioma cells and microglia was variable and weak. Additionally, we showed that microglia and glioma cells exhibit different types of diffusive migratory behaviour. Microglia movement fit a simple random walk, while glioma cell movement fits a super diffusion pattern. These results show that glioma cells stimulate microglia motility at the infiltrative margins, creating a correlation between the spatial distribution of glioma cells and the pattern of microglia motility.
TZO - Working memory performance in glioma patients is associated with functional connectivity between the right dorsolateral prefrontal cortex and default mode network
<p>Data files hosted on Figshare for "Working memory performance in glioma patients is associated with functional connectivity between the right dorsolateral prefrontal cortex and default mode network".</p> <p>Contains functional connectivity matrices, clinical variables, and working memory performance scores of 45 glioma patients.</p>
Evolving therapies, neurocognitive outcomes, and functional independence in adult survivors of childhood glioma
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ALKBH5 promotes tumour proliferation, migration, and invasion by regulating the lncRNA MIR210HG/Mir-206/WEE1 signalling pathway in glioma
<p>GRAPH</p>
Resume Table: Angiocentric Glioma
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Data repository for the article: Fluorescence lifetime imaging unravels the pathway of glioma cell death upon hypericin-induced photodynamic therapy.
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Gene alterations, clinical informations and survival data of gliomas with/without corpus callosum involvement
<p>The raw dataset of this study contained the gene alterations, clinical informations and survival data of glioma patients. Gene alterations data were obtained by Next-generation DNA sequencing of glioma samples of patients. Clinical informations were obtained from Electronic medical records and follow-up. The survival data were obtained by follow-up of patients. In order to explore gene alterations and their correlation with the survival of glioblastoma (GBM) of corpus callosum (CC) involvement (ccGBM), this dataset was analyzed in detail. A total of<b> </b>30 ccGBM and 88 non-ccGBM were finally included. The ccGBM had higher incidence of <i>PDGFRA </i>(33.3% versus 9.1%, P=0.004) alterations than non-ccGBM. <i>PDGFRA </i>amplification (<i>PDGFRAamp</i>, 33.3% versus 9.1%, P=0.004) and missense mutation (<i>PDGFRAmut</i>, 20.0% versus 3.4%, P=0.011) both had higher incidence in ccGBM than in non-ccGBM. <i>PDGFRA </i>alteration was significantly associated with the occurrence of ccGBM (OR=4.91 [95%CI: 1.55-15.52], P=0.007). The ccGBM of <i>PDGFRAamp </i>achieved shorter median PFS (8.6 versus 13.5 months, P=0.025) and OS (12.4 versus 17.9 months, P=0.022) than non-ccGBM of <i>PDGFRAnon-amp</i>. The ccGBM of <i>PDGFRAamp</i> combined with <i>PDGFRAmut</i> (<i>PDGFRAamp-mut</i>)<i> </i>had shorter median PFS (7.6 versus 8.9 months, P=0.022) and OS (9.6 versus 17.8 months, P=0.006) than non-ccGBM of <i>PDGFRA</i> wild type and non-amplification (<i>PDGFRA-w, non-amp</i>). Compared to ccGBM of <i>PDGFRA-w, non-amp</i>, the ccGBM of <i>PDGFRAamp</i> and <i>PDGFRAamp-mut </i>both had shorter median PFS and OS (P<0.05). Hazard ratios (HRs) of <i>PDGFRAamp</i> for PFS and OS of ccGBM were 3.08 (95%CI: 1.02-9.35, P=0.047) and 5.07 (95%CI: 1.52-16.89, P=0.008) respectively, HRs of <i>PDGFRAamp-mut </i>for PFS and OS were 13.16 (95%CI: 3.19-54.40, P<0.001) and 16.36 (95%CI: 2.66-100.70, P=0.003) respectively. The <i>PDGFRA </i>alterations is significantly associated with the occurrence and poor prognosis of ccGBM.</p>
Inter and Intra-tumour Heterogeneity of Paediatric-type Diffuse High-Grade Glioma Revealed by Single-Cell Mass Cytometry
<p>raw data (fcs file) from mass cytometry experiments </p>
Fig. 1 in Iridoids and bis-iridoids from Valeriana jatamansi and their cytotoxicity against human glioma stem cells
Fig. 1. Chemical structures of compounds 1–10 from Valeriana jatamansi.
Fig. 3. Key ROESY correlations for compounds 6 and 9 in Iridoids and bis-iridoids from Valeriana jatamansi and their cytotoxicity against human glioma stem cells
Fig. 3. Key ROESY correlations for compounds 6 and 9.
Phase I-II Everolimus and Sorafenib in Recurrent High-Grade Gliomas
ClinicalTrials.gov study NCT01434602. IPD Sharing: NO. Countries: 1. Publications: 0.
A Registry-Based Cohort Study on the Clinical Outcomes of Spinal Cord Glioma Resection Via the Dorsolateral Sulcus Approach
ClinicalTrials.gov study NCT07066475. IPD Sharing: YES. Countries: 1. Publications: 0.
Aloxi for Prevention of Chemotherapy Induced Nausea and Vomiting in Malignant Glioma Patients Receiving Irinotecan With Bevacizumab
ClinicalTrials.gov study NCT00636805. IPD Sharing: Not stated. Countries: 1. Publications: 0.
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These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.
Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.