Glioblastoma (GBM) research papers

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Tumor-associated astrocytes augment cholesterol synthesis to support glioblastoma growth through alternatively spliced Quaking (QKI) isoforms. reports: Glioblastoma (GBM) is a highly aggressive brain tumor with limited treatment options. Tumor-associated astrocytes (TAAs) are crucial components of the GBM microenvironment, yet the contribution of alternative splicing (AS) in TAAs to tumor progression remains unclear. Transcriptomic and molecular analyses of GBM-associated astrocytes revealed a GBM-induced isoform switch in the RNA-binding protein Quaking (QKI) from the QKI-6 isoform to QKI-5 isoform.

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Transfer Learning Strategies for Pathological Foundation Models: A Systematic Evaluation in Brain Tumor Classification. reports: Deploying pathology AI at individual hospitals faces challenges including limited cases and adapting pretrained models to local data. Brain tumor classification, with diverse diagnostic categories but few cases per institution, represents this challenge. Foundation models may offer a solution, but optimal transfer learning strategies remain unclear.

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Spectral discrimination of pediatric SF188 and adult glioblastoma stem cells by deep learning-enhanced Raman profiling. reports: Pediatric and adult glioblastomas (GBM) represent biologically distinct entities requiring age-tailored therapeutic strategies. However, rapid and non-invasive methods to distinguish these molecular subtypes remain an unmet clinical need. This study evaluates the potential of confocal Raman spectroscopy combined with deep learning as a label-free diagnostic tool to differentiate pediatric from adult GBM based on intrinsic biochemical fingerprints.

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Differential migration mechanics and immune responses of glioblastoma subtypes reports: Glioblastoma remains a deadly cancer driven in part by invasion of tumor cells into the brain. Transcriptomic analyses have identified distinct molecular subtypes, but mechanistic differences that account for clinical differences are not clear. Here, we show that, as predicted by the motor-clutch model of cell migration, mesenchymal glioma cells are more spread, generate larger traction forces, and migrate faster in brain tissue compared to proneural cells. This is a preprint and not peer reviewed.

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BRAF/MEK Inhibition Induces Cell State Transitions Boosting Immune CheckpointSensitivity in BRAFV600E-mutant Glioma reports: Resistance to BRAF plus MEK inhibition (BRAFi+MEKi) in BRAFV600E-mutant gliomas drives rebound, progression, and high mortality, yet it remains poorly understood. This study addresses the urgent need to develop treatments for BRAFi+MEKi-resistant glioma in novel mouse models and patient-derived materials. BRAFi+MEKi reveals glioma plasticity by heightening cell state transitions along glial differentiation trajectories, giving rise to astrocyte- and immunomodulatory oligodendrocyte (OL)-like states. This is a preprint and not peer reviewed.

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Attenuation of malignant phenotype of glioblastoma following a short course of the pro-oxidant combination of Resveratrol and Copper reports: BackgroundWe investigated a novel therapeutic approach to glioblastoma (GBM) that targets cell-free chromatin particles (cfChPs) that are released from dying GBM cells and aggravate the oncogenic phenotype of living GBM cells. cfChPs can be deactivated by oxygen radicals (OR) generated upon admixing the nutraceuticals Resveratrol (R) and Copper (Cu). Oral administration of R-Cu leads to generation of OR which are readily absorbed to deactivate cfChPs. This is a preprint and not peer reviewed.

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YAP controls cell migration and invasion through a Rho-GTPase switch reports: Delineating the mechanisms controlling the invasive spread of non-diseased and transformed cells is central to understanding diverse processes including cancer progression. Here, we found that Yes-associated protein (YAP), a central transcriptional regulator implicated in controlling organ and body size, modulated a Rho-GTPase switch that drives cellular migration by transactivating the Rac1-GEF protein TRIO through direct modulation of its intronic enhancer. Additionally, YAP and TRIO may promote invasive behavior through putative crosstalk with STAT3 signaling, a potential downstream target. This is a preprint and not peer reviewed.

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Causal associations between gut microbiota and cancers reports: BackgroundEmerging evidence suggests that the gut microbiota is associated with various cancer-related outcomes. Recent studies using Mendelian randomization (MR) have indicated a causal relationship between gut microbiota and several types of cancer. However, these conclusions remain controversial. This is a preprint and not peer reviewed.

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