Glioma Diagnosis and Treatment

This study shows that cell-free DNA (cfDNA) can track glioblastoma tumor burden and treatment response over time using in vitro models.

This study identifies genetic changes in IDH-mutant gliomas that correlate with treatment response and tumor evolution using longitudinal genomic data from 206 patient samples.

This study examines how the size of glioblastoma spheroids affects their invasion and response to temozolomide therapy.

This study uses a 3D hydrogel model to investigate TMZ resistance in GBM by examining drug response and migration in heterogeneous cell populations.

The paper identifies speech-related neural activity in IDH-mutant gliomas using electrocorticography, showing task-based and resting-state distinctions that could improve surgical outcomes.

The paper uses single-cell spatial analysis to identify SPP1+/GPNMB+ myeloid cells in pediatric high-grade gliomas that suppress CD8+ T cells and promote tumor growth.

This study uses multi-omics approaches to analyze pediatric low-grade glioma and identifies immune-related differences linked to BRAF mutations.

This study examines how patient-derived glioblastoma cells from different tumor regions respond to adhesion and metabolic inhibitors, showing heterogeneity in drug sensitivity linked to migration and adhesion properties.

This study identifies DNA-PK as a synthetic lethal target in TP53-deficient SHH medulloblastoma, showing that inhibiting DNA-PK enhances radiosensitivity and improves survival in preclinical models.

This study shows that cholinergic neuron activity promotes both healthy OPC and DMG proliferation through muscarinic receptors, with specific nuclei driving growth in different brain regions.

This paper develops a 3D brain vascular niche model to study GBM invasion and gene signatures, revealing glia-vascular contact influences transcriptional adaptation and poor prognosis.

This study identifies FEN1 as a driver of glioblastoma stem cell survival and temozolomide resistance, showing FEN1 inhibition can enhance TMZ efficacy in aggressive tumors.

This study shows DCX enhances glioblastoma metabolism by regulating glutamine synthesis and metabolism-related genes, supporting tumor proliferation through energy homeostasis.

The paper identifies treatment-resistant persister cells in glioblastoma that exploit macrophage lipid metabolism to sustain tumor growth and immune evasion, suggesting lipid-targeted therapies could improve outcomes.

This paper updates TCGA glioma classifications to align with WHO-2016 and WHO-2021 guidelines using molecular profiling data, achieving high reclassification rates.

This paper identifies CD99 as a therapeutic target in K27M+DMGs, showing that a novel anti-CD99 antibody reduces tumor growth and enhances radiation efficacy in preclinical models.

This study analyzes spinal cord diffuse midline glioma using genomic and transcriptomic data to identify location-specific cellular and molecular features and suggests epigenetic therapies.

This study investigates DEPDC1's role in GBM radioresistance, finding that its downregulation enhances radiosensitivity through NF-κB upregulation.

This study identifies nuclear factor I (NFI) as a driver of dysregulated purine metabolism in DIPG, showing that targeting ATIC reduces tumor progression in mice.

This study shows an oncolytic herpesvirus expressing a CXCR4 antagonist reduces GSC stemness and migration in vitro and in a mouse model.

This paper establishes a humanized mouse model of glioblastoma using patient-derived xenografts to study immune infiltration and tumor heterogeneity, finding immune cell profiles similar to recurrent human GBM.

This study identifies EGR1 as a key driver of sex differences in glioblastoma tumorigenicity, showing it mediates survival and treatment response differences between males and females.

This study identifies CPI203, a BET inhibitor, as a compound that consistently down-regulates DNA synthesis genes across multiple glioblastoma lines.

This study investigates how oncogenic mutations in gliomas influence the tumor microenvironment through integrative multiomic and spatial transcriptomic analysis of glioma samples.

This paper develops a 3D GBM model with pericytes to study TMZ resistance, finding that pericytes increase TMZ resistance in GBM spheroids by upregulating CCL5.

This study investigates the combination of DNA methyltransferase inhibitor decitabine and PD-1 inhibitor in high-risk pediatric brain tumor models, finding improved survival in some subtypes.

This study uses single-cell multiomics to identify regulatory programs and plasticity regulators in glioblastoma, revealing MYT1L as a key repressor of malignant plasticity.

This study identifies CDK9 as a conserved dependency in Myc-driven medulloblastoma and shows that CDK9 inhibition disrupts Myc-driven transcriptional programs, leading to anti-tumor effects.

The paper identifies VAMP5 as a therapeutic target for gliomas with high NDRG4 expression, showing it downregulates PLK1 and other genes, with NDRG4 as a predictor of treatment sensitivity.