Glioma Diagnosis and Treatment

This study identifies the neuronal H+-Asic1a axis as a regulator of neuron-glioma synapses, showing reduced tumor growth in Asic1a-deficient mice.

The paper develops EGFRvIII-targeting peptides using in silico modeling and phage display to detect and target refractory glioblastoma tumors without affecting wild-type EGFR.

The paper identifies an epigenetic neural signature in glioblastoma that correlates with poor prognosis and therapeutic vulnerability.

OpenPBTA provides a collaborative platform to genomically characterize 1,074 pediatric brain tumors and 22 cell lines, offering analysis modules and somatic datasets for research and clinical applications.

This study uses an explainable AI model to classify chronic inflammatory responses as prognostic markers for glioma using TCGA data, identifying five inflammatory profiles linked to survival outcomes.

This study develops human iPSC-derived tumor models to investigate the cooperative effects of H3.3K27M and PDGFRA mutations in DMG, identifying therapeutic vulnerabilities.

The paper identifies three biomarkers predicting response to NK cell immunotherapy in recurrent GBM using immune profiling and validation techniques.

This study shows dopamine receptor antagonists have sex-dependent effects on neural stem/progenitor cells, potentially reducing radiation-induced cognitive decline in glioblastoma treatment.

The paper combines five RNA-seq datasets to create a reference landscape of human brain tissues and tumors, enabling comparative gene expression analysis across normal and neoplastic samples.

This study identifies FCGRT as a prognostic factor in glioma, showing its role in promoting tumor proliferation and invasion through interaction with CIgG.

This paper introduces a conditional H3.3K27M mutation in mice to model paediatric diffuse intrinsic pontine glioma, showing dwarfism with intact growth hormone signaling.

This paper develops a functional precision medicine approach using metabolic imaging to predict glioblastoma treatment response early in ex-vivo organoids, identifying responder and non-responder groups and a new molecular signature.

The paper uses single-cell analysis of GBM patient samples and xenografts to identify regulatory networks driving treatment-induced tumor evolution and proposes a framework for precision medicine.

The paper develops an in silico disease model for DIPG with TP53 and H3K27M mutations to identify potential drugs for repurposing.

This study introduces an individual-level structural abnormality detection method for frontal glioma patients and finds unique and shared atrophy patterns linked to molecular biomarkers.

This study demonstrates a device that attracts and traps glioma cells in vitro and in vivo using Hepatocyte Growth Factor (HGF) as the attractive medium.

This study shows that synaptic proteins in glioblastoma cells contribute to tumor progression and lethality in Drosophila models.

The paper identifies PD1 signaling regulation as a prognostic marker in glioblastoma using gene regulatory network analysis across two cohorts.

This study investigates the role of TCF12 in oligodendroglial cell proliferation and its regulation of signaling pathways in gliomas.

This study evaluates the feasibility and survival impact of applying the clinical standard of care to glioblastoma mouse models, showing improved outcomes when treatments are combined.

This paper shows that combining ONC201 with radiation improves GBM treatment efficacy by targeting glioma-initiating cells in vitro and in vivo without increased toxicity.

The paper identifies ROS1 fusions in various glioma types through genomic and transcriptomic analysis, showing they are not restricted to specific subtypes.

The paper identifies recurrent structural variations in the lncRNA gene CCDC26 in DIPG patients, linking them to increased expression and association with MYC and proliferation.

This study identifies how PI3K/mTOR signaling and Trp53 loss determine the heterogeneity and excitability of BRAFV600E-induced brain tumors in mice.

The paper identifies functionally distinct subgroups of glioblastoma stem cells (GSCs) by analyzing cross-species chromatin accessibility, showing that epigenetic regulation is controlled by developmental origin.

This study shows that combining quetiapine, atorvastatin, and radiation extends survival in glioblastoma mouse models by exploiting a metabolic vulnerability.

This paper shows that glioblastoma produces ImpL2, which disrupts neuronal insulin signaling, leading to neurodegeneration and premature death, and that restoring insulin signaling can rescue these effects.

The paper introduces the Chinese Glioma Genome Atlas (CGGA), a resource providing genomic and clinical data for glioma patients, along with analysis tools for data exploration and research.

This paper demonstrates that overexpressing neural transcription factors can convert glioblastoma cells into neurons, inhibiting their proliferation and offering a potential therapeutic strategy.