Glioma Diagnosis and Treatment

This study identifies KHDRBS3 as a factor promoting self-renewal and temozolomide resistance in glioblastoma stem-like cells, suggesting it as a potential therapeutic target.

This study identifies DNA-methylation and RNA-expression signatures that improve grading of IDH-mutant astrocytomas beyond current methods.

This study shows ERK signaling promotes resistance to TRK inhibitors in NTRK fusion-driven glioma mouse models and suggests MEK inhibition as a potential combination therapy.

This study develops a repeat-biopsy model in mice combined with ultra-fast cycling technology to analyze immune response changes in gliomas over time and in response to treatment.

The paper identifies hybrid cells in human glioma with both neuronal and glial electrophysiological and transcriptomic features using Patch-sequencing and a new computational tool.

This study identifies the trigeminal root entry zone as a pontine-specific niche that supports gliomagenesis driven by H3.1K27M and co-occurring mutations.

This study shows that PDGF-BB overexpression in p53 null OPCs increases H3K27me3 and promotes proliferation by altering transcription.

This study shows that oncometabolite D-2HG drives enhancer hypermethylation in IDH-mutant gliomas, leading to hyporesponsive microglia and reduced immune reactivity.

This study generates human cerebellar organoids to model medulloblastoma subgroups G3 and G4, showing their ability to sustain tumor growth and respond to anti-tumour compounds.

This study identifies LOX-mediated cleavage of the vascular matrix as a mechanism driving glioblastoma infiltration and suggests targeting LOX as a therapeutic strategy.

This study shows thyroid hormone promotes differentiation of medulloblastoma cells, reducing tumor growth by reversing EZH2-mediated repression of NeuroD1.

The paper identifies cerebellar damage patterns in children with brainstem tumors and links them to specific behavioral disorders using segmentation and predictive modeling.

This study identifies two cortical thickness subtypes in brainstem tumor patients using normative modeling, linking them to tumor growth patterns and clinical outcomes.

This study identifies a neurovascular progenitor cell type in glioblastoma that links distinct malignant lineages and influences tumor composition and survival.

This paper applies a fetal neural progenitor cell classification to adult diffuse gliomas, finding distinct THY1-CD24-EGFR+ and THY1-CD24-EGFR- cell populations across IDH mutant and IDHwt gliomas.

This study shows that constitutive TrkB kinase signalling, independent of ligand, reduces actin filopodia dynamics and cell migration, and can be inhibited by Trk inhibitors.

This study identifies cellular and molecular mechanisms of tertiary lymphoid structure (TLS) formation in glioblastoma, showing TLS correlate with improved survival and are driven by CD4 T cells expressing lymphotoxin β.

This paper uses an in-silico model to show that localized biopsies and macrophage density at the tumor edge improve predictions of recurrence in high-grade gliomas.

This study integrates MRI and genomic data from GBM patients to identify common molecular signatures and link them to tumor locations, highlighting dysregulated neurotransmitter receptors and synaptic activity.

This study identifies recurring cell states across adult-type diffuse gliomas and reveals a shared astrocyte-like glioma stem cell population driving intratumoural heterogeneity.

This study shows imipridones induce GABA accumulation in diffuse midline gliomas, which can be used for non-invasive imaging and therapy.

The paper shows how gene regulatory network topology in glioma stem-like cells influences drug resistance and treatment escape, suggesting strategies to overcome resistance through combinatorial therapies.

The paper identifies sex differences in microglial inflammatory responses in glioblastoma, showing that genes on the inactive X chromosome drive these differences.

This study identifies CTPS1 as a vulnerability in MYC-driven medulloblastoma and shows that combining CTPS1 and CHK1 inhibition synergistically reduces tumor growth in vivo.

This study uses spatial transcriptomics to analyze a DIPG-infiltrated brainstem, identifying invasion markers and ligand-receptor pairs involved in tumour-TME crosstalk.

This paper develops a validated protocol for using Oxford Nanopore methylation sequencing on FFPE samples to classify brain tumors, enabling point-of-care diagnosis.

This study identifies PIEZO1 as an oncogene in glioma that promotes astrocyte reactivity and is associated with worse prognosis in male patients.

This paper develops a method using migratory cortical interneuron precursors to deliver therapeutic agents directly to glioblastoma, improving survival in mice.