Glioma

P1, N=20, Recruiting, University of Alabama at Birmingham | Trial completion date: Feb 2026 --> Feb 2028 | Trial primary completion date: Feb 2026 --> Feb 2028

P1, N=50, Recruiting, Shanghai Juncell Therapeutics | Trial completion date: May 2025 --> May 2027 | Trial primary completion date: Dec 2024 --> Dec 2026

Despite poor overall outcomes, incremental progress across targeted, immune, and delivery-based approaches supports a patient centered strategy emphasizing clinical-trial enrollment, molecular profiling and symptom focused care.

Both in vitro and in vivo experiments demonstrated that exosomal miR-151a-3p promotes glioma cell migration, invasion, proliferation, and epithelial‒mesenchymal transition, thereby increasing tumour aggressiveness. These findings highlight the NamiR-151a-3p/PDE4D/FAK/YAP axis as a promising therapeutic target for GBM.

This strange case was similar to a previously reported tumour reported in the literature, which clustered perfectly with our case. Further reports are needed to confirm the hypothesis that this neoplasm represents a novel tumour type.

Furthermore, corynoline treatment significantly inhibited the growth of GBM in vivo and was shown to modulate the STAT3/Bcl-2 signalling pathway. These results suggest that corynoline exerts antitumour activity against GBM by inhibiting the STAT3/Bcl2 pathway, indicating that corynoline might be a promising agent for the treatment of GBM.

WP1066 is safe, has minimal toxicity, and induces anti-tumor immune responses in pediatric brain tumor patients. Phase II investigation of WP1066 at the MFD in this patient population is warranted.

N4BP2 promoted genome rearrangements (including chromothripsis), formation of extrachromosomal DNA (ecDNA) in drug-induced gene amplification, tumorigenesis, and tumor cell proliferation in an induced model of human high-grade glioma. Analysis of more than 10,000 human cancer genomes revealed elevated N4BP2 expression to be predictive of chromothripsis and copy number amplifications, including ecDNA.

Mechanistically, P4HB promoted STAT3 phosphorylation in microglia, driving their pro-tumorigenic M2 phenotype. These findings establish P4HB as a regulator of glioma progression via IL-6/STAT3-mediated microglial polarization, highlighting its potential as a therapeutic target for GBM.

Treatment was well tolerated, with only grade 1-2 adverse events reported. Larger randomized studies are needed to validate efficacy and long-term safety.

Contemporary glioma cohorts showed prolonged survival outcomes compared to historical cohorts. An association between anatomic localization and molecular subtypes was also established in this Chinese glioma cohort.

This multimodal approach identified a corpus callosum-specific invasion signature in glioma stem-like cells, revealing how local microenvironmental cues shape transcriptional reprogramming during infiltration. These findings provide new insights into the spatial heterogeneity of gliomas and highlight potential molecular targets for therapies designed to limit tumor spread through white matter tracts.