Glioma

P1, N=50, Recruiting, University of California, San Francisco | Suspended --> Recruiting

P1/2, N=68, Recruiting, Washington University School of Medicine | Not yet recruiting --> Recruiting

Ferroptosis inducers (sorafenib, erastin) heightened LDH release and reduced viability, while inhibitors (ferrostatin-1, U0126) had opposing effects...STXBP1 functions as a tumor suppressor in glioma, regulating ferroptosis and EMT. It shows potential as a therapeutic target in glioma management.

Furthermore, static magnetic fields have been reported to increase apoptosis, inhibit proliferation, and may offer a complementary treatment with low toxicity. These findings suggest that magnetic-field-based approaches offer an innovative strategy for GBM treatment.

Drug sensitivity analysis revealed differential half-maximal inhibitory concentration (IC50) values for 20 anticancer agents between risk groups. Our findings suggest that SOX21-AS1 may influence the tumor microenvironment through the modulation of the immune checkpoint CD274, potentially serving as a novel prognostic indicator and a target for immunotherapeutic strategies in GBM.

This multi-omics framework identified ACP2 as a lysosomal regulator of glioma aggressiveness and immune remodeling. ACP2 functions as a robust biomarker of malignancy and may represent a candidate target for therapeutic exploration in glioma.

The proposed FGF-ViT provides a clinically relevant multimodal imaging and generalizable framework for preoperative IDH genotype prediction in gliomas, enabling reliable application across centers and incomplete multimodal conditions.

Achieving meaningful survival benefit for patients with DMG requires a multidisciplinary approach bridging neuro-oncology, advanced imaging, and nanomaterials development. Future research must prioritize four key areas: (1) optimizing NP properties for superior brainstem penetration, (2) leveraging DMG-specific markers for active delivery, (3) integrating theranostics for real-time monitoring, and (4) developing scalable, clinically compliant manufacturing.

Through structure-based virtual screening, our results suggest that Ziprasidone and Apomorphine may disrupt the BARD1-XRCC5 interaction...Our findings unveil a novel LLPS-mediated mechanism by which BARD1 confers TMZ resistance in GBM, positioning it as a prognostic marker and a therapeutic target. Targeting the BARD1-XRCC5 axis presents a promising strategy to overcome chemoresistance.

Collectively, this study identifies the RBP-J/NNMT/SAA3 axis as a critical stromal-driven mechanism of immune evasion in glioma and provides a rationale for targeting metabolic-epigenetic pathways to improve immunotherapy outcomes. Schematic Diagram Illustrating the Molecular Mechanism by Which RBP-J Promotes Immune Evasion in Glioma via Activation of NNMT in CAFs, Leading to H3K27 Demethylation-Mediated Upregulation of SAA3 and Subsequent Reprogramming of M2 Macrophages.

MET fusions are actionable oncogenic drivers across several cancers, and their detection has therapeutic relevance with approved inhibitors. This case expands the spectrum of MET-driven CNS tumors and suggests that CLIP2::MET fusion may represent a distinct molecular subset of glioneuronal tumors relevant to precision oncology.

However, elevated expression of poliovirus receptor (PVR) and the immune checkpoint T-cell immunoreceptor with immunoglobulin and ITIM domain (TIGIT) on tumor-infiltrating leukocytes suggests a potential resistance mechanism to virotherapy. Combining rQNestin34.5 v.2 with TIGIT blockade enhances therapeutic efficacy compared to monotherapy, identifying IDH1-R132H as a potential predictive biomarker for oncolytic virotherapy response.