Glioma

Combined radiomics-clinical models achieved numerically higher performance, but current evidence remains limited by retrospective designs, internal validation, and methodological heterogeneity. These models should be considered adjunctive rather than replacement tools, and prospective multicenter external validation with standardized workflows is required before clinical implementation.

Although paraspinal peripheral nerve sheath tumors (including neurofibromas and schwannomas) occur frequently in the NF conditions, there is also a risk of intramedullary spinal cord tumors in people with NF1 and NF2-SWN. Here, we discuss the presentation and diagnosis of the various forms of NF, the intramedullary spinal cord tumors that occur in NF1 and NF2-SWN, and their diagnostic and treatment considerations.

Mechanistic analysis revealed that the active peptide uniquely competes with Wnt5a, the endogenous ligand of ROR1, for receptor binding. To our knowledge, this report provides the first evidence implicating ROR1/2 as a viable therapeutic target in DIPG and establishes macrocyclic peptides as a promising modality for its pharmacological inhibition.

The review addresses rationale testing for BRAF alterations, selection, and monitoring of targeted therapies, management of treatment-related toxicities, approaches to resistance, and priorities for future research. It aims to provide practical, evidence-based guidance for clinicians while highlighting gaps to inform prospective studies.

P1, N=35, Completed, Shenzhen Zhenxing Medical Technology Co., Ltd

P=N/A, N=40, Recruiting, Hospital Italiano de Buenos Aires

P1/2, N=30, Recruiting, Aveta Biomics, Inc. | Trial completion date: Jan 2026 --> Jun 2027 | Trial primary completion date: Dec 2025 --> Dec 2026

In vitro, MRC2 depletion reduced proliferation, clonogenicity, migration, and invasion, accompanied by decreased CDK4 and CDK6 protein levels and changes in β-catenin and EMT-related markers. Together, these findings support MRC2 as a candidate prognostic biomarker associated with aggressive glioma phenotypes and warrant further mechanistic and in vivo investigation.

Our study defines a clinically relevant inflammatory cell death signature that integrates tumor cell state plasticity, genomic instability, and immune microenvironment dynamics in glioma. PA.Sig may serve as a prognostic biomarker and provide a rationale for combinatorial strategies targeting cell death pathways and immune modulation.

In addition, EV-enriched non-coding RNAs, such as miR-25-3p, miR-3591-3p, and lncRNA H19, regulate PI3K-AKT-mTOR, JAK2/STAT3, and related pathways to promote myeloid reprogramming, immune escape, and temozolomide resistance...Targeting EV biogenesis, release, uptake, or specific immunosuppressive cargoes may provide promising opportunities to overcome resistance and improve immunotherapy for glioma. Future studies should focus on deciphering EV-mediated immune regulatory networks, identifying robust glioma-specific EV biomarkers, standardizing EV detection platforms, and developing precision EV-based therapeutic strategies.

In recent years, derivatives of olaparib and rucaparib have been radiolabeled for noninvasive imaging of PARP1 expression and targeted radionuclide therapy of PARP-expressing tumors. Methods for the chiral separation of precursor permitted radiolabeling of [211At]talazoparib without the need for separation from its inactive 211At-labeled enantiomer after radiolabeling, and scaled-up production was optimized. [211At]talazoparib exhibited promising potential as a targeted radiotherapeutic, particularly for settings where locoregional administration is warranted.

Additionally, the manuscript emphasizes novel therapeutic strategies, such as nanomedicine, oncolytic virotherapy, immunotherapy, tumor-treating fields, and phytochemical-based interventions, as well as the increasing significance of artificial intelligence and machine learning in diagnosis and personalized treatment. Lastly, this review integrates mechanistic and translational insights to establish a framework addressing blood-brain barrier limitations, therapeutic resistance, and immune evasion, thereby facilitating the advancement of precision medicine approaches for enhanced GBM outcomes.