Glioblastoma

SFRT was associated with longer survival in non-elderly patients, possibly reflecting selection of poorer-risk patients for HFRT. In elderly patients, HFRT was noninferior regardless of MGMTp status, supporting its use as a less intensive approach with comparable survival and reduced treatment burden.

P=N/A, N=20, Enrolling by invitation, King's College Hospital NHS Trust

Importantly, CD206 expression was not increased in M1 macrophages after contact with spheroids, and was lower in M2 macrophages loaded with B4C nanoparticles compared to control M2 macrophages. BMDMs are promising carriers of B4C nanoparticles for BNCT due to their ability to cross the in vitro BBB model toward the glioblastoma microenvironment.

FAM135B acts as a critical negative regulator of GBM angiogenesis, whose low expression contributes to high tumor angiogenic potential and poor patient prognosis. Mechanistically, HNF4A transcriptionally upregulates FAM135B, which then binds to and stabilizes the IKK complex, inactivating the NF-κB signaling pathway and downregulating IL-6 expression, ultimately inhibiting the JAK/STAT-mediated angiogenic process. FAM135B also remodels the GBM tumor microenvironment by reducing M2 macrophage infiltration. Targeting the HNF4A/FAM135B/NF-κB/IL-6 signaling axis provides a novel and promising therapeutic strategy for GBM anti-angiogenic therapy.

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.

We further found that TNFα-NFκB mediated the activity of CXCL8 and suppressed ferroptosis, leading to the malignant biological behavior of GBM cells. The CXCL8-TNFα-NFκB axis restrains the TME of ferroptosis and leads to poor prognosis in GBM patients, indicating that it is a potential biological mechanism for GBM.

P=N/A, N=250, Recruiting, University of Colorado, Boulder

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

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

Gene set enrichment analysis linked high PS to immune-evasive pathways, including Notch and IL-6/JAK/STAT3 signaling, along with increased expression of DNA repair gene RAD50, suggesting a potential association with radiotherapy response. This AI-based pathomics framework offers a robust and interpretable tool for immunoprofiling and outcome prediction, paving the way for precision radiotherapy and Treg-targeted therapeutic strategies in glioblastoma.

In this study, we observed that NF1 mutation was associated with poorer OS in a cohort of Korean GBM patients across several analyses. Given the limited sample size (N = 11), these findings should be interpreted as exploratory; however, they provide hypothesis-generating evidence suggesting that NF1 may serve as a potential complementary biomarker in assessing the prognosis of GBM patients in future clinical evaluations.

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.