temozolomide

P2, N=75, Recruiting, Institut de cancérologie Strasbourg Europe | Not yet recruiting --> Recruiting | Trial completion date: Mar 2027 --> Jul 2029 | Trial primary completion date: Mar 2027 --> Jul 2028

P2, N=23, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Mar 2026 --> Nov 2026

P=N/A, N=100, Not yet recruiting, Hospices Civils de Lyon

We found that β-lapachone acts synergistically with TMZ to inhibit GBM cell proliferation, epithelial-mesenchymal transition (EMT), and angiogenesis by suppressing NF-κB activation through blockade of p65 nuclear translocation. These results provide a solid preclinical foundation for combining β-lapachone with TMZ as a promising strategy to counteract TMZ resistance in GBM.

P1/2, N=90, Recruiting, St. Jude Children's Research Hospital | Active, not recruiting --> Recruiting | N=46 --> 90

P=N/A, N=110, Recruiting, Istituto Oncologico Veneto IRCCS | Not yet recruiting --> Recruiting

CRT significantly improves survival in IDH-wt/TERTp-mut grade 2 to 3 gliomas with favorable safety.

Our study offers the first proof that XHP causes AMPK inhibition-mediated mitochondrial dysfunction, activates both the NLRP3/caspase-1/GSDMD and caspase-3/GSDME signaling, and promotes pyroptosis in GECs, thereby effectively suppressing tumor angiogenesis and prolonging survival of tumor-bearing mice when combined with TMZ.

POT1-AS1 promotes TMZ and radiation resistance in GBM by regulating ferroptosis through the IGF2BP2/GPX4 axis. Targeting this pathway may offer a new therapeutic strategy for overcoming GBM treatment resistance.

The identified qMSP cut-off value (0.242) based on the procedure described in this study provides a robust prognostic stratification tool for GBM patients. High MGMT methylation correlates with improved survival, supporting its integration into clinical decision-making. Further multi-center validation studies are warranted to establish standardized MGMT assessment methodologies.

Here we show that PGC1α (Peroxisome Proliferator-activated Receptor Gamma coactivator-1 Alpha) upregulates Mfn2 (Mitofusin 2) enhancing mitochondrial-fusion in GBM cells contributing to survival under profound Temozolomide (TMZ) stress...Notably, this further corroborates with our observations in the patient samples and clinical data where upregulation of Mfn2 was concurrently observed with elevated levels of PGC1α simultaneously leading to poor prognosis. Thus, this study provides critical insights into the molecular regulation of mitochondrial dynamics-dependent survival mechanisms in GBM that could further be exploited to design future therapies.

MB-FUS plus temozolomide is a safe combinatorial therapeutic approach for individuals with high-grade glioma, with the potential to improve survival and enable non-invasive plasma biomarker-based disease surveillance (sono-liquid biopsy), warranting randomised controlled trials.