temozolomide

This study reveals a new functional role of APOE that leads to chemoresistance in patient treatment. Our findings suggest the potential of combined administration of BLT-1 to overcome TMZ chemoresistance and improve treatments for patients with pNETs.

In vivo, NRTL-24 demonstrated superior tumor-targeting ability, significantly prolonging median survival compared to untreated and temozolomide-treated groups while maintaining favorable safety. This NQO1-responsive linker technology enables precise payload activation in tumor while minimizing off-target effects, establishing NRTL-24 as a promising therapeutic candidate. The strategy provides a blueprint for enzyme-targeted ADC development through tumor- selective linker design.

Furthermore, IFN-γ facilitates erastin- and RSL-3-induced ferroptosis of tumor cells, particularly in temozolomide (TMZ)-resistant cells. Additionally, OMV-C-C@RSL-3 synergistically suppresses GBM growth in vivo. Thus, biosynthetically engineered OMV-C-C integrates intrinsic immunomodulatory activity with ferroptosis enhancement to strengthen glioblastoma immunotherapies, offering a versatile platform to overcome limitations in brain tumor immunotherapy.

A mechanistic pharmacokinetic-pharmacodynamic model incorporating the clock network recapitulated experimental observations and enabled prediction of treatment timing. Our findings highlight the importance of timing in GBM therapy and propose combining circadian profiling with mathematical modeling to personalize GBM chronotherapy.

Additional chorioallantoic membrane (CAM) and brine shrimp lethality tests supported its potent bioactivity, with a lower LD50 (50.24 µg/mL) compared to temozolomide (125.82 µg/mL). These findings indicate that the α-conopeptide from C. planorbis possesses multi-target anticancer activity targeting via SHH and FGFR1 loop signaling pathway, structural stability, and superior cytotoxic potency against GBM, highlighting its potential as a novel marine-derived therapeutic agent.

VAL-083 (30 mg/m2/day) combined with radiation therapy was generally safe and well tolerated. Adverse events aligned with previous studies. This regimen, compared to standard-of-care TMZ, showed potential benefits in terms of disease progression and overall survival. Trial registration ClinicalTrials.gov ID NCT03050736, dated: February 13, 2017.

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

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.

An actinomycin D assay analyzed FBXL16 mRNA stability. RBM7 promotes TMZ resistance by suppressing mitochondrial dysfunction and ferroptosis through destabilization of FBXL16. Targeting the RBM7-FBXL16 axis may represent a novel strategy to overcome GBM chemoresistance.

Glioblastoma (GBM) remains associated with poor outcomes, with a median survival of 15-18 months despite maximal safe resection, radiotherapy, and temozolomide. CAR T-cell therapies are advancing toward bispecific and armored constructs with locoregional delivery, while oncolytic viruses such as DNX-2401 and PVSRIPO demonstrate potential for durable responses in select patients. Looking ahead, progress is likely to arise from biomarker-informed, multimodal regimens that integrate targeted agents, next-generation immunotherapies, and precision-guided strategies, while embedding translational endpoints into trial design to address the complex biology and therapeutic resistance of GBM.

Patients were assigned to three arms: (A) PD-1 antibody plus gemcitabine and docetaxel; (B) PARP inhibitor combined with temozolomide; or (C) tinengotinib (TT-00420), a small-molecule aurora kinase inhibitor currently in clinical trials. This study demonstrated the feasibility of using genomic molecular subtyping to guide the precise treatment of osteosarcoma. We also revealed that the abnormal genomic and transcriptomic profiles caused by MYC amplification could be suppressed by tinengotinib.

Olaparib and temozolomide (OT) combination therapy is in clinical trial evaluation for rhabdomyosarcoma (RMS). The combination of OT + alpelisib also kills RMS cells which are resistant to standard-of-care combination chemotherapy and was effective in preclinical xenograft mouse models at curbing tumor growth. Our work defines a common resistance pathway in RMS and has credentialled PIK3CA/AKT inhibition as a preclinical strategy to kill therapy resistant RMS.