P2, N=33, Suspended, Weill Medical College of Cornell University | Trial completion date: Dec 2025 --> Jun 2026 | Recruiting --> Suspended | Trial primary completion date: Dec 2025 --> Jun 2026
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Trial completion date • Trial suspension • Trial primary completion date
This study highlights the prognostic significance of lncRNAs associated with PCD in glioma and provides computational evidence for their potential as therapeutic targets. While the results suggest novel avenues for treatment development, they must be interpreted cautiously due to the lack of experimental validation. Future studies should aim to validate these results through controlled clinical trials and explore underlying molecular mechanisms.
This platform comprises GIC-targeting exosomes that carry siRNA for Notch1 and mitoxantrone to reduce the stemness of GICs and kill residual GICs and glioma cells, respectively, and an immune activator (interleukin-12), which can remodel the immunosuppressive tumor microenvironment, ultimately suppressing postoperative GBM relapse. Our work provides a perspective into the effective inhibition of postresection recurrence of GBM.
These results highlight the potential of stratified, multi-organ evaluation frameworks with multi-evaluator consensus in LLM benchmarking for clinical applications. Overall, this consensus-based approach demonstrates that locally deployed LLMs can provide a transparent, accurate, and auditable solution for integration into real-world pathology workflows such as synoptic reporting and cancer registry abstraction.
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Journal
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TP53 (Tumor protein P53) • ROS1 (Proto-Oncogene Tyrosine-Protein Kinase ROS)
Clinically, the Notch ligand JAG1 was upregulated in recurrent high-grade glioma patients treated with the oHSV CAN-3110 and correlated with poor prognosis. Heightened EGFR activation in senescent cells was a mechanism to escape cell death, which created a unique opportunity for cetuximab as a senolytic agent. Combination therapy reduced EGFR signaling and induced macrophage-mediated antibody-dependent cellular cytotoxicity, thereby increasing the anti-tumor therapeutic efficacy of OD-0J1.