Glioma

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.

P1, N=12, Active, not recruiting, University of Florida | Recruiting --> Active, not recruiting

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.

In conclusion, circNEIL3 stabilizes SPI1 mRNA expression by binding to U2AF2, thereby promoting glioma progression and temozolomide resistance. Implications: Our findings offer a new mechanistic insights into gliomas drug resistance, and targeting the circNEIL3/U2AF2/SPI1 axis represents a promising approach to counteract TMZ resistance in gliomas.

The recent patent data show how selective BRD9 degraders represent a significant step forward in terms of efficacy and selectivity, with promising results in preclinical models of acute myeloid leukemia (AML), synovial sarcoma (SS), and Huntington's disease (HD). Despite several critical issues, the selective degradation of this epigenetic target shows great potential to be an innovative therapeutic strategy.

P1, N=102, Recruiting, Jazz Pharmaceuticals | Trial primary completion date: Dec 2025 --> Jul 2026

P1/2, N=55, Recruiting, Institut de Recherches Internationales Servier | N=42 --> 55

P1, N=78, Active, not recruiting, University of California, San Francisco | Recruiting --> Active, not recruiting

P=N/A, N=50, Recruiting, Massachusetts General Hospital | Trial completion date: Apr 2026 --> Apr 2027 | Trial primary completion date: Sep 2025 --> Sep 2026

P=N/A, N=1650, Recruiting, European Organisation for Research and Treatment of Cancer - EORTC | N=1250 --> 1650 | Trial completion date: Dec 2026 --> Jul 2038 | Trial primary completion date: Aug 2026 --> Dec 2027

P=N/A, N=43, Active, not recruiting, Beijing Neurosurgical Institute