temozolomide

Our findings reveal an intrinsic SLFN11-dependent vulnerability in ccRCC that synergizes with alkylating agents to induce an acquired PARP-1 dependency, thereby sensitizing BRCA1/2-WT tumors to PARP inhibition. Therefore, this work uncovers a potential therapeutic strategy for targeting SLFN11-high kidney cancers.

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

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.

Post-operative re-RT appears to be associated with enhanced survival and minimal toxicity in patients with rGBM following temozolomide chemoradiation. Our study suggests a novel clinicogenetic criterion for re-RT after re-OP in rGBM, which requires further validation.

Overall, our findings suggest that TMZ may induce oncogenic miRNA expression as part of an adaptive response, while ruxolitinib may counteract this effect. Targeting miRNA-mediated regulatory networks in combination with pathway inhibition may represent a promising strategy to overcome therapeutic resistance in glioblastoma.

Despite current standard therapies, including surgery, radiotherapy, and temozolomide treatment, median survival remains less than 15 months, underscoring the urgent need for novel therapeutic strategies, with microRNAs representing a promising approach...Our study indicates that miR-219 may modulate tumor-related processes through the negative regulation of target genes such as REST and AKAP13, while its overexpression appears to reinforce the effects of irradiation and TMZ by reducing malignant properties in GBM cells, in both 2D and 3D, and in increasing apoptotic susceptibility in GBM spheroids. Collectively, these findings support further investigation of miR-219 in the context of GBM therapy and suggest that it may contribute to improved treatment responses and reduced treatment resistance.

P1, N=10, Active, not recruiting, University of Chicago | Trial primary completion date: Jun 2025 --> Dec 2026

Accordingly, these genes can be incorporated into clinical prognostic models and provide panels of genes for selecting personalized and appropriate therapeutic approaches. Overall, key genes can be suggested as influential genes associated with temozolomide-resistant glioblastoma cell lines.

P1/2, N=10, Completed, University Hospital, Antwerp | Active, not recruiting --> Completed | Trial completion date: Jun 2027 --> Aug 2025 | Trial primary completion date: Jun 2027 --> Aug 2025

P2, N=27, Recruiting, Tianjin Medical University Cancer Institute and Hospital | Not yet recruiting --> Recruiting

P1/2, N=20, Active, not recruiting, University Hospital, Antwerp | Trial completion date: Dec 2025 --> Jul 2027 | Trial primary completion date: Dec 2024 --> Jul 2027

P2, N=70, Recruiting, Abramson Cancer Center at Penn Medicine | Trial completion date: May 2026 --> Jul 2028 | Trial primary completion date: May 2026 --> Jul 2028