A combination of the ΔVFTK-NG-GM-CSF virus with vinorelbine prolongs mouse survival compared to the treatment of mice with either agent alone. Our study suggests that vinorelbine is a promising agent to combine with oncolytic vaccinia virus for the management of ovarian cancer.

P1, N=70, Recruiting, PharmaMatrix Holdings Ltd | Trial completion date: Dec 2026 --> Dec 2027 | Trial primary completion date: Dec 2026 --> Dec 2027

We identify the microtubule targeting agents lexibulin, colchicine, and combretastatin A-4 as three compounds that bind to the colchicine-binding pocket of the a/b tubulin dimer, and which show increased efficacy in a P47S liver cancer cell line compared to parental cells with WT p53. We find evidence for an unusual mechanism underlying this increased efficacy: our data indicate that the P47S variant shows increased ability to bind to the peptidyl-prolyl isomerase PIN1; this leads to decreased PIN1-cyclin D1 complexes in P47S cells, along with increased cell cycle arrest in response to lexibulin. IMPLICATIONS: These findings support the growing literature that particular mutant forms of TP53 may have specific therapeutic vulnerabilities that can be targetable; improved understanding of these unique vulnerabilities can lead to improved understanding of p53 function.

We induce a patient-derived xenograft model (KT-47) to develop blastemal predominance after chemotherapy and to become resistant to vincristine, actinomycin-D, and doxorubicin (VAD). These findings are validated in additional Wilms tumor models. Overall, resistance is associated with de-differentiation to a stem-like state and is driven by ABCB1 upregulation, suggesting that therapeutic strategies targeting chromatin regulation and drug efflux may be relevant in therapy-resistant Wilms tumor.

P3, N=395, Active, not recruiting, Children's Oncology Group | Trial completion date: Mar 2026 --> Nov 2026

The Cell Counting Kit‑8 assay was used to investigate the effect of SIVA‑1 silencing on drug sensitivity in AGS/DDP cells by measuring the IC50 of Adriamycin, DDP and vincristine. In conclusion, silencing SIVA‑1 has been shown to modify sensitivity to DDP and biological function in drug‑resistant gastric cancer cells, either directly or indirectly. This phenomenon may be associated with the Bcl‑2/BAX‑mediated, mitochondria‑dependent apoptosis pathway.

Furthermore, drug sensitivity profiling identified a positive correlation between the risk gene MTDH and sensitivity to Vincristine and Gemcitabine. This study presents a reliable risk-stratification tool that bridges autophagic mechanisms with personalized chemotherapy guidance. The online version contains supplementary material available at 10.1007/s13205-026-04756-5.

P1, N=24, Completed, Medical University Of Vienna | Recruiting --> Completed

Drug sensitivity analysis revealed that UBE2D3-low tumors were more responsive to vincristine, bosutinib, and ambazone [median inhibitory concentration difference (IC50 diff.) P<0.01], supported by favorable molecular docking affinities. Correspondingly, its loss appears to correlate with advanced disease, an immunosuppressive tumor microenvironment (TME), and unfavorable prognosis. This potential role in modulating immune cell dynamics and drug sensitivity positions UBE2D3 as a promising biomarker for prognostication and personalized therapy selection in KIRC.

P3, N=88, Completed, Cairo University

By establishing specific correlations between biochemical and behavioral parameters, this study provides mechanistic insights into VCR-induced neurotoxicity. It proposes 4-PSQ as a promising therapeutic candidate for preventing or reversing chemotherapy-related cognitive and emotional dysfunctions.

The combination therapy based on the in situ vaccine FOLactis and intravenous PD-1 monoclonal antibody showed a certain degree of anti-tumor effect, and was safe and well tolerated in patients with advanced hepatic malignancies.