paclitaxel

Our real-world study provides preliminary evidence that bevacizumab may confer differential prognostic benefits in AOC patients undergoing NAC followed by IDS, contingent upon tumor MVD quantified via CD34 immunohistochemistry, though it is important to acknowledge the lack of independent external validation for these findings. This potential biomarker-driven therapeutic heterogeneity preliminarily underscores the possibility of developing adaptive treatment algorithms that stratify patients based on angiogenic susceptibility profiles, which may lay a foundation for exploring precision administration of anti-VEGF therapy in a cost-effective paradigm.

Non-cytotoxic concentrations of olverembatinib significantly increased the sensitivity of ABCB1-overexpressing cells to paclitaxel and vincristine. Additionally, olverembatinib activated the ATPase activity of ABCB1 in a concentration-dependent manner and exhibited potent binding affinity to ABCB1 in docking simulations. These findings suggest that olverembatinib holds promise as a potent reversal agent for MDR, paving the way for its integration into novel combination chemotherapy regimens to improve cancer treatment outcomes.

These findings suggest that rupestonic acid is a promising candidate for HCC treatment. They also underscore the potential of rupestonic acid in the design and development of lead compounds for HCC treatment and identify ENO1 as a viable therapeutic target.

P2, N=162, Completed, MedSIR | Active, not recruiting --> Completed

P2, N=20, Completed, University of Nebraska | Active, not recruiting --> Completed | Trial completion date: Nov 2026 --> Dec 2025

Paclitaxel, gemcitabine, and cisplatin (all p < 0.05) may be more useful in EC patients with high expression of targeted srlncRNAs in the GDSC database. The EC-18 PDO was more resistant to three drugs, which aligned with clinical observation. The srlncRNA signature (AL121906.2, AP002761.4, BX322234.1, LINC00662, LINC00908, VIM-AS1, and ZNF236-DT) could guide prognosis prediction and treatment choices for EC patients.

Docetaxel (DTX), a chemotherapeutic agent derived from paclitaxel (PTX), has received approval from the US Food and Drug Administration (FDA) for the treatment of BC and various other malignancies...Furthermore, key challenges limiting clinical translation are analysed. This paper provides a theoretical foundation and practical guidance for rationally designing DTX nanomedicines, accelerating their transition from laboratory research to clinical application and offering new hope for BC treatment.

P3, N=130, Not yet recruiting, AIDS Malignancy Consortium | Trial completion date: Dec 2029 --> Nov 2027 | Trial primary completion date: Mar 2028 --> Dec 2026

Our findings indicate that the FBXW7-MAP7 axis plays a critical role in regulating the malignant phenotypes and PTX sensitivity of PTX-resistant LUAD cell lines, suggesting a potential therapeutic strategy to improve the efficacy of PTX-based therapies in LUAD.

DUO-O met its primary PFS endpoints for first-line durvalumab plus carboplatin/paclitaxel and bevacizumab followed by durvalumab, bevacizumab plus olaparib maintenance versus carboplatin/paclitaxel and bevacizumab followed by bevacizumab in the non-tBRCAm HRD-positive and non-tBRCAm ITT populations. Further insight into long-term benefit is anticipated with additional follow-up.

This review concludes that natural compound-NPs therapies constitute a transformative and synergistic strategy for BC therapy. To realize their full clinical potential, interdisciplinary collaboration is essential for optimizing manufacturing processes and validating predictive biomarkers. Future research efforts must focus on the rational design of intelligent, multi-responsive nanosystems that are specifically tailored to the molecular subtypes of BC. Ultimately, establishing robust regulatory frameworks and scalable manufacturing pathways is imperative to successfully bridge the gap between promising preclinical results and tangible clinical benefits for patients.

A967079 (10 µM), a selective TRPA1 antagonist, significantly lessened the cytotoxicity caused by PTX. Additionally, PTX causes sensorimotor and cognitive neuropathy, which was reversed by Li+ treatment. These findings suggest that Li+ may act as a neuroprotective agent, preventing neuronal damage caused by PTX via TRPA1 channel pathways.