Cervical Cancer

P=N/A, N=288, Recruiting, ISA Associates, Inc. | Trial completion date: Jun 2026 --> Mar 2027 | Trial primary completion date: May 2026 --> Jan 2027

P1, N=63, Recruiting, Regor Pharmaceuticals Inc. | Not yet recruiting --> Recruiting

P1/2, N=41, Not yet recruiting, Second Affiliated Hospital, School of Medicine, Zhejiang University

P=N/A, N=750, Active, not recruiting, National Cancer Institute (NCI) | Recruiting --> Active, not recruiting

P3, N=410, Completed, Grupo Español de Investigación en Cáncer de Ovario | Active, not recruiting --> Completed

Mechanistically, transcriptomic and lipidomic analyses reveal that PEG-FA@ZIF-8@FIS exerts its anticancer effects by downregulating aquaporin-3 (AQP3) expression, which subsequently disrupts tumor lipid metabolism. By linking AQP3 inhibition to metabolic impairment via a targeted delivery platform, this work establishes a highly biocompatible and effective translational strategy for cervical cancer intervention.

Piceid exhibited dose-dependent cytotoxicity against HeLa cervical cancer cells, inducing marked morphological alterations, although with a higher IC₅₀ than doxorubicin. These findings suggest that piceid may serve as a promising candidate for multi-target immune-modulatory activity to prevent the progress of Cervical Cancer.

GAS is a rare, distinct, and highly aggressive cervical adenocarcinoma with poor long-term outcomes and limited responsiveness to standard therapy. Improved diagnostic strategies and tailored treatment protocols are urgently needed.

Apoptosis induction was validated by DAPI staining and Annexin V-FITC/PI flow cytometry, while in ovo chorioallantoic membrane assays demonstrated significant inhibition of neovascularization. Overall, these results establish ligand aromaticity as a key factor governing anticancer activity, providing insight into structure-activity correlations and highlighting the potential of Cu(I) complexes as promising candidates for further anticancer therapeutic development.

P=N/A, N=1000, Not yet recruiting, The Cleveland Clinic

Because they require standardized gene-expression inputs and have not undergone prospective clinical validation, they should not be used as standalone tools for clinical diagnosis, risk stratification, or treatment decision-making. Overall, our findings identify candidate transcriptomic markers associated with PTC occurrence and lymph node metastasis and provide a basis for future translational evaluation.

In vivo experiments further confirmed the significant antitumor effects and the favorable safety profile of H101. These findings suggest that the antitumor effects of H101 are associated with the downregulation of HPV16 E6/E7 and the activation of the p53-p21 pathway, involving both p53-dependent and p53-independent mechanisms.