This exploratory pharmacodynamic biomarker analysis identifies three 3-cytokine panels associated with prognostic risk stratification in metronomic chemotherapy for metastatic gastrointestinal cancer. As this single-arm trial cannot distinguish prognostic from predictive value, findings are hypothesis-generating. Prospective external validation is required before clinical translation, and exploration in combination with immune checkpoint inhibitors is warranted.
The system is constructed using celecoxib (CXB)-loaded poly(d,l-lactide-co-glycolide) (PLGA) nanoparticles and subsequently camouflaging them with mesenchymal stem cell membranes with high CXCR4 expression...This dual modulation of the chemokine network significantly improves the therapeutic efficacy of CAR-T cells against solid tumors. Our approach represents a promising strategy for advancing CAR-T cell therapy toward clinical applications for soild tumors.
By integrating genetic causal inference, in vitro experiments, and network pharmacology, our study systematically reveals that celecoxib may exert therapeutic effects by targeting against cervical cancer by targeting NEU1 and modulating CD25 on CD45RA+ CD4+ non-regulatory T cell-related immune pathways. This finding highlights both the novelty and the translational potential of this approach.
P2/3, N=58, Terminated, Wake Forest University Health Sciences | N=100 --> 58 | Suspended --> Terminated; Study initially suspended following an audit and need of amendment to address deficiencies. PI requested to terminate due to lack of support.
This study provides a diagnostic model for osteosarcoma metastasis and proposes that MYC/TNFRSF21 drive metastasis via a "necroptosis‑immune exemption" axis, suggesting new therapeutic strategies.
Moreover, intervention with the PTGS2 inhibitor celecoxib counteracted the tumor-promoting functions of OTX1 and demonstrated tumor-suppressive effects in in vivo OS models. Herein, results demonstrate that OTX1 drives OS malignant progression by transcriptionally activating PTGS2, which in turn modulates apoptosis- and invasion-related molecules. Targeting the OTX1/PTGS2 axis may represent a promising therapeutic strategy for OS, particularly in high-risk patients with aberrant OTX1 expression.