The data obtained indicated that PEE, either alone or in combination with MET, has strong neuroprotective potential against STZ/HFD-induced diabetes. These safeguarding effects are probably because of its strong anti-inflammatory and antioxidant properties.

P1, N=1033, Completed, Massachusetts General Hospital | Active, not recruiting --> Completed

This study suggests that the Tak-Met-LEME combination treatments may inhibit BC progression by increasing CD8+ CD28+ T cell population in tumor tissue and decreasing tumor progression.

P2, N=86, Completed, Wake Forest University Health Sciences | Active, not recruiting --> Completed

P=N/A, N=72, Completed, Cairo University | Not yet recruiting --> Completed

P4, N=14, Active, not recruiting, University of Virginia | Recruiting --> Active, not recruiting | N=20 --> 14 | Trial completion date: Apr 2026 --> Jul 2026 | Trial primary completion date: Apr 2026 --> Jul 2026

However, the killing activity of CD126 CAR-T cells against RPMI 8226 cells decreased after co-culture with macrophages, likely due to interactions between the CAR-T cells and the macrophages. These findings highlight the significant role of macrophages and inflammatory responses in MM progression and in modulating the efficacy of CAR-T cell therapy, providing valuable insights for the optimization of immunotherapeutic strategies.

By combining clinical outcomes with targeted biomarker analyses in a randomized design, this pilot study will assess whether taVNS alleviates metformin-associated GI intolerance without impairing glycaemic efficacy, and will provide feasibility data, effect-size estimates, and biomarker selection for future confirmatory trials. Trial registration International Traditional Medicine Clinical Trial Registry (ITMCTR) http://itmctr.ccebtcm.org.cn/, Identifier: ITMCTR2025001086.

Our findings showed that Vimentin overexpression and the EMT phenomenon are strongly associated with poor OS and DFS in resectable PDAC, underscoring their potential as prognostic biomarkers and therapeutic targets.

Further analyses identified the METTL3/ACC1/FASN axis as a critical downstream pathway, with metformin suppressing m6A modification and expression of Fatty acid synthase (FASN) and Acetyl-CoA carboxylase 1 (ACC1) transcripts - effects reversed by METTL3 overexpression. These findings establish METTL3 as a central mediator of metformin's metabolic and antiproliferative activities in HCC, uncovering a previously unappreciated epitranscriptomic mechanism by which metformin impedes tumor progression.

BMI and blood variables did not identify subgroups with luminal or triple negative bc who benefitted from metformin nor those with HER2 positive bc who did not benefit.

P3, N=212, Not yet recruiting, Fundación Instituto de Investigación Sanitaria de Navarra