Pancreatic Adenocarcinoma

P1, N=18, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Apr 2026 --> Apr 2027

P2, N=42, Completed, HonorHealth Research Institute | Active, not recruiting --> Completed

P=N/A, N=150, Not yet recruiting, Assistance Publique - Hôpitaux de Paris

P=N/A, N=42, Chongqing Medical University First Affiliated Hospital; Chongqing Medical University First Affiliated Hospital

P1, N=398, Recruiting, Astellas Pharma Global Development, Inc. | Trial completion date: May 2027 --> May 2028 | Trial primary completion date: Nov 2026 --> May 2028

P2, N=40, Completed, HonorHealth Research Institute | Active, not recruiting --> Completed | N=24 --> 40 | Trial completion date: Aug 2025 --> Nov 2025

Expression of glutathione peroxidase 4 and acyl-CoA synthetase long-chain family 4 and Hippo signaling proteins, TAZ and YAP, were also altered. PDK4 influenced ferroptosis in pancreatic cancer cells via an effect on Hippo signaling with implications for gemcitabine resistance.

Overexpression of CDC6 significantly promoted glycolysis and tumor progression in pancreatic cancer, whereas these pro-tumor effects were markedly abrogated by THBS1 knockdown. Collectively, our findings demonstrate that CDC6/THBS1/AKT signaling drives glycolysis and accelerates pancreatic cancer progression, suggesting that the CDC6/THBS1/AKT axis may serve as a promising therapeutic target for pancreatic cancer.

P1/2, N=20, Not yet recruiting, University of Arkansas

P=N/A, N=10, Completed, CCTU- Cancer Theme | Active, not recruiting --> Completed

P1, N=330, Recruiting, Pfizer | Trial completion date: Sep 2028 --> Jan 2029 | Trial primary completion date: Sep 2027 --> Jan 2028

We identified cytarabine and methotrexate as significantly more effective in the 9p21 compromised BLCA cells. Analysis of morphological alterations further supported a genotype-specific activity of nucleoside analogs, nominating gemcitabine as a drug with greater efficacy in this context...Synergy between cytarabine and inhibitors of PRMT5 (MRTX1719) and MAT2A (AG-270) was mediated by a differential activation of DNA damage and replication stress markers, suggesting an exploitable vulnerability. In fact, rational drug combinations with ATR/CHK1 pathway inhibitors increased efficacy while maintaining 9p21-specificity. Finally, we confirmed the effectiveness of these combinations in cell models of pancreatic adenocarcinoma and pleural mesothelioma, two tumor types with high prevalence of MTAP loss and, most notably, in bladder cancer patient-derived organoids, underscoring the strong translational potential of our findings.