Pancreatic Cancer

P2, N=37, Recruiting, Ningbo Medical Center Lihuili Hospital

P=N/A, N=200, Recruiting, ARTIDIS AG

P=N/A, N=2048, Completed, Medizinische Hochschule Brandenburg Theodor Fontane

P1, N=300, Recruiting, M.D. Anderson Cancer Center | Active, not recruiting --> Recruiting | N=117 --> 300

P=N/A, N=300, Active, not recruiting, Massachusetts General Hospital | Trial completion date: Dec 2025 --> Dec 2026 | Trial primary completion date: Dec 2025 --> Dec 2026

P=N/A, N=700, Recruiting, Masaryk Memorial Cancer Institute | Trial primary completion date: Dec 2025 --> Jun 2026

We experimentally validated several actionable findings, including tepotinib to target the IRAK1/4-cholesterol pathway in glioblastoma, brigatinib to target the MARK2/3-Hippo pathway in pancreatic cancer and gilteritinib to overcome MET mutation-driven drug resistance and metastasis. To facilitate exploration of our data, we provide KIRHub, a web-based tool that allows identification of existing inhibitors of wild-type and mutated kinases to guide precision oncology.

Although PKM-ASO monotherapy had a limited effect in an immunodeficient mouse model of PDAC, synergy between PKM-ASO and anti-CTLA-4 immune checkpoint blockade (ICB), which targets Tregs, restricted tumor growth in an immunocompetent mouse model. Our findings provide preclinical support for combined antisense therapy and ICB for PDAC patients, highlighting the critical role of PKM2 in the TME and its potential as a therapeutic target.

Compact gene signatures stratified stage and survival and generalized to TCGA and ICGC cohorts. Functional assays confirmed greater invasiveness, altered redox balance, and mitochondrial dependence in advanced disease, suggesting stage-associated metabolic vulnerabilities.

Additionally, PCDH1 activated the NF-κB pathway by promoting nuclear translocation of P65, and inhibition of NF-κB with SC75741 reversed PCDH1-induced EMT, confirming that PCDH1 promotes pancreatic cancer metastasis via the NF-κB/EMT axis. PCDH1 acts as an oncogene in pancreatic cancer, promoting cell invasion, migration, and EMT progression through the NF-κB signaling pathway, making it a potential therapeutic target.

The SNORA64 interactions with apoptotic inhibitor molecules and downregulation of pro-apoptotic molecules significantly sustain cellular viability. Therefore; SNORA64 can be used to increase the cell sensitivity to death during treatment.