Pancreatic Ductal Adenocarcinoma

NcRNAs play central roles in regulating glycolysis and metabolic adaptation in PDAC and represent promising targets for diagnosis and therapy. Further studies are required to validate key regulatory networks and translate these findings into clinical applications.

P2/3, N=900, Recruiting, AbbVie | Not yet recruiting --> Recruiting

P1, N=58, Active, not recruiting, Boehringer Ingelheim | Trial completion date: Jun 2027 --> Mar 2027 | Trial primary completion date: Jun 2027 --> Mar 2027

P3, N=288, Recruiting, Tianjin Medical University Cancer Institute and Hospital

P2, N=60, Recruiting, Memorial Sloan Kettering Cancer Center | Trial completion date: May 2026 --> May 2027 | Trial primary completion date: May 2026 --> May 2027

Primary tumor location was associated with site of recurrence. Neoadjuvant and adjuvant therapy significantly reduced ER and increased OS.

Notably, YIYA stabilises KRAS by preventing its autophagy-mediated degradation, thereby sustaining a proliferative state. This study identifies YIYA as a glucose-responsive lncRNA that links KRAS signalling to metabolic reprogramming in PDAC.

Mechanistically, CXCL10 signaling activated the ERK/MAPK pathway, and ERK inhibition abolished its tumor-promoting effects. This study establishes that CXCL10 drives PDAC progression through CXCR3-dependent ERK/MAPK activation, positioning this axis as a potential therapeutic target.

Inhibition of FABP5 using BMS-309,403 suppressed syngeneic KPC subcutaneous tumor growth without serious side effects. Conclusively, this study demonstrates that high IPFD enhances PDAC carcinogenesis, growth, and metastasis with enrollment of FABP5 upregulation, indicating that FABP5 inhibition may represent a potential therapeutic strategy for PDAC.

Analyzed variables included demographics, tumor characteristics (location, stage), NAC regimens (FOLFIRINOX, GEMCAP, gemcitabine monotherapy), response to therapy (RECIST criteria), surgical outcomes (resection rate, R0 resection), CA19-9 levels, neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and survival outcomes (overall survival (OS) and progression-free survival (PFS))...Elevated pre-treatment CA19-9, NLR, and PLR may identify patients less likely to benefit from NAC. Biomarker-driven trials are warranted to optimize patient selection and personalize treatment strategies, especially in resource-constrained settings.

Our data indicate that GATA4 functions through the coordinated action of multiple inflammatory factors that are required for ADM/PanIN formation but are dispensable for PDAC development. Collectively, these findings challenge current paradigms of PDAC initiation and progression.

Genetic depletion of Fbln3 led to reduced tumor progression and increased Cd8 + T cell infiltration in mice. Together these findings identify a previously unknown signaling axis driving immunosuppressive phenotypes in PDAC, uncovering multiple potential nodes to relieve the immunosuppressive pressures within the PDAC TME.