Pancreatic Cancer

Collectively, these findings establish DCLK1 functions as a context-specific amplifier, exacerbating aggressive tumor progression and chemotherapy resistance in pancreatic cancer. Targeting the calcium/DCLK1 signaling axis may therefore enhance the efficacy of adjuvant therapies in pancreatic cancer.

The integration of molecular diagnostics, advanced imaging technologies, and AI may enable a paradigm shift in PDAC detection, transitioning from late to early-stage diagnosis and potentially improving survival rates. However, further clinical validation and standardization of these technologies are essential to ensure their widespread clinical adoption. The future of PDAC detection lies in a multimodal, personalized approach, optimizing diagnostic accuracy and early intervention for high-risk individuals.

Our findings suggest that STINGKO CAR-T cells stand to benefit from STING agonists to improve CAR-T cell therapy for immune-deprived cancers such as pancreatic cancer.

Targeting class I HDACs, alone or combined with KRAS/MAPK inhibitors, represents a promising therapeutic strategy that concurrently disrupts both epigenetic and oncogenic pathways to treat KRAS-mutant cancers and overcome resistance, warranting clinical evaluation.

Targeting the PINCH-1/Notch1/AKT axis presents a novel theragnostic strategy to simultaneously disrupt the fibrotic tumor microenvironment and inhibit tumor growth in PDAC. (188 words).

Collectively, these findings reveal that UBE2T drives p53 positive feedback degradation to enhance glycolysis of PDAC, leading to excessive lactate production, which promotes H3K18la in CAFs and subsequent ECM deposition. Targeting UBE2T represents a potential strategy to improve the efficacy of immunotherapy in PDAC.

Integrating germline testing into surveillance redefines the management of familial PC. It uncovers hereditary susceptibility beyond classical criteria and supports cascade testing. PC also arises in mutation-negative HRI. #NCT05724992.

We successfully developed TIPE2-downregulated NKG2D-CAR-T cells that exhibited enhanced activation and cytotoxicity while limiting apoptosis and exhaustion against NKG2D ligand-expressing pancreatic tumors, highlighting TIPE2 as a promising intracellular immune checkpoint target for optimizing CAR-T cell therapy in solid tumors.

Metformin pretreatment significantly enhanced PBMC-mediated cytotoxicity against tumor cells and patient-derived organoids in ex vivo co-culture systems. Our findings establish the SLC5A11-AMPK-PD-L1 axis as a novel mechanism linking metformin to tumor immunity, providing a molecular rationale for combining metformin with checkpoint inhibitors in cancer immunotherapy.

P=N/A, N=450, Recruiting, Origin Sciences | Trial completion date: Dec 2025 --> Dec 2027 | Trial primary completion date: Jun 2025 --> Jul 2027

Erastin, a ferroptosis inducer, enhanced ferroptosis in CEP55-deficient cells and counteracted the tumor-promoting effects of CEP55 overexpression. In vivo, CEP55 silencing reduced tumor growth and altered ferroptosis markers. Our findings establish CEP55 as a novel driver of PC progression via ferroptosis suppression, supporting its potential as both a prognostic biomarker and a therapeutic target for combination strategies aimed at overcoming PC resistance.