A. Bianchi

CREB drives acinar cells to ductal reprogramming and promotes pancreatic cancer progression in preclinical models of alcoholic pancreatitis

This study shows CREB promotes acinar-to-ductal reprogramming and pancreatic cancer progression in alcoholic pancreatitis models by enhancing fibrosis and tumor growth.

Cell-specific nanoengineering strategy disrupts tolerogenic signaling from myeloid-derived suppressor cells to invigorate antitumor immunity in pancreatic cancer

The paper develops CXCR2-homing nanoparticles to specifically target PMN-MDSCs in PDAC, reducing arginase activity and enhancing T-cell activity without causing neutropenia.

Metabolic enzymes moonlight as selective autophagy receptors to protect plants against viral-induced cellular damage

This study shows that metabolic enzymes act as autophagy receptors in plants to degrade defense executors during viral infection, revealing autophagy as a tolerance pathway rather than an antiviral defense.

Binding of the TRF2 iDDR motif to RAD50 highlights a convergent evolutionary strategy to inactivate MRN at telomeres

The paper identifies a third example of convergent evolution where the TRF2 iDDR motif binds human RAD50 at the same site as the yeast MIN motif, inhibiting MRN nuclease activity at telomeres.

Neutrophil-Mediated Stromal-Tumor IL-6/STAT-3 Signaling Underlies the Association between Neutrophil-to-Lymphocyte Ratio Dynamics and Chemotherapy Response in Localized Pancreatic Cancer: A Hybrid Clinical-Preclinical Study

This study shows that neutrophil-to-lymphocyte ratio (NLR) dynamics predict chemotherapy response in pancreatic cancer and that targeting NLR improves chemosensitivity by modulating IL-6/STAT-3 signaling.

Distinct Mechanisms of Innate and Adaptive Immune Regulation Underlie Poor Oncologic Outcomes Associated with KRAS-TP53 Co-Alteration in Pancreatic Cancer

Combined MEK and STAT3 inhibition reprograms stromal inflammation to overcome immunotherapy resistance in pancreatic cancer

This paper shows that combining MEK and STAT3 inhibitors reprograms stromal inflammation and enhances immunotherapy response in pancreatic cancer.