DYRK1B Inhibition Enhances Macrophage-Mediated Tumor Suppression in Pancreatic Cancer

Recent research has identified the kinase DYRK1B as a key regulator of macrophage activity in pancreatic ductal adenocarcinoma (PDAC). Inhibiting DYRK1B shifts macrophages from a tumor-promoting (M2) to a tumor-suppressing (M1) phenotype, enhancing their ability to attack cancer cells. This phenotypic change is mediated through the activation of the NF-κB signaling pathway. In mouse models, combining DYRK1B inhibitors with immune checkpoint blockade therapies significantly reduced tumor growth and improved survival rates. These findings suggest that targeting DYRK1B could be a promising strategy to boost the immune system's response against PDAC.