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Abstract
Pancreatic ductal adenocarcinoma (PDAC) is an aggressive cancer with poor outcomes, partly due to dysfunctional vascularization and complex tumor-stromal interactions. This dissertation investigates the role of the RNA-binding protein HuR in regulating extracellular vesicle (EV) cargo and signaling within the PDAC tumor microenvironment. We demonstrate that HuR modulates EV content, affecting endothelial cell behavior and vascular integrity, and explore therapeutic strategies to disrupt EV-mediated communication. Our findings reveal novel mechanisms by which HuR contributes to PDAC progression and identify potential targets for improving treatment outcomes.