Files
Abstract
The overwhelming majority (~90%) of patients with pancreatic ductal adenocarcinoma (PDAC) will be treated with systemic standard-of-care chemotherapeutic regimens at some point during their care. These treatments have limited benefits for patients, in addition to causing adverse side effects. One of the contributing factors to poor treatment response is PDAC?s characteristically dense stroma and heterogeneous tumor microenvironment. For instance, pancreatic stellate cells (PSCs) and cancer associated fibroblasts (CAFs) in pancreatic tumors promote fibrosis, which is associated with poor prognosis and resistance to therapy.
Herein, this thesis describes a novel function of tumor intrinsic HuR in the PDAC tumor microenvironment and proposes a method of direct and specific inhibition of HuR in PDAC tumors. In doing so, we aimed to address the need for improved treatments for PDAC, by both manipulating the tumor microenvironment to improve therapeutic efficacy and optimizing a novel, targeted delivery method for payloads.