Pancreatic cancer is a disease that is very difficult to detect, treat, and in almost all cases, lethal. Due to its high resistance to most treatments, research has focused on the development of combined-modality treatments. In this dissertation, we evaluated different approaches combining immunotherapy and chemotherapy to treat a murine pancreatic carcinoma in a pre-clinical transgenic mouse model. The first set of studies evaluated the use of an inhibitor for the TGF-β pathway alone and in combination with a MUC1 cytoplasmic tail vaccine. Results indicated that the TGF-β inhibitor, when combined with the vaccine, removed the protective effect of the MUC1 vaccine. A second set of studies determined the efficacy of administration of a cyclooxgenase 2 inhibitor injected at the tumor site. We observed no increase in survival in this model and mode of administration. A third set of studies evaluated the combination of the MUC1 monoclonal antibody MAb-AR20.5 with the chemotherapy drug gemcitabine. Through these studies, we determined that the most efficacious dosing schedule was administering MAb-AR20.5 5 or 7 days post-gemcitabine treatment. This study emphasized the importance of knowing the optimal time of the immune system recovery from chemotherapy to allow the immunotherapy to work effectively. The final set of studies designed a novel method for developing biomarkers for evaluation of immunotherapies. Through the use of microarray analysis of splenocytes, we determined a gene expression profile for an efficacious response to an immunotherapy. This method has the potential to be used in the clinic to develop new biomarkers for monitoring cancer immunotherapies.