Pancreatic cancer (PC) is one of the five most fatal forms of cancer. Despite decades of advances in cancer therapy for many other types of cancer, there has been minimal impact on the overall survival of PC patients. Two reasons may explain this clinical roadblock. First, symptoms often present late when the disease has spread to many organs, when surgical interventions aiming to cure patients do not work. Second, PC is highly resistant to cancer drugs. The ability of drugs to reach and kill PC cells is very poor compared to other types of cancer. This is due to the intense inflammation that surrounds the cancer and causes blood vessels within the tumour to collapse. As a consequence of the scarce blood supply within the tumour, cancer drugs cannot penetrate in sufficient quantities to shrink tumours in patients. This inflammation is provoked by the build-up of fibroblasts, a non-cancerous cell type that borders the cancer. Many laboratories worldwide have shown that the accumulation of fibroblasts can block drug delivery to the cancer. This has led to a new vision for cancer therapy in the future whereby drugs that attack fibroblasts as well as cancer cells are given to patients in parallel. The idea behind this theory is that one drug would attack fibroblasts to increase blood supply, and provide the second cancer-killing drug access to the tumour cells. To accomplish this goal, we need to be able to isolate, study and learn how cancer fibroblasts cause inflammation within the tumour. I have now developed cell-based studies to separate cancer cells and fibroblasts. This will allow me to monitor the true role of fibroblasts, and how they cause the menacing inflammation that limits the drug delivery to neighbouring cancer cells. In this application, I will study the biology of how fibroblasts mediate inflammation in pancreatic cancer.