Pancreatic cancer stem cells and inflammation: milestones achieved and challenges ahead

The inflammatory mediators tend to activate or regulate an array of signaling mechanisms to trigger cancer stem cells and mediate malignancy. In acinar cells, cholecystokinin stimulation activates and translocates nuclear factor kappa B to the nucleus to activate transcription factors and secretes proinflammatory cytokines. An effective balance between proinflammatory and antiinflammatory cytokines determines the outcomes of several cancers, including pancreatic cancer (PC). A strong correlation between acute/chronic pancreatitis and incidence of PC is known. The incidence of PC mortality is increasing globally at alarming rate. Though surgical resection is prescribed for advanced PC, the presence of a small stem cell population after surgery accounts for relapse. Therefore, for an effective therapy, an understanding between tumor inflammatory microenvironment and PC stem cells is very important. This chapter is aimed at consolidating several tumor stem cell markers and their association with inflammatory molecules/inflammation for the development of antiinflammatory-based stem cell targeting therapy. Key milestones in this area are collected along with the ongoing strategies and challenges to develop an effective PC stem cell therapy.