Molecular biology, models, and histopathology of chronic pancreatitis and pancreatic cancer

BACKGROUND: Pancreatic ductal adenocarcinoma (PDAC) and chronic pancreatitis (CP) represent frequent, and devastating diseases of the pancreas. Although the treatment for both conditions has improved over the past decades, overall prognosis remains poor necessitating the development of new treatment options, which in turn requires a deeper understanding of the underlying pathophysiology including genetic, molecular, and histopathologic changes occurring in both diseases. METHODS: Review of the literature. RESULTS: Significant progress has been made in the field of pancreatic research deepening our understanding of PDAC and CP development and maintenance. The landmark findings will be outlined in this article drawing attention to the common pathologic pathways of both diseases. On a histopathologic level, PDAC development from precursor lesions has been described in detail. Furthermore, genetic changes during PDAC initiation and maintenance have recently been discovered. However, the exact role of many molecular alterations found in PDAC remains unclear. In CP, new concepts have changed our understanding of the disease and the finding and characterization of pancreatic stellate cells have given us a better understanding of the mechanism of pancreatic fibrosis, a hallmark of CP. CONCLUSIONS: Our growing knowledge of the underlying molecular and histopathologic changes occurring in PDAC as well as CP has given us an unprecedented insight into the causes and mechanisms of PDAC and CP development.