Chronic pancreatitis as a driving factor for pancreatic cancer: An epidemiological understanding

Core Tip

Core Tip: The United States has a high incidence of pancreatic cancer (PanCa) cases that result from chronic pancreatitis (CP). This link between diseases is well-established in many scientific studies and clinical practices. In CP, the chronic inflammation of the pancreas causes DNA mutations and cellular changes that may make one prone to cancerous tumors. The CP is responsible for the persistent damage and fibrosis as a consequence of continuous inflammation of the organ over time. Such chronic inflammation promotes DNA mutations and oxidative stress, and damages cells thus leading to an increased risk of carcinogenesis. On a long-term basis, these alterations can cause the development of pancreatic intraepithelial neoplasia, a precancerous stage prior to pancreatic ductal adenocarcinoma (PDAC), which is another name for PDAC; it’s also regarded as the most prevalent type of this ailment. An example is that hereditary pancreatitis patients have up to 40% lifetime risk by age 70 years. Non-genetic CP also increases risks, although not very greatly. Development of PanCa is partly associated with CP risk factors like genetic mutations such as protease serine 1, serine protease inhibitor kazal type 1, cystic fibrosis transmembrane conductance regulator, heavy alcohol use, and smoking.