Genetic pathways in pancreatic tumorigenesis

Tumorigenesis is a multistep process. The accumulation of newly acquired capabilities promotes cell autonomy, eventually transforming normal cells into malignant cells [1]. The predominant mechanism may be the accumulation of genetic alterations, providing certain selective advantages, in a select subset of genes [2]. Our understanding of the development of pancreatic cancer is hence based upon the identification and characterization of the genes that are mutated in this tumor type. Although the term "pancreatic cancer" comprises several histopathologically distinguishable tumor entities, including acinar cell carcinomas, pancreatoblastomas, solid-pseudopapillary tumors, mucinous cystic tumors, and intraductal papillary mucinous neoplasms, it commonly refers to pancreatic ductal adenocarcinomas, which represent the most common form of pancreatic neoplasms [3]. We focus here on a comprehensive summary of the genetic alterations identified in pancreatic ductal adenocarcinomas and their functional implications for pancreatic cancer tumorigenesis.