Pathology of pancreatic tumors

Abstract

Pancreatic ductal adenocarcinoma (PDA) is the most common cancer of the pancreas. It is an aggressive cancer that leads to rapid progression, high disease stage at presentation and diagnosis and therefore complicate treatment approaches. It has a peak incidence in the 7 th to 8 th decades of life and most are high stage at diagnosis and not surgically resectable. PDA is associated with multiple risk factors including environmental, dietary, chronic diseases and genetic. KRAS has been the most frequently altered oncogene in PDA (somatic KRAS mutations are present in >90% of cancers), clearly indicating that this gene is a driver of tumorigenesis in the pancreas. Frequently altered tumor suppressor genes have also been identified in PDA, including p16/CDKN2A, TP53, and SMAD4/DPC4, and these genes also represent drivers in pancreatic tumorigenesis. ROR2 plays an essential role as a prognostic marker of survival in patients with PDA and could be considered a potential therapeutic target in the future. Positive Nectin-2 and DDX3 expression were associated with the progression and poorer prognosis in pancreatic adenocarcinoma patients. Advancement in cancer genetics have improved the understanding of the disease and serve as screening and also prognostic markers. Here we review the pathology of PDA and other pancreatic tumors.