ABSTRACT
Pancreatic ductal adenocarcinoma (PDAC) is among the dangerous human cancers, is the 10th highly prevalent cancer, and the fourth sole cause of cancer-related mortality in the United States of America. Notwithstanding the significant commitment, the forecast for people with this burden continues to have a five-year survival rate of just 4-6%. The most critical altered genes within PDAC consist of K-ras the proto-oncogene which is usually mutationally activated above 90% cases and tumor suppressors likeTrp53 are altered at 55%. To face the burden of pancreatic ductal adenocarcinoma, a variety of genetically engineered pancreatic cancer mice models have been created over the last past years. These models have distinctive features and are not all appropriate for preclinical studies. In this review, we focus on differences between two mice models K-rasLSL.G12D/+;Pdx-1-Cre(KC) and K-rasLSL.G12D/+; Trp53R172H/+; Pdx-1-Cre(KPC) in terms of their modeling biology and their clinical relevance.
