In these, primary tumour initiation and growth is driven by expression of constitutively-active KRas (LSL-KRasG12D) in combination with either deletion of an allele of p53 (p53fl/+ generating the KPflC mouse) or expression of mutant p53s (either LSL-mutp53172H or LSL-mutp53270H generating the KP172C and KP270C mice respectively) under control of the pancreatic-specific Cre recombinase, Pdx-Cre. Here, KRAS is linked to neoplasm.