The E-cadherin-GFP mouse was therefore crossed with either wild-type mice expressing Pdx1-Cre, mice bearing a Pdx1-Cre-driven initiating KrasG12D mutation alone, Pdx1-Cre; KrasG12D; p53−/− mice, or Pdx1-Cre; KrasG12D; mutant p53R172H mice and monitored for ∼150 days to allow tumor formation to occur. The gene discussed is TP53; the disease is neoplasm.