This indicates that acquisition of mutant p53R172H, which we have shown previously to drive an invasive and metastatic program over and above the loss of p53 in pancreatic cancer (Morton et al., 2010b), could partially achieve this by allowing early tumor dissolution via mobilization of E-cadherin-based cell-cell contacts (Figure 5F). Here, TP53 is linked to familial pancreatic carcinoma.