Next, we found that either the transfection with p53 K381/382R vector before exposing cells to SAHA/5-AZA (Figure 5B), or the silencing of p53 (Figure 5C) or the treatment by c-Myc inhibitor (Figure 5D), less efficiently counteracted the reduction of BRCA-1, suggesting that the disruption of mutual support between mutp53 and c-Myc contributed to BRCA-1 downregulation and to DNA damage induction in pancreatic cancer cells. Here, TP53 is linked to pancreatic neoplasm.