We demonstrate for the first time that ATM disrupts binding of PKCζ to partitioning defective 6 homolog (Par6), an aPKC signaling partner, and that inhibition of expression of Par6 significantly reduces transformed growth and invasion of pancreatic cancer cells, suggesting that aPKC/Par6 signaling is an important mediator of the transformed phenotype of pancreatic cancer cells. This evidence concerns the gene PARD6A and pancreatic neoplasm.