KRAS and familial pancreatic carcinoma: An in vitro and in vivo mouse model of kras-driven pancreatic cancer cells with or without concomitant atm knockdown revealed significant increase in genomic instability and accumulation of double-strand DNA breaks (as shown by colocalized foci stain for γ-H2AFX and 53BP1) in atm-deficient cells and tumors compared with cells and tumors with intact atm [75].