Mutant KRAS and p53 cooperate to drive pancreatic cancer metastasis

Researchers at The University of Texas MD Anderson Cancer Center have discovered that mutant KRAS and p53, the most frequently mutated genes in pancreatic cancer, interact through the CREB1 protein to promote metastasis and tumor growth. Blocking CREB1 in preclinical models reversed these effects and reduced metastases, suggesting an important new therapeutic target for the deadly cancer.