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Date Time 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. “To our knowledge, this is the first study to show how these two major genetic drivers work together to promote tumor growth and metastasis,” Kim said. “We learned that signaling downstream of mutant KRAS directly promotes mutant p53 activity. This discovery provides not only a new therapeutic target but unveils a vast transcriptional network that is activated downstream of these mutant proteins.”

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