Abstract:<div>Abstract<p>Activating <i>KRAS</i> mutations, a defining feature of pancreatic ductal adenocarcinoma (PDAC), promote tumor growth in part through the activation of cyclin-dependent kinases (CDK) that induce cell-cycle progression. p16<sup>INK4a</sup> (p16), encoded by the gene <i>CDKN2A</i>, is a potent inhibitor of CDK4/6 and serves as a critical checkpoint of cell proliferation. Mutations in and subsequent loss of the p16 gene occur in PDAC at a rate higher… Show more
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