Abstract
Direct KRASG12C inhibitors have shown promising clinical activity in cancers bearing KRASG12C mutation and sotorasib, in particular, is approved for the treatment of these patients. While intrinsic and acquired resistance to this drug limits its utility, the mechanisms underlying such resistance remain to be elucidated. Aurora A Kinase (AURKA) has been considered as a key druggable KRAS effector and mediates adaptive resistance to direct KRASG12C inhibitors. We have previously demonstrated synergistic antitumor effects when the mitotic cell regulator WEE1 is inhibited in combination with AURKA inhibition and explored this strategy to prevent or overcome sotorasib resistance.
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