Dual-targeting of MEK and CDK4/6 in KRAS-mutated Non-Small Cell Lung Cancer

Abstract

Discovering new ways to modulate the responsiveness of non-small cell lung cancer (NSCLC) to treatment represents one of the forefronts of cancer research. KRAS mutations, present in roughly 30% of NSCLCs, lead to increased levels of cellular proliferation and decreased responsiveness to treatment modalities. The present study examined the RB/p16/CDK4 pathway as a way to modulate the responsiveness of these cell lines. The diverse downstream effects of these pathways suggest that molecular profiling of NSCLCs may assist clinicians and researchers to predict the effectiveness in the application of particular therapeutics.