CDK4 and CDK6 upregulation promotes DNA replication stress, genomic instability and resistance to EGFR targeted therapy in lung cancer.

A preprint abstract from biorxiv.org discusses the genetic interactions in lung cancers driven by oncogenic forms of the epidermal growth factor receptor (EGFR). The study focuses on the co-alterations of cell cycle regulators CDK4 or CDK6, which are commonly found with oncogenic EGFR. The researchers found that upregulation of CDK4/6 overcomes EGFR inhibitor-induced cell cycle arrest and leads to replication stress, DNA damage, and genomic instability. This upregulation also contributes to resistance to EGFR targeted therapies. However, the study also shows that a combination of EGFR and CDK4/6 inhibitor treatment can alleviate genomic instability and EGFR inhibitor resistance in preclinical models. This research sheds light on the genetic interactions in lung cancer and their clinical implications. [Extracted from the article]

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