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Resistance inevitably develops despite the initial efficacy of using tyrosine kinase inhibitors of epidermal growth factor receptors (EGFR‐TKIs) for treating patients with non‐small cell lung cancer (NSCLC). Recent studies highlight a link between alternative splicing and cancer drug response. Therefore, the study aimed to identify deregulated splicing events that play a role in resistance to EGFR‐TKI. The results support the role for defective autophagy in acquired resistance to EGFR‐TKIs and identify splicing regulation of ATG16‐L1 as a therapeutic vulnerability that could be explored for improving EGFR‐targeted cancer therapy.
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