fig1

Osimertinib acquired resistance among patients with EGFR-mutated NSCLC: from molecular mechanisms to clinical therapeutic strategies

Figure 1. On-target mechanisms of osimertinib-acquired resistance in EGFR-mutated NSCLC and strategies to overcome them, including EGFR secondary mutations and amplification observed in first-line and second-line treatment. Created with BioRender.com (https://BioRender.com/18y6p5u). EGFR: Epidermal growth factor receptor; TKI: tyrosine kinase inhibitor; JAK-STAT3: Janus kinase-signal transducer and activator of transcription 3; Ras-Raf-MEK-ERK: Ras-rapidly accelerated fibrosarcoma-mitogen-activated protein kinase kinase-extracellular signal-regulated kinase; PI3K-AKT: phosphatidylinositol 3-kinase-protein kinase B; EMT: epithelial-mesenchymal transition; PDK1: phosphoinositide-dependent kinase 1; NSCLC: non-small-cell lung cancer; ATP: adenosine triphosphate.

Cancer Drug Resistance
ISSN 2578-532X (Online)

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