1. Figure 1. Resistance mechanism against first generation epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI). (A) Mutations in the EGFR gene. T790M mutation induces conformational changes on the ATP-binding pocket of EGFR–tyrosine kinase domain, inhibiting interaction with the drug target site. (B) Activation of alternative signaling pathways. MET amplification, and overexpression of phosphoinositide 3-kinase (PI3K)/AKT, mitogen-activated protein kinase (MAPK), and AXL bypass the dependency on EGFR activation and can promote survival and proliferation. (C) Phenotypic changes, small cell lung cancer transformation, and epithelial-mesenchymal transition (EMT) confer resistance to EGFR-TKI. SCLC: small cell lung cancer.
Figure 1. Resistance mechanism against first generation epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI). (A) Mutations in the EGFR gene. T790M mutation induces conformational changes on the ATP-binding pocket of EGFR–tyrosine kinase domain, inhibiting interaction with the drug target site. (B) Activation of alternative signaling pathways. . .
Tuberc Respir Dis Oct;79(4):