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Fig. 3 | Journal of Hematology & Oncology

Fig. 3

From: MET inhibitors for targeted therapy of EGFR TKI-resistant lung cancer

Fig. 3

MET amplification causes EGFR-TKI resistance by activating EGFR-independent phosphorylation of ErbB3 and downstream activation of the PI3K/AKT pathway, providing a bypass resistance mechanism in the presence of an EGFR-TKI. MET can also activate PI3K/Akt signaling through ErbB3. In EGFRm NSCLCs with MET amplification, EGFR-TKIs can still inhibit EGFR phosphorylation but not ErbB3 phosphorylation, leading to persistent activation of PI3K/Akt signaling via ErbB3 in an EGFR-independent manner

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