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. 2023 May 29;26(7):107006. doi: 10.1016/j.isci.2023.107006

Figure 1.

Figure 1

Frequency of MET amplification and MET overexpression in 28 patients with NSCLC who had disease progression on ALK (n = 15), ROS1 (n = 8) or RET (n = 5) tyrosine kinase inhibitors (TKIs) (refer to Table S1 for details)

(A) Left: Pie chart visualizing the frequency of MET amplification or on-target ALK/ROS1 mutations as potential resistance mechanisms to ALK, ROS1 or RET TKIs in 27 patients with liquid (blood, pleural effusions, cerebrospinal fluids) biopsies (LBx) available. Patients P6 and P27 tested positive for MET amplification. Right: Pie chart visualizing the frequency of MET amplification, MET overexpression or on-target ALK/ROS1 mutations as potential resistance mechanisms to ALK, ROS1 or RET TKIs in 8 patients with tumor or cytological biopsies (TBx) available. Patients P24 and P27 tested positive for MET amplification (P24 also showed MET overexpression) and patient P26 tested positive for MET overexpression without MET amplification.

(B) FISH and IHC analyses of patients P24 and P26 progressing on TKIs presumably by MET alterations. Left: patient P24 harbored an ALKv1-rearranged NSCLC relapsing on lorlatinib and had MET amplification. Right: patient P26 harbored a CD74-ROS1-rearranged NSCLC relapsing on crizotinib and had MET overexpression without MET amplification. As indicated in the images, scale bars refer to 5, 100 and 200 µm, respectively.