Figures & data
Figure 1. The mechanisms of acquired resistance of EGFR-TKIs. The secondary T790M mutation of EGFR leads to decrease the affinity to EGFR-TKIs. Irreversible TKIs bind with high affinity to receptors carrying the T790M mutation. MET or IGF activation induces activation of PI3K/Akt pathway independent of EGFR activation. In these cases MET-specific inhibitor or HGF-inhibitor, inhibition of parallel pathway is a feasible strategy.
![Figure 1. The mechanisms of acquired resistance of EGFR-TKIs. The secondary T790M mutation of EGFR leads to decrease the affinity to EGFR-TKIs. Irreversible TKIs bind with high affinity to receptors carrying the T790M mutation. MET or IGF activation induces activation of PI3K/Akt pathway independent of EGFR activation. In these cases MET-specific inhibitor or HGF-inhibitor, inhibition of parallel pathway is a feasible strategy.](/cms/asset/1d8256e3-cb14-42ca-9c9d-29f03768841b/kcbt_a_10927221_f0001.gif)
Figure 2. Tumor volume changes seen on CT (A) before the first erlotinib treatment; (B) 2 mo after the first erlotinib treatment.
![Figure 2. Tumor volume changes seen on CT (A) before the first erlotinib treatment; (B) 2 mo after the first erlotinib treatment.](/cms/asset/f5318fa7-eea5-4550-858b-67478f140d4e/kcbt_a_10927221_f0002.gif)
Figure 3. Tumor volume changes seen on CT (A) before the gemcitabine treatment; (B) 2 cycles after gemcitabine retreatment.
![Figure 3. Tumor volume changes seen on CT (A) before the gemcitabine treatment; (B) 2 cycles after gemcitabine retreatment.](/cms/asset/e7d06673-ed0b-4065-adcc-8304ffed54ba/kcbt_a_10927221_f0003.gif)