Figure 4

The frequency of acquired EGFR-TKI resistance in 26 patients. Secondary T790M mutation was the most common mechanism, found in 11 patients (42.3%). Four patients had other co-existing resistant mechanisms (MET:2, AXL:1, PI3KCA:1). Increased AXL expression was observed in 5/26 patients (19.2%), while MET gene amplification was noted in 3/26 patients (11.5%). One patient acquired a mutation in the PIK3CA gene and 2 patients showed increased CD56 expression, suggesting neuroendocrine differentiation. Conversion from L858R-mutant to wild-type EGFR-expressing cells occurred in 1 patient, and 7 patients (26.9%) did not exhibit any known resistance mechanisms.