Table 2.
Characteristics of patients with detected EGFR amplification.
| Patient | Sample type | EGFR activating mutation | T790M status | Pre-existing/acquired EGFR amp | Other potential concomitant resistance mechanisms |
|---|---|---|---|---|---|
| 2 | P | 21L858R | + | Acquired | − |
| 9 | P | Del19 | + | Pre-existing | AXL amp# |
| 16 | P | Del19 | + | Pre-existing | MET amp, EGFR C797S |
| 18 | P | Del19 | + | Acquired | CDKN2A/2B del |
| 20 | P | 21L858R | + | Pre-existing | PIK3CA E545K & SCLC |
| 23 | Ta & P | Del19 | + | Pre-existing | − |
| 24 | CSFa & P | Del19 | + | Unknown | CDKN2A del |
| 26 | T | Del19 | + | Unknown | EGFR L718V |
| 28 | Ta & P | Del19 | − | Unknown | MET amp |
| 29 | T | Del19 | + | Acquired | − |
| 30 | T & P | Del19 | + | Acquired | EGFR C797S# |
21L858R, EGFR 21L858R mutation; CSF, cerebrospinal fluid; amp, amplification; Del19, EGFR 19 deletion; P, plasma; T, tissue; AXL amp#, EGFR copy number gain was observed upon RECIST disease progression, while AXL amp was detected upon clinical disease progression with further copy number gain of EGFR; EGFR C797S #, EGFR C797S mutation was detected only in plasma, while EGFR amp was detected in both tissue and plasma upon abivertinib progression in P30.
EGFR amp was identified in P23, P24, P28 by tissue or CSF, but not in plasma.