| No change | T790M | SCLC | Wild-type | p value |
---|
Total (n = 101) | 46 (45.5) | 50 (49.5) | 1 (1.0) | 4 (4.0) | |
EGFR mutation types |
E19del (n = 51) | 21 (41.2) | 27 (52.9) | 0 | 3 (5.9) | 0.447 |
L858R (n = 42) | 19 (45.2) | 21 (50.0) | 1 (2.4) | 1 (2.4) | 0.601 |
Uncommon (n = 8) | 6 (75.0) | 2 (25.0) | 0 | 0 | 0.371 |
EGFR TKIs |
Afatinib (n = 38) | 21 (55.3) | 14 (36.8) | 0 | 3 (7.9) | 0.130 |
Erlotinib (n = 32) | 12 (37.5) | 19 (59.4) | 1 (3.1) | 0 | 0.168 |
Gefitinib (n = 31) | 13 (41.9) | 17 (54.8) | 0 | 1 (3.2) | 0.747 |
- A total of 101 patients underwent re-biopsy for investigation of acquired resistance after discontinuation of EGFR TKI. The most common mechanism was acquisition of T790M mutation, followed by conversion to EGFR wild-type, and transformation to small-cell lung cancer. No difference was found in the rate of acquired resistance mutations according to initial EGFR mutation type and treatment regimen
- Data are shown as n (%) per each group
- SCLC small-cell lung cancer, E19del exon 19 deletion, L858R L858R point mutation, Uncommon uncommon mutations