| |
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
