Table 4.

Acquired resistance mechanism after the use of epidermal growth factor receptor tyrosine kinase inhibitors according to mutation type and treatment regimen

	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