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Table 4 Acquired resistance mechanism after the use of epidermal growth factor receptor tyrosine kinase inhibitors according to mutation type and treatment regimen

From: Comparison of epidermal growth factor receptor tyrosine kinase inhibitors for patients with lung adenocarcinoma harboring different epidermal growth factor receptor mutation types

  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
  1. 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
  2. Data are shown as n (%) per each group
  3. SCLC small-cell lung cancer, E19del exon 19 deletion, L858R L858R point mutation, Uncommon uncommon mutations
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