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. Author manuscript; available in PMC: 2014 Jun 9.
Published in final edited form as: Nat Med. 2013 Nov 7;19(11):1389–1400. doi: 10.1038/nm.3388

Table 1.

EGFR-activating and resistance mutations in adenocarcinoma of the lung

Mutation Frequency in EGFR-mutant lung adenocarcinoma (%) Clinical properties
Response rate to EGFR TKIs
Median PFS
Median OS
% Reference Months Reference Months Reference
Exon 19 deletions 45 82.8 13 11.5 13 30.8 171
84.8 170 9.0 14 34 174
63 171 11 12 17.7 172
64 172 14.6 171 33.1 173
70 173 12 174
9.3 172
9.8 173
L858R (exon 21) 40 67.3 13 10.8 13 14.8 171
60.9 170 9.6 14 8 174
50a 171 8.4b 12 20.5c 172
62 172 9.7 171
5 174
6.9 172
Exon 20 insertions 2–9 The variable response to EGFR TKIs is thought to be related to the effect of varying insertion length on the drug-binding pocket175. Median OS of 16 months176 in one series and 4 years in another177.
G719X 3 ~50 178 8.1 179 16.4 179
L861X 2 60 179 6 15.2
Exon 19 insertions 1 Case series report responsiveness to erlotinib180
T790M 0.5–3 (in some case series) Associated with lack of response to EGFR TKIs in patients with EGFR-activating mutations41,179
a

P = 0.39 compared to exon 19 deletions in this series.

b

P = 0.075 compared to exon 19 deletions in this series.

c

P = 0.65 compared to exon 19 deletions in this series.

PFS, progression-free survival; OS, overall survival.