Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
1 i, l3 d% O; P F( x: f/ r# P, i# t. o
. P" n2 O$ P7 Z& x. H' u2 j
Sub-category:. e2 c/ v. J; h
Molecular Targets
?% d: ?0 Y: N8 W' z
9 ]% E+ e3 b( x. [% m6 Z5 k9 z6 P6 J1 q
Category:6 |+ \" w# p0 ]- L% K, \
Tumor Biology " `5 G) `. m/ O' w
# Q0 N! k) B5 l( U* ?
2 ? I8 l( K3 N+ a
Meeting:
) E6 {$ k; H% `3 h$ u' t% ~9 z2011 ASCO Annual Meeting
4 l F( W, H, s* x9 o0 V, i. j$ g: z* a
6 x' k. E/ [% B
Session Type and Session Title:
2 u/ x5 [/ o2 S3 y1 ]* h9 R* P. kPoster Discussion Session, Tumor Biology # j `$ A, F: z5 }8 h. ~" \# L
' O9 T- W7 Z6 y% k
6 s6 Z3 a# ^9 p. X4 t0 a6 pAbstract No:1 v' x5 s) ~4 Z) D9 D+ [
10517
. l" e$ n9 e3 A- R! L
, j$ A: d7 s# f$ `9 Q# B6 Q6 t" J: P- c( K0 g
Citation:* f, A( |: J& S
J Clin Oncol 29: 2011 (suppl; abstr 10517) 1 c7 D% t* E5 ?4 P; _6 r) V8 q$ N6 b+ S
, R+ n3 L R( W$ J: ~, G& R
$ a% X8 n# `8 y) D# v8 X
Author(s):, K; k) \9 f* p+ ]6 }; w; M0 f
J. Yang, X. Zhang, J. Su, H. Chen, H. Tian, Y. Huang, C. Xu, Y. L. Wu; Guangdong Lung Cancer Institute, Guangdong General Hospital & Guangdong Academy of Medical Sciences, Guangzhou, China; Guangdong Lung Cancer Institute, Medical Research Center of Guangdong General Hospital, Guangzhou, China; Guangdong Lung Cancer Institute, Guangzhou, China; Guangdong Lung Cancer Institute, Guangdong General Hospital & Guangdong Academy of Medical Sciences, Guangzhou, China ( l a5 S7 U% {/ \5 _
; ~, }% ?; C' `" U* C% I. Y
, I- S) s+ @$ {2 Q. Y5 c. z7 \
, Y4 g+ t0 s. Z" S2 o- ~3 G- nAbstracts that were granted an exception in accordance with ASCO's Conflict of Interest Policy are designated with a caret symbol (^) here and in the printed Proceedings.( [/ W# U' n, B: X# h, |
" o+ U$ c- l# d1 R. Q
Abstract Disclosures' I6 ^4 L/ V Q( U
/ |2 k; y+ {1 x0 E
Abstract:
* o" E4 [( y. [9 J/ w: f0 Q$ F' i s: K% N
. Z% K2 T+ D$ z! f0 E6 }Background: The fusion of the anaplastic lymphoma kinase (ALK) with the echinoderm microtubule-associated protein-like 4 (EML4) and epidermal growth factor receptor (EGFR) mutations are considered mutually exclusive. Advanced non-small cell lung cancer (NSCLC) patients with EML4-ALK did not benefit from EGFR tyrosine kinase inhibitors (TKIs). Methods: Multiplex reverse transcriptase-polymerase chain reaction (RT-PCR) followed by sequencing was performed for EML4-ALK fusion status detection. EGFR and KRAS mutations were determined by direct DNA sequencing. Positive results of EML4-ALK fusion were also confirmed by RACE-coupled PCR sequencing. Results: From April 2010 to January 2011, 412 patients (398 with NSCLC; 14 with SCLC) were tested for mutation status of EGFR, KRAS and EML4-ALK respectively. Frequency of EML4-ALK fusion was 10.6% (42/398) in NSCLC patients. No patients with SCLC were found to have positive EML4-ALK fusion. Frequency of concomitant EGFR and EML4-ALK gene mutations was 1.0% (4/398) in NSCLC patients, and their variants of EML4-ALK gene mutations were Variant 1 (3 patients) and Variant 6 (1 patient); being never smokers, all of them were diagnosed with advanced (3 with stage †W and 1 with stage IIIB) adenocarcinoma harbouring wild type KRAS. Two female stage †W patients with double gene mutations (1 with L858R and Variant 1; 1 with exon19 deletion and Variant 6) received first-line gefitinib which is one kind of EGFR TKIs and achieved partial response. Conclusions: Though being rare events, NSCLC patients harbouring concomitant EGFR mutation and EML4-ALK gene fusion are sensitive to first-line EGFR TKIs. Whether they could also benefit from ALK inhibition after failure to EGFR TKIs warranted further investigation.4 c) i% ~6 ^# @2 x& U
! A: o6 J2 N0 a* v8 \* |' b - B8 j; U& M4 _% q- z1 n' V: X
|