Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page - Y: c3 O+ T, H' ?* a7 n9 d) H
6 Y7 l8 G4 C9 c7 h8 O P5 \- E' x1 n! B- e
Sub-category:
& C" _" w. b& ^, p' v6 [$ }Molecular Targets 1 J+ J4 g( A( S4 P/ [. A& ]
* M) D4 r) G/ @& R
* B! B2 R2 k5 f5 TCategory:" @# j- D$ `; G! o% {' L6 C" b
Tumor Biology
% ?; j# T2 V7 a# [, i0 ?1 F0 B& n
6 r x1 I& X% v1 M( y. Z
3 K) N/ E& q- Z9 E7 z+ MMeeting:
, S4 j3 B5 F6 r( _9 J2011 ASCO Annual Meeting ' T+ f7 N0 V, n1 ]5 ^( u
6 B% w0 u/ X3 R4 {' K- J3 K
: J f. |: {) q% q/ C" `Session Type and Session Title:4 X) F+ n. z# Y: x) `/ ^
Poster Discussion Session, Tumor Biology
. K" F" T+ f3 I3 R
9 i9 a6 ]6 X0 @' L4 v0 R
& f5 ]+ }$ g3 K' v1 @0 X; xAbstract No:$ O/ p5 a7 p9 B) U4 \. q
10517 # i+ Y2 s" Q9 E5 |# ~. a
( u% M3 z$ W* E0 N
6 d$ L: U6 q: }3 MCitation:* ]! e! A) ~' Q3 ^ I; X
J Clin Oncol 29: 2011 (suppl; abstr 10517) & l3 F/ ]" L+ v `
; G- Q5 x1 K5 N5 L
. _- }; a' G+ o6 c
Author(s):
5 k5 F9 D7 H5 SJ. 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 # S: b; U1 v" I3 a4 w- q
7 ?0 g( c# [# Q7 |% g. H9 U3 E; `+ D6 H4 F3 H
2 t* u3 f5 m p0 S9 g2 cAbstracts 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.3 S) ^& w1 h! j0 M0 V; |9 K; F9 D
! C3 ^+ T4 w+ y; u' K& mAbstract Disclosures: D' m8 u) L/ {
0 @) Y( u8 H/ {( y3 tAbstract:
+ n- `" D4 q1 `3 W+ P
6 o1 M; L& y% Y6 }. J# C6 U; U1 b6 N+ P$ f$ o% ^' K/ Y. N
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.
0 C7 O+ }6 u+ I3 Y4 k6 ~% U7 `, R/ C5 U& O. p+ A) p9 O, }3 ~$ A5 b
% t8 h; [9 o+ U9 z9 g3 I. C
|