Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page $ [$ `. T6 z& a6 \! P0 D
: n" H) M! J' a" `
. F8 |* P4 k3 p/ w f9 f3 _
Sub-category:/ E1 w! h- w* F2 l$ u
Molecular Targets , z& B# J$ Q9 D) ^# [) U; [
: u8 h# T1 k, h( }4 f7 K7 j- d- Y7 T$ a
Category:
& J4 S% e% j( _# o# _0 QTumor Biology
* }, @$ e+ p3 E9 w7 n8 g. R" w; y' }9 H
. L0 O1 N4 a# z+ o' @/ bMeeting:4 d4 ^( l; U- H) h
2011 ASCO Annual Meeting
# e$ g. z: T n, C" k- B2 l2 @4 Q: E* S7 I) k9 E
) q0 ?, p7 w$ v; C/ hSession Type and Session Title:& u% M" L2 n/ u1 D; K
Poster Discussion Session, Tumor Biology
0 \. _8 T0 b5 N0 L
! |7 U9 ^! E+ k4 Z6 x& q, k. [% C0 y# b( H+ A
Abstract No:
! q. y, R9 U/ b4 v10517
% Y% q' r$ c1 m& j- F9 ?: a; s7 d' W' _
4 ] b$ W3 e3 I' g
Citation:
! f2 C" i: T J* k& I6 TJ Clin Oncol 29: 2011 (suppl; abstr 10517)
" E% z8 Q9 n* U0 _, O/ z. E/ h) |6 v2 d8 t0 k
/ U' [. H q. c9 g4 q: q
Author(s):# ?2 c6 X+ r9 H# T d
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
k; ^4 I/ q4 {! f$ Q: O* n) L! P( M
6 T/ |4 }; i, \4 W) e1 ?" P1 z. [: K% i
0 t6 H7 g! h! L' F2 GAbstracts 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.& n& t0 o# Q; `- a8 m: b# b9 ?) ~
. ^* U$ }6 C5 Y# q" eAbstract Disclosures, _5 I) ~8 u! I
2 M, ? Z2 B1 Z' e
Abstract:
7 _3 {1 v, {6 y, k2 |6 y* H: g: l" `5 B* i& O0 f0 Q
7 v K T2 Z4 u$ {& JBackground: 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., J- G+ G+ R+ e8 D3 O1 X1 S
& v" U% [) r3 Z( m/ l3 Z# L
, q, q; e) }- X7 \- z |