Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
2 i! U7 h% ?" H$ [$ n+ [9 `* K2 r9 ^) k0 C: W* J
. A; u' ]& Q+ e
Sub-category:9 z( a- V: O ?! z* |
Molecular Targets
: r( P1 K0 \. R; h5 Y. A: w6 N K
9 a6 x6 Y( |% c# @( r
Category:
8 K7 t& y& b. d$ PTumor Biology 0 I% F9 M4 V; ?( F) t" l) h- R
* Y* ]. l1 x; b8 {: G
* o, @) w# {0 e1 l+ tMeeting:
8 f8 u- ]$ z. K/ g) X2 z2011 ASCO Annual Meeting
! X4 i( {4 {* \" U8 n: C; c- q; x/ V' f5 j# A1 d' ~5 W( s
' ^( r$ V a/ y% ^9 j2 k. g
Session Type and Session Title:5 p2 B( p4 E, ^0 o- x# U
Poster Discussion Session, Tumor Biology
0 B; ~7 q# j; U% Y
: g7 |* {; z6 ~( @4 n$ ?& P" T
2 A! X/ d' w+ X% R" K7 rAbstract No:
: ?. e7 q [( o: }6 p2 j5 I10517
/ D* Z q+ u# t: Z9 j: T# b+ E2 d* e& s3 t4 P
2 E" w/ d; G; I& X3 F6 V1 Z! ?Citation:
) b, s" {- Z/ H+ k4 C' `J Clin Oncol 29: 2011 (suppl; abstr 10517)
3 `- ]% C- \( l* C: R. x4 E$ G5 Z, k6 ]
1 {1 f+ o9 W( y8 M
/ g; E% {- c% f! W) YAuthor(s):
& H/ Z2 ?! F5 \/ QJ. 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
0 W; o" U/ K' V/ j j, ?! l& `2 {5 Q3 b7 U3 p& t' }
: S; ?) w. G! D3 e1 ?' e, P. p
% `4 q5 P/ D7 g0 E' a y5 q5 FAbstracts 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.
9 I' C" [% z1 }, Q, `) ]: S0 h- n! H1 _7 r
Abstract Disclosures5 }& k* l& M4 z* {; Q+ H W( V" t z9 ~
1 @* ?: }9 S' Q, `+ y8 n
Abstract:
$ r# u8 h6 n% M" X7 N* }9 t" s8 I% E* x
! }+ a. {+ f9 s$ Y/ D" Y
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./ j& Z F- [ K) c
8 `/ o) R, C6 j
% Y2 D' l2 y. W& M$ E
|