Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page + K# a. S5 |, k3 j. O6 M' `" B
`6 J$ |) k, Y7 j% G$ I! [) H
" Z+ N$ {' J* [# q7 cSub-category:% Z9 j" j6 T1 h/ T2 U5 ` m) R$ S
Molecular Targets ) @0 q" p) U5 q5 D! _; Q4 M) d
8 B8 L: k9 ?4 [& O2 s3 \% p2 f$ |
- [+ f2 B6 S8 \' C
Category:! z, t0 O5 \, K' y; b! H0 `( X
Tumor Biology
$ @9 t k9 R5 h- n% A! Z. E" @# v. N4 L
4 z+ V; P% ~) Z$ l. b0 y9 VMeeting:
5 d# C# S0 X ?* |; n4 m2011 ASCO Annual Meeting ! f$ |- d' a% _# b, E' L$ I- ?
+ W4 R0 L# O6 \. B/ e2 v7 w% @4 M3 p5 C# s' j/ |. c9 F/ D4 V2 U
Session Type and Session Title:
% L6 Y4 R& e5 W# D7 ZPoster Discussion Session, Tumor Biology
7 |: r* E" C% Q9 t x6 N( D# ~( k4 M7 k0 ?% U0 k. s
6 E% e: K3 i7 f/ P* c
Abstract No:9 ?* b, O$ h% F& _( o* U! e
10517 ' }1 n! S0 C+ C9 o$ _3 E' R/ o$ b. u" [
2 A8 A& D# L7 C/ F$ G) ` k
1 C* O- H' \( F; \
Citation:. a# i n5 Z; I6 {' Y" e
J Clin Oncol 29: 2011 (suppl; abstr 10517)
" F4 u& n: e/ h* T' c. F" W4 ^( J5 _, D. y2 V
/ _5 }$ u6 D. {Author(s):' `4 S2 P2 x/ B! e' W
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
+ f) n' Y7 C# D: \: E" M3 p6 _( C! a# p( f6 @; }9 G
9 w. Y& Z; p" e: H; _* v
. ]) M5 W* N0 j
Abstracts 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./ \2 B1 X1 H3 Q$ b7 \; Y% }; X' D) n
' w- I% g1 s) }! Q# q9 E0 nAbstract Disclosures
8 k" D6 b1 w3 u. M, s2 @: w& I8 c- e$ k& [4 l
Abstract:# I( T& E" P1 u3 A% ]% x Q
' K/ {- N" X$ m% U5 k6 X- [9 C# i8 ^' F. _: b+ T' a: _
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./ k: ?* f! L+ U8 z% @$ X8 N) g
3 P2 r- ]9 j7 i8 y
' O* C% O' O0 A' S3 A |