Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
6 E; u" h2 h, H! }8 s0 Z( x
1 }5 T* q0 S1 A4 g
) Q, W+ W# O7 V) u. nSub-category:
0 f- ?! A4 M5 \, f. QMolecular Targets 5 U T( ^3 Q9 [0 n# J
7 Q# g; k* U6 F/ E* H2 V. a* @" u
" g- U' C, Q+ P/ c7 b5 G' @; QCategory:
4 c. u- c9 V U5 yTumor Biology
4 g- ^6 K2 b% \
9 J0 W, o6 _( \! b' Y5 `) T# \7 c8 a
Meeting:& {6 M/ l3 v: B1 m6 g1 a2 x
2011 ASCO Annual Meeting
3 m6 R7 v/ w5 z, r. ^0 z) y/ `8 {
. J8 ]+ G& b7 H- \
9 K6 ~2 U1 C% N1 H# R& X+ oSession Type and Session Title:
2 Y2 |/ w$ Z4 P) |3 e& P* {. N- aPoster Discussion Session, Tumor Biology
0 B. Z" O* s% Y) u9 c W, S; r0 X# `4 K/ @3 {/ Q
3 M7 y; L3 Z5 f( u: y
Abstract No:5 b* k+ B c+ J$ W
10517 7 q. k7 Z6 a, P7 ]+ s
r' I3 R% R- A; o1 B1 r6 u% ^- Q2 |
1 c: g1 u2 b& i4 s" V( z7 GCitation:0 A* G. W* a# C& a/ J+ {
J Clin Oncol 29: 2011 (suppl; abstr 10517)
* D. b; i% \2 N3 s
- D E' R) y6 N( S
7 c5 B$ h ~: `, j( }Author(s):
1 V0 W. V+ u% J& K5 s- [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 % A7 R/ g; V( C, `) B" G _; O
. t. m: @) \7 A, g
5 \0 A2 q: E0 d* o' F; x7 l) M( _; ]" a) C
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.
. {4 C/ c. `* T0 A& V( k7 v4 Y
: `! V: m) {% ^/ r6 M/ n/ z6 HAbstract Disclosures S* t; P( u. J+ r' C
0 k& A5 T* _7 V; |( P: D- @
Abstract:
0 q4 r" \& D. g( O/ h' `* g7 A+ W' ]% E0 Z7 \. Q
- p$ K, M f; M( ^4 p& ?
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 s3 M& ?$ Y) c& L/ W
. e7 u# d- v0 E+ v; R% M0 m4 ~
. i- e& D9 Y& T0 [ |