Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page . t0 L, D) i* F, ?
- C5 h @- R- Z* Z7 V* n* F# N5 ]; |1 h, w8 H
Sub-category:4 I- ?/ u; Z4 j* k% M6 V
Molecular Targets
& S# M* r0 f, Q4 S. T/ K
; Q9 d. P6 h% {! g! U; C
2 q/ ^7 \& f( X$ @Category:: T* @( S3 W8 _' F# z4 L
Tumor Biology 1 x x0 w# B: R( A1 i/ T
( H/ c y5 l, _( v2 A
* K/ F9 `6 c$ h# u5 ?( TMeeting:
: K; u* F& E6 Z* @2011 ASCO Annual Meeting 8 C) i/ J; j- v) b7 p) y9 b
2 h$ y- Z5 {- I: w' x: ~2 S0 H3 S2 J R Z! e2 |3 f
Session Type and Session Title:
: s2 X1 Z2 V, T) V% P4 G, S* cPoster Discussion Session, Tumor Biology 5 c4 _3 }2 f' x4 e) a2 `
: e3 d* a k% t: Z/ Q9 a
# T- L9 m) J9 o+ z4 p2 e! CAbstract No:( Q" R% C+ \8 \! H1 C" a4 b# o: Y
10517 $ {/ |5 z. [# q/ d8 J
# _9 y( T; @# l4 X7 G8 |
8 D) v: f. S- L+ n CCitation:* W8 I) S7 i; B8 k' {% f5 e+ k) k
J Clin Oncol 29: 2011 (suppl; abstr 10517) ) p, \# j; {. ]5 f# W
8 g. H2 e, x) u: J* K$ q5 y
; e9 Y) `; N. J7 TAuthor(s):
$ v# n. d6 _4 {& S0 {" a9 }+ S! I8 |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
* s9 W0 ?6 k" f+ c7 n4 b
. P, Z+ B/ P! V* ?# D3 H w/ F U. U4 e; @) a+ M3 o) G6 M: ]8 Z
& a$ D" x. ^! V
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.
N7 X, A5 F O$ _$ w% l3 v" h
5 v5 u) I5 Q) S8 M ]+ v( c6 SAbstract Disclosures
5 J2 p' r# B7 n: k8 \
9 J9 q- D l ?, |+ c% d; ?0 jAbstract:
( H% T, P: K6 P( Y" B" ?1 l* R+ K' @, Q+ l/ \
8 F: @: E6 ], [; _; FBackground: 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.
' |# C1 j2 ]* L1 w* n, X2 ?; h) z% `. C! ]5 K( R4 ]% u* a
2 l$ t" c, N% d# s1 r' `$ D
|