Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page - O. E/ ]9 U1 b1 p6 f4 v; g
6 k! G2 P3 t9 I+ u8 Y8 q; T$ R% H- Y* z$ K$ H% s6 W
Sub-category:
# E, U( ]3 G, E0 ZMolecular Targets
$ T9 ?/ L: B& u
9 H$ N" j( k/ B3 c4 J/ x W5 X( r3 B7 g( V5 n* |4 |
Category:6 _% G! K2 X; x* A" E! i7 R% Z
Tumor Biology
/ V( _3 r! j0 w% q& t
% ~" X. s* t/ I5 Y. N1 k$ N
3 m+ l) _- C: [8 s( eMeeting:
# D' Q+ U& l1 m8 V' a9 C( E2011 ASCO Annual Meeting
: n" u7 Z+ ]5 R F% P9 B/ }0 J3 h' E c6 U) M5 f# x# y
1 T& b2 F% I0 c6 r( nSession Type and Session Title:
# T- d- k2 `; u$ k- f8 SPoster Discussion Session, Tumor Biology 0 g( O2 J, v# y* ]3 T3 h
# U6 x3 i# R1 ?% S+ V- o
2 J0 _) m. g: R O* B5 TAbstract No:! K' c' [2 S4 U( x* a% }& W
10517
) Y) w- ?( |+ v2 j8 j( g: H4 n4 p
! `! ^( V( K$ M1 W
Citation:
* f, F5 T' h2 }& w1 ]) NJ Clin Oncol 29: 2011 (suppl; abstr 10517) $ {! I( a* ~3 ]( G- U# u
9 x7 l" f' v Q
: Q2 {3 \% Y l* xAuthor(s):
8 F( g# f9 b2 eJ. 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 & Q1 f g) G! W4 @ {) ]' _
& G: n/ J" k/ s6 o- r# B# x5 O3 x& N, S
1 L& z% r! k- ~
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.5 A4 w/ k, ~4 u% a& l8 |2 K
, h* g2 l. F$ t0 R8 t
Abstract Disclosures4 \- C9 M( T( f! q# X
1 J9 i' k6 J# k) d/ z+ l! cAbstract:: ~# }3 o; ~+ O
/ v0 P V6 |7 k! u0 u- M j
: s, r& I' q2 x- h3 z% SBackground: 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.: d4 |% @8 R7 c, \ I6 k3 ~
0 K5 `2 |" h& P. d F) y
: q9 O) T# Y" \5 ~% t+ ` |