Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
$ g* V( i1 q+ _* |
* V% z4 _% p u. {, d$ l3 Z- l1 ~8 _8 @( [* j3 V6 J# q# `+ ^
Sub-category:6 N6 B2 g& g9 v- R( g2 B8 d& c
Molecular Targets
1 t( m" n; Z. {+ D f% D) ~) [3 v, Z
6 m- Z4 `6 _3 g; `$ Q; vCategory:; N2 J4 O% g. O' e4 e6 B) H1 P) R
Tumor Biology 6 H. t0 L& S6 U- F
2 `1 ?7 l# z8 q r, H4 i: d; k% ^9 H
, i7 Y" F! X! \& x/ R9 EMeeting:9 j. R* q u5 h/ n, K9 w3 f: `
2011 ASCO Annual Meeting
& \ a& s. B0 B0 v! G' @
1 W; p3 h: ^1 a7 a
' T p# F V3 \. LSession Type and Session Title:2 r/ }, p& z7 s. i0 M2 ]' d7 {
Poster Discussion Session, Tumor Biology
* H" p( T2 B# y4 `4 z5 ?! `6 h+ i- g! h# H6 W. [# p2 e& e- t
6 T6 n3 ~, m( A4 n
Abstract No:
$ D. y( |- R* l- f10517
6 R |! N& a6 _ t. k) u
7 y+ g4 i* v( |1 M; \: Z* t/ b6 B- a+ @1 i
Citation:
0 ^7 d! o. _ {; n0 _5 f( L- J |J Clin Oncol 29: 2011 (suppl; abstr 10517)
8 |1 S6 N4 i/ n) ^9 v* X6 g* D1 t* S5 T: A. [7 i8 n0 r
5 @' l3 B P9 d$ S. Y6 r3 KAuthor(s):
- _ z2 P, s* fJ. 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 1 w6 v- i, {/ b0 M4 f# o9 V
, J7 ^# n1 _! \4 w+ j; S5 O7 u( O' q! F( M. V
8 ^; m9 d& y9 e) I
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.
& W+ R3 V6 b' }/ L% |; H0 i5 x3 `0 k I, v
Abstract Disclosures* ?& u6 y; O& e, a! J3 M
6 O8 n% B& f1 l* L' N h* M4 g; I
Abstract:2 `2 j1 Q- r* v- J4 G3 k
' \/ f; e) x# p
% t H, X9 m" A& M+ I! v2 I% QBackground: 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.
+ u: r; ^ i6 o4 m+ N+ R1 g e
) U( E9 p$ h' u% D
" j2 \% y/ F4 p4 O. U; O+ a/ o |