Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
6 Y& f% h9 B2 W& A
) D5 k0 ?8 F) i# ]. j
: U& F6 W' N7 a, P. Y8 S" ]Sub-category:
+ Q7 H8 D$ V' |1 Q% l3 }Molecular Targets & l4 |6 c1 S5 r2 C
7 `/ Y- c* x6 C
4 w8 E4 ?* t4 B8 X9 M) ]
Category:
) o/ X6 Z- W; d( M& N. FTumor Biology
8 S/ I* Q. w& }9 z! s2 r( c8 g2 d0 Y% v7 F
$ N& }& t1 R' |3 t6 w# _Meeting:" V) |& A. m& O7 P6 @/ M% L, M
2011 ASCO Annual Meeting " L$ x3 z8 l0 g- B" k
0 X0 f1 W% y1 O3 @2 t* j, U* ~4 l1 v' U0 B
Session Type and Session Title:% S. v- g3 e9 l& s1 f5 k* _! W3 J) j
Poster Discussion Session, Tumor Biology ! Y, C; b2 {0 A
D9 z" ]$ r# l' o. p, S' p) [* u( _! v( U
Abstract No:3 ]0 K% S0 A6 F# X1 C& N
10517
5 i% t( [8 M5 S; y4 h9 g
8 O! n1 R$ p! U5 i: l+ j' L4 F- ]) O+ X2 g: R+ k0 U
Citation:
2 @. G2 h: L5 S+ U0 I3 Y; f* Q6 K, _5 xJ Clin Oncol 29: 2011 (suppl; abstr 10517) # ~1 J# e5 s+ U
' o: @) \& w% M. Q
* K7 R1 |9 T/ f' A. SAuthor(s):- s" t+ v% u' j
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 1 i- _; ]( F2 e" \% U) N
- x0 r/ z$ p P4 S
! Y9 O6 O: O& Z1 M I/ W2 W* g
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.
8 }: G0 X& g) {& ?
% x. |2 S6 f# H( ?+ P' lAbstract Disclosures
" f3 p; A( m5 c8 j* z( B- ^7 r& r& v; w! T( ^
Abstract:
) ~& h1 _( j* {7 L0 u `: ~/ @
u2 C- Y' Z5 O, t, X
% ~# Y: |0 q0 L# h6 nBackground: 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.
/ Z( e7 F: M/ r
' @4 r4 W3 k% y6 Z 3 r- `1 E6 D! u4 ^
|