Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page 0 C& y* I f- w, j
. X0 b$ Y/ G9 ?9 ]
& x- {1 x; i! o
Sub-category:
5 y L% z+ u& ^% w* N2 `Molecular Targets
* g6 E! h4 z; ~6 l ^( ~4 z
1 g1 a# ^4 t) w8 w1 I; K; ?, M ?- L$ `7 A7 A8 A/ y
Category:* [& i% l2 H3 @4 L1 q, h
Tumor Biology
) U8 E% ?" E6 f: l
P& X; ?& n$ V" f6 E- r( b
# h% k+ L# i( d' r* t/ F( xMeeting:
! z9 J! G# N& _/ w2011 ASCO Annual Meeting 8 }: q: U/ J" a, \, H
N3 n7 z/ \1 {
" x! h8 w$ e B$ z$ `6 @Session Type and Session Title:; j9 a/ m0 _2 m9 b( L
Poster Discussion Session, Tumor Biology
6 F$ p, t/ r c: Z. J9 y+ |( m& |) E4 F1 ]" \' t
2 U9 V& U3 i7 [6 v1 C
Abstract No:& _# ?8 y5 F! y" l# ]; C& G; z
10517 ' j7 d q" ?* ]( {' A) v) p4 t, G4 f0 F
* V; f& Y3 w5 f0 _# C; v
v9 y% s2 C. ]( S
Citation:
# b$ ^# d0 { a3 ]2 @9 {0 cJ Clin Oncol 29: 2011 (suppl; abstr 10517) " }9 B* v% y8 V9 g/ R6 ?4 R" }0 X
4 s6 m/ Y/ l0 x; h8 C6 h! ~
! Z$ B/ j0 {; p& u2 j+ mAuthor(s):
\, d5 I1 e5 `2 A2 t, cJ. 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
3 a8 F$ ~6 x; J- ]
0 A$ m* y! U- \/ B4 e H( J1 a
. x k6 x9 Z% Z6 P4 |8 q, P, d$ m4 v. n
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.& J$ K" c R- `8 x5 n) d% y
% d" l+ `2 O, G- o/ Q9 C. h
Abstract Disclosures
" S/ c0 w) W2 Y x. H* S8 {. T1 m) J H) z. j# [! s5 [# i1 c
Abstract:
# V8 S/ h: \2 ^! h' j& x, x8 g+ ^. Z: C9 C7 l
, v4 a# w' {5 V: V DBackground: 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.
, h4 t* R+ _0 |0 ], l/ d& |) [' b$ {. e( E: p
1 E6 ~. h9 `) _: h) K' w6 a! X: @
|