Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
; y9 v( K5 k( s/ h/ |, J5 v' p; s0 W- a7 ?' x
. a& X) \& e& O( eSub-category:
) H" g% R/ O* |) ?) h1 y- U# u* ]Molecular Targets 6 w4 f0 e7 g& R$ P
4 k/ p/ o/ J6 {
7 m; i2 k7 l, U. uCategory:
& R0 L" X& G% P9 U3 RTumor Biology . O7 I! M2 f: X
) s A, Z5 e, K" {4 I9 y& ?0 |8 b5 D# _! w8 b
Meeting:
& |. ~4 r/ R2 V' L# c2011 ASCO Annual Meeting
2 I9 `. n& b) M
8 U. v6 U w( v6 z
1 y, [7 K" l, K" mSession Type and Session Title:
* D A4 H% y9 ]' J2 Y# L& t: j: |Poster Discussion Session, Tumor Biology
% D2 z. ~, ?8 U" S1 d! `8 B3 t
- y j& m+ ^# _( s* e- M/ W; b! v) h& _. j
Abstract No:8 y2 z9 O( C) H6 u5 d
10517 # V9 x/ Q" `) r
5 T+ S% z$ {. o0 l
1 n# W* r) O, ]7 [( i8 l3 ]+ L' WCitation:
3 W4 c1 @+ ^2 {# QJ Clin Oncol 29: 2011 (suppl; abstr 10517) ! @ N, J& j2 h. Q, z/ Z
% n, B w# {& H/ Y$ y
! `; H; M, h$ }Author(s):. }9 P+ }' l. u/ ~- u0 ?
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 " T; `( Z% U, l
* `7 d \' J. D2 w; T% J; S% H, h' B
7 F' Q, W3 J* U3 g2 U
; \% U" q( p: uAbstracts 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.
; x# e: q) c7 m0 X2 w( V, M" e* S2 B5 [( V. \8 Y- w$ V* T' c" y" W
Abstract Disclosures
& @8 t. [/ q! d1 ^7 x8 _1 h
* c' n( z* Q; cAbstract:9 F1 g: z' N* w, N m: x1 T
6 _2 [* q+ B4 i! t* w* C
V! K6 a5 T, n. V1 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.
6 ]) x8 D6 z% Q! r; z0 W& v
" M1 h& M& g5 P2 w/ w) j3 s
. `$ S# ?3 t/ S; A, G3 {3 V |
4 I, o- K+ S& s2 R: Z
显身卡
