Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
N ]) I$ Z/ [8 v! _5 h5 t$ M C2 @- ~# g
, G& ^0 c" A) e' }* L0 RSub-category:
$ M$ e( i8 _% V" @2 ^6 UMolecular Targets ! v, z, T" M2 J& B; U2 X" @9 F
9 }( P" o5 N; ]
% C: p B" P; |0 z
Category:
# B$ q# T0 H3 r- I: d5 RTumor Biology * o6 V2 v( O( R# W
8 Z# g8 i3 j \ }
9 Z) L9 u, M: G
Meeting:; X [8 w+ H ~5 T: g5 G& a
2011 ASCO Annual Meeting $ _- r" S- I5 Y' [7 z
0 q* t5 L# A4 z# n
" s; x) b+ k9 W7 JSession Type and Session Title:
' ^" d+ q8 H9 R2 F+ H7 n% w; DPoster Discussion Session, Tumor Biology
, W' ?8 r8 l6 }1 t+ ^
4 V$ y7 Q# x; S2 {4 f! |7 j! s% ^" I5 b8 B5 e4 q4 `
Abstract No:
, W' _ y2 E- z8 X4 Y10517
9 P, D8 O! @# W% K$ M4 s9 V( I: q5 V' D% i
; r" q- I# [3 J" r: ]Citation:
3 P) d! } D5 C y# l6 }J Clin Oncol 29: 2011 (suppl; abstr 10517) 3 z6 ~' o7 W& }! Z1 Z6 I. H
! L6 n5 m& I* { C* K
8 O7 z: A u( q9 h' E2 |, ^Author(s):
+ ?% p1 X% ^) B. H( X# R( i2 X( mJ. 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
0 Y9 S1 C1 O* I, o9 {4 v# e7 y
! K. {. c' A2 R- p# ~# x% F
8 c( v; V" o, I4 | p' y# ~( r5 h" H: i, U7 J. A6 ~" k F' 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, t$ v8 j$ I0 F% E5 T; @8 Q# x- E9 Z$ _+ A$ A% {6 }" `# [
Abstract Disclosures/ G+ U G( h3 C Q& w) M# B2 L
' X8 G* H3 m5 B4 r) I% ^7 HAbstract:% M' p7 s% l) X& m
6 S3 j. D& R9 f1 k9 e7 ~
' D% {# b7 M2 z1 {6 P1 ?: cBackground: 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.: [ K$ K, @ H- g8 }) H# n% z
7 f L+ v: \' X& h3 h
4 z) N, h8 M/ [2 t5 F7 d7 G0 _ |
|
11011102001537 )
+ u4 f+ ^( Y. Y, Q' t- h7 q& I
显身卡
