Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page 2 B; d- D8 [6 T2 F# _- A
U. r! o2 V0 ^. X$ O
/ {$ j3 m' E! [: xSub-category:6 y& t, B: I6 j) D% R4 _; A
Molecular Targets 3 d7 j+ C1 Q4 z; C {, b
% X% N2 O: }3 K( j: d
, r8 `: R5 J* w8 }# r( V! V
Category:8 W! r1 n: R- c9 k: ^% E0 ]$ o
Tumor Biology : X' P$ f: [% k5 A
7 j; K8 W: h. K4 M! K8 f( M. c1 k# p* s1 Q/ o
Meeting:
0 p" \& w/ o0 u0 d, a! d2011 ASCO Annual Meeting
* V2 Y' L4 V0 z: S0 j9 k# K3 u9 O: [2 v, w7 L& X2 v+ C' P+ Q
- C- h6 R# Q. l/ M* _1 | L3 g6 ]; |Session Type and Session Title:( g6 Y# G# E+ U. F" }
Poster Discussion Session, Tumor Biology ; [1 p6 m4 z' [( d9 F7 e* X6 i
. o6 G9 L8 h P
+ N: g: @; U/ e2 m4 H( X* `Abstract No:
3 ]7 |8 V5 W' p% l10517
4 {( ^5 d- B: H/ g' a; |( }7 x) Z5 ~$ U2 `9 |( R2 `: d# G
" j1 i, T2 x! [7 F& w
Citation:
/ {; @- W" o" tJ Clin Oncol 29: 2011 (suppl; abstr 10517)
% C) w8 D3 S( D# C1 ^4 L
5 E' C* A7 M9 T# G8 O* R/ T' O! P e; K" m. ?# I. U
Author(s):
) y$ s5 V7 `, U8 Q, [ E) LJ. 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 r0 i P% G9 B( u0 u4 {: ~
) I3 `$ `7 v% ]2 K- N+ J" L2 }! E/ Y
. B7 o; v2 F0 V+ t) \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.
* y7 H$ D* x% ]! S: W, y( M6 \0 d2 v& M, s# W5 i: t
Abstract Disclosures; M7 D1 X$ Y+ T- I1 s
- H( M: D0 O, b* U3 V1 O
Abstract:
& T9 y* }- \5 c9 x1 c( c; N5 _1 @, h
5 B" n( m; I! Q$ ~
Background: 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.
" }' [$ T. E; W$ v8 S0 }
9 [! S) h. ^1 J' X% N5 i
% z7 V/ U+ Y, f& Y, e! C+ a |
- E8 ]/ [6 h* g( G8 M
显身卡
