Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page " W, ?1 \ q! X% F& ] Y" E
% H6 {: P, U9 o! z& ?# ~2 f/ Y! Y8 k3 l& n& J7 d
Sub-category:( Y6 X% u8 x3 e' ?
Molecular Targets % W' i, n0 V7 B( D* D
3 ?% b0 c3 z5 e5 P+ _9 u1 e2 x/ O9 i. n
Category:2 B$ u: ^- H! ~7 P+ X# h8 ~$ O
Tumor Biology
+ A/ ]" n6 {$ ?2 v/ U! B. o4 ?0 ?
" C ^2 M; h1 r. HMeeting:
$ J" C& H7 G( E: _* e( m2011 ASCO Annual Meeting - S. c ~" Y! _; ~$ L. C
7 ^# {/ N+ c7 j/ D5 {
9 A3 P8 g2 t3 v6 c1 A; xSession Type and Session Title:
$ y$ U1 m7 m, y1 E% o; b3 k2 e& lPoster Discussion Session, Tumor Biology
: X" a' V8 o- Q0 a4 F) Q. b( b4 B* P- D+ o( ]1 d
5 V6 X) \- d7 b( g" V" PAbstract No:
" Z6 j( }1 C% q0 G10517 * B4 w& q! j. |! l9 X3 u. O
5 m9 `* E: N7 } T, _1 m/ J' t3 J5 a
, ~& L7 b* A7 r6 v
Citation:
+ d7 X2 Q4 {6 J7 {* i* kJ Clin Oncol 29: 2011 (suppl; abstr 10517) + ~, B& }0 Z: h
1 Y1 ` k2 v9 G2 @0 N
2 S. _& g/ j' a
Author(s):
% O2 U: f0 S' vJ. 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 : ^$ @) b+ P) N
* x# _* b; y$ O
& ~3 E' z7 n" j- S) P( g3 _
; {8 \5 e8 I* T: sAbstracts 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.
. B+ g6 |. D/ F5 \8 D, {/ a' \% D6 y
Abstract Disclosures
; ]2 y+ I0 {7 ]5 l) n# `* t8 F! z% h2 A8 c/ v# p
Abstract:+ v7 C' k5 @, b+ h* x/ ^
# N _, G% L, |# v
# Q9 u! Y6 Q8 Q: P
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+ G4 `9 p6 w8 C0 `6 Z
1 G+ i9 A! @( i. }" S& \5 Q , G/ l4 i- U& Z! }+ H
|
7 r% |8 C; k5 |4 }" y
显身卡
