Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page 7 w2 R0 Q9 ?9 \+ ^/ {9 {/ v" \
+ u6 M+ o5 \: o) ?
8 Q3 T* G* L% K! ?8 b
Sub-category:
5 S. C# x$ Y: e( f& ^! xMolecular Targets ; }7 k* g$ }, u4 p) o2 e- F
3 ^# B1 l# N0 @: i( k L
% _7 J8 t: x7 E! Z% _( gCategory:
* q3 R8 u/ U5 P# R: t! mTumor Biology ( f! {% e* ^. [0 K/ w' I
, T5 z" B/ }5 e5 |! Q1 l$ d
; ?8 e5 P5 g. \8 T; HMeeting:
( Z& ~0 I. c% j' } o9 n* g& q2 B3 l2011 ASCO Annual Meeting 2 h9 n2 F9 e- h. Z9 B9 _& b
! ?4 N7 `* \# o. S4 R5 n: ?
2 F( J& A5 g5 ~0 RSession Type and Session Title:
$ Y, |7 `$ E+ i* \Poster Discussion Session, Tumor Biology 2 q4 G |( {. g3 }) g" q
; v/ [( ` h @2 K8 H, e
/ K6 i/ f0 X5 w2 ZAbstract No:
# d# ^6 K9 X% W0 Y+ a1 K10517
`, Z- K# ~6 ]6 y
9 s% D& k! r) o( a+ D0 ]7 c- t# D% k( _$ N
Citation:
9 }& V; i+ m* D5 ^J Clin Oncol 29: 2011 (suppl; abstr 10517)
1 I% u# z5 B. G" I; s- _% e }5 N4 S+ `( ~4 p) X2 U& Y
9 \# q* `" P- ^8 V5 @* w& x# n
Author(s):, I5 r2 e, ]" C" i- D: ^
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
. n* n7 S9 d$ T/ f d G4 I9 e$ ]1 ~2 f) ~& d0 f- l) V
/ S' U+ x5 ^" _0 g: `' W
, i7 W A* S, y e( C5 RAbstracts 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.
' s9 n) @" F0 v7 ?7 g1 G, P9 L2 A8 u1 \( m5 _
Abstract Disclosures. G2 h1 A. C& Z( u+ Q% Q
4 k2 R* I" b1 }' hAbstract:
* X2 J& p# Z* l7 u. z6 d( B8 B5 o( Y- `9 [; a5 o) C6 o2 i: U! q* ?
: g* I$ z7 m7 e& O! O# ^8 bBackground: 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.9 v$ H! \; n+ C& H
) `, Y& q4 |! v# _) s6 X. j' h9 x 3 R9 v0 a* E/ z5 g9 h* G9 L- f; I6 e! Q3 f
|