Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
7 F* |( O' ]: _5 [" K( {
. _7 p L2 ^* f1 A3 V* P8 _* A" g, P
" ]1 p/ m; B2 Z0 ?4 i4 T; }- u9 MSub-category:
* z% n- _/ I# M+ m$ W" EMolecular Targets + w7 {6 B0 k1 }% q/ p4 {# R
/ {( j7 t2 T* h+ X1 t3 |/ q
5 S- j9 @$ ?3 Y+ P1 ~Category:
6 u# e3 u6 p# h& R9 e- a2 STumor Biology ) x/ C, w0 P: U( X
, {5 q1 F/ w8 s2 I: n- W3 M
% ?0 r. E" w1 n2 N
Meeting:, f" D& E- H, U
2011 ASCO Annual Meeting
2 `- x2 r6 x7 u( F6 e0 s$ \* C, ? _/ H/ \
3 k! L( `! ~+ `, f+ w% T
Session Type and Session Title:
5 j# Q k7 T( kPoster Discussion Session, Tumor Biology 6 _9 x: z2 W" X) m6 \* a3 ]. a- R t
3 G% T0 w6 L3 F8 Q3 A! h8 l2 U F+ ]! _9 }
Abstract No:
K2 n2 V" a6 p6 F10517
3 O) S& J( e4 G. t
X3 S! c! B- s" ?4 _1 J6 w2 n, b c8 j. y3 r' h
Citation:
! f$ o1 y& B. |, j8 E+ x# UJ Clin Oncol 29: 2011 (suppl; abstr 10517) 3 I) O: C1 c' v( i
$ P0 M% q" E4 `7 A X! J& I
, M" g% D9 e! ?- R& A& ~
Author(s):& o% _+ J, ]5 P) I
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
! k5 W6 j2 ~5 ]& y
+ b; X( ?9 r4 m! ]1 q3 z. F) C6 g: y4 @5 H* g7 A, ~" w. l0 s8 N
3 \! o/ B' {; p2 A: w, }. G( A
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.6 l" ~8 T8 v5 `# Q
0 B, B" c2 Q( N9 F( uAbstract Disclosures) A( K1 i# @7 h2 h/ v- O$ B$ W* D
2 d/ Y2 n" \) X' f
Abstract:
/ ~( t/ A q# m3 N3 w4 y
+ a* ~" m: X8 g% x4 F# L; Z
W1 D. I- ~) @( ?8 ^6 MBackground: 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.; d ^+ }! O S8 [
8 A+ u/ g; s+ H( c9 l) }
9 \9 O( _1 h: z4 E |