Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page 6 l( X* |6 d( H: Z9 W
% I- b1 K1 c' R# x2 M
0 o% M! X, k" A
Sub-category:9 x( J9 h1 V+ r. Q# U1 _ N1 J
Molecular Targets % z5 C; t+ l/ U$ H
( q- m5 C+ g3 Y
1 u) Y$ P7 Q6 I' `0 {; O' iCategory:
V8 p, a6 y$ P. E g4 dTumor Biology $ |3 {: N a; T- g1 d3 w
6 }. b5 F& ^ n4 \' ?
+ m" `# R5 |9 K* [Meeting:
: e3 b- J7 E1 X1 d( ~5 Y2011 ASCO Annual Meeting # C V/ G2 G. u4 s0 {& h
$ G2 B+ u7 J& X$ @
1 z( h7 V; S5 U0 o% c0 T4 V6 D9 WSession Type and Session Title:
/ x/ e J5 p$ Y sPoster Discussion Session, Tumor Biology # r7 P: Z, K' a9 w( S7 B
' t4 b) ]/ P, p1 _
; K$ ]6 f! g& J6 O' b
Abstract No:
" m' y# U7 X E10517
5 M) M7 m( m& i1 _6 w" n% o: k0 ^! K3 M: `1 {
p. M: u6 T! K6 A6 p; y9 t! u' w
Citation:
3 G$ F. C9 v+ `& v2 X. WJ Clin Oncol 29: 2011 (suppl; abstr 10517) ; t: B0 R$ L/ M3 Q; Z" E' d+ X
3 C& l6 A9 E7 _: `4 x* a& p' R
% a; G2 f* x3 ~- K& CAuthor(s):
& L/ c6 [; O9 [ BJ. 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 , x+ E" m- q4 r* C3 W
- a1 W2 h% R8 z6 B6 m7 u
3 K% T2 o( u) l) o0 Y+ X: F
9 [1 K5 p9 j; q7 F$ YAbstracts 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.
- X% y% I6 M3 @% U* w
8 K* u9 ^% s2 P5 vAbstract Disclosures" p0 U0 G1 ]9 b' s7 x
9 ^1 N! a2 b# d, u1 H" L
Abstract:7 M5 I9 S2 r; \
: ]7 V1 U4 O5 [ }' W: i x/ X; B+ K3 b2 N+ E, v& j5 m' t/ X& S
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.! y9 w" B+ g% o* n- c
' A6 o0 m1 O& Z& ~ X m; W6 s
) K0 E+ i9 |/ |/ C8 m |