Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
5 I3 h" Z& R l+ k- }8 x6 }; ~, N, C% k# ~1 |
# o* p8 R. T; q2 B( ^9 A
Sub-category:5 t# D8 y# p2 y; h% x8 [& n
Molecular Targets
@) r5 ?7 W" c$ ^* I7 `
7 U- Q7 p3 d& {. `( h' q: ?" }$ b, [# O: d+ @
Category:6 ?4 h5 n B5 h
Tumor Biology : w3 k) b$ n. `+ T- X
& J: a. C- `/ O+ u; F; ?' C) A( ^# c q. b( `
Meeting:
& u+ s2 h/ g, s2011 ASCO Annual Meeting " m2 a' y# j3 u6 I) N/ Z
0 P# F3 n8 q4 |9 I* `3 {
/ C! V. y. h; _. M
Session Type and Session Title:
4 ~$ G9 C3 c0 w5 z s: x- |8 tPoster Discussion Session, Tumor Biology ! ^- ~7 d8 t1 n
5 ]0 ]2 e; a( V5 x" A6 i" F. v: G# n( L' z! D. b/ U" V: Z
Abstract No:
) m p% [+ v* J% R8 Q- `10517 : t) t" f! q% R* r! r- V
$ S- I. v1 n# N2 D
& s# J8 k* v, _5 oCitation:8 p; K% F4 i- `
J Clin Oncol 29: 2011 (suppl; abstr 10517) " P) h" c% K3 d# |9 w5 G8 m
9 `: [1 B0 l5 y: ~% a
8 q0 U% P3 J f! }9 X. c' B
Author(s):
: J& R* @6 K" |7 o3 [. pJ. 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 ; c) {6 _: v# |+ S0 F2 c V
" Q6 ~( ~- \ Z: n* x4 ^: F+ v; L5 T: F1 L8 X; c) z2 r) A
! p) E ` Y# t/ c4 }; J' A. G
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.
" l$ M$ h: z( r0 [2 D) {, K! }5 ~9 h. k) I0 S/ C) [. m ?
Abstract Disclosures
' x. W" }4 m# E- |
; R0 i8 t M2 A4 a- e8 dAbstract:8 X; q1 t! o# t8 s0 z8 [; R$ {5 O
9 ]5 H+ s. A- b( a) M
# d+ m# |4 y# ]! u! k: h& n1 y6 y
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.
9 @; t& u/ W4 w5 M
) I* _+ o) O" ^4 n; S2 f t
5 V- t( t; p: j6 Y3 ? |