Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
9 p! A) R" U, I8 N, e
4 _# E, c' W2 \$ L0 L! z& L+ S) D. _
& v. `( J2 k% n' t4 PSub-category:
2 a( I* b/ C2 p3 a6 f: lMolecular Targets 7 \, L/ k' I) R0 z! T8 f
$ \" `8 u+ L4 n3 Q4 s" e
7 ~% d0 o4 |/ g! ?# b
Category:% o' c `& y# I" F" A
Tumor Biology
* t4 R9 I: w; g! G9 U3 z9 g" O; m3 B+ [6 Q$ b/ n' K
! }* m( t1 Z K8 D7 V" W9 X4 w
Meeting: h+ L6 Z- [4 U; Q( |: U3 g
2011 ASCO Annual Meeting
0 Z# s1 e* ~; L$ [, |. d# i
6 r# x$ R, t+ q5 k7 k3 y) {
. l" A6 O% j( `9 i# j2 ~& VSession Type and Session Title:& Y' ?2 C6 e6 g
Poster Discussion Session, Tumor Biology
8 [5 R0 r0 B. S1 q4 J( ]/ \1 E* B$ E# i
9 M+ V1 g/ E: c! Q' T' @9 [1 v% n2 C
Abstract No:& _2 X& l9 o* {% L, {6 x$ C: V
10517
- E! q2 o" B- f. `, {( c5 \1 R: o$ s; d( I5 ^# v* |% e# H
8 y0 X: D) a3 J5 ~: t& T8 t
Citation:/ T! M' D$ f# H2 Q3 `6 v7 Y
J Clin Oncol 29: 2011 (suppl; abstr 10517)
4 ~5 T+ Q q( w' S: P8 l2 L
6 p9 I! z, ^- h
' I; @8 B% T8 h9 J+ [ O! TAuthor(s):
; F; s) y, r* i: C( [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
( l7 ^7 w0 D1 J) e2 U0 E* |8 W
. q( z' }4 b" `+ s* ?4 }- @% S. j$ I6 s. n
! T1 U# b' c( c2 Q: `; VAbstracts 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.
- E- [( Z+ U5 I' p% P# z& s
/ d$ l5 x6 k" l. z; S* d/ F' BAbstract Disclosures
0 c" O9 n0 `. E' ~( m t1 p
1 ?/ S/ V7 c: x- \ l" QAbstract:
9 @9 k* ]4 }2 V: Y/ |
, Z/ s4 d; y( V$ S6 F. |, u7 |9 j5 T7 B5 T9 r7 w; 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.
$ ~ J: L2 u$ b* i$ ^! z& E: ^; s
" y2 N5 L- g3 M3 G |