Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
6 \2 \; E$ u% D9 A8 U: K- c: R
' P7 z+ u0 n" l* I& l: R* q0 c4 W- a+ V+ g. p- W; N! w
Sub-category:/ g0 D' ?8 i$ x
Molecular Targets 1 D1 [7 O, O8 E4 ^1 |
" r$ ~: ?# l+ k# g
6 J- F* e, v4 T9 {
Category:% I# i7 l5 n, `5 }2 d# d" ]
Tumor Biology
* |/ W# y+ P( O) L2 B8 |# d/ ]* L- H9 o
1 C" @# y9 x/ H4 nMeeting:5 X( {; h' Z! X2 W9 ]
2011 ASCO Annual Meeting
+ B. `& ?! { q6 `; W) c% S
* o- w. y2 O$ A" l" P) Q) |; s$ P$ K2 a4 p* R- |
Session Type and Session Title:
8 L; T6 B) |6 B( XPoster Discussion Session, Tumor Biology
4 j- O, X' ?2 J4 Z z0 B/ h- G* \) g3 `
" N% N. y% ?- E c- T, F
Abstract No:
1 \! J) c- a2 Q7 x7 K$ S+ B& ]10517 " Y* G0 [- L* ~
9 X! w: J8 [( Z7 b6 j
* C) l% q7 Y, w: i. W& QCitation:
; a+ p ?- Y& c0 r, p& @) y" AJ Clin Oncol 29: 2011 (suppl; abstr 10517) ) ^: ~3 Y: F. p7 [1 b
2 R l$ Q, s( n. y8 s
Z6 z8 L8 U+ n% {- AAuthor(s):
8 s7 ^1 A, d* d; w3 ZJ. 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
3 {* p: e5 F$ v- K; l3 y, m1 s6 }) G4 |4 B9 X
! \ {& T4 \+ O# I/ ], _' s' Y7 R2 F2 L- z
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.
* D1 Q( e) K! ~! ^- [- \0 H
5 M' R* M y" ]9 R9 [$ X rAbstract Disclosures* G- H/ k) l; K' U1 ~
( r9 w& z4 _" }6 c3 @! d' l1 V- wAbstract:) z! D. Z! J" x0 p. t" L( Z
# ^& O; Y. Q6 F6 p0 g0 q# K/ M4 D0 ?8 @
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.
4 \3 k6 L' T/ }" s
* u% H+ Y! q) C8 ]# f* F9 o2 n 1 k. U- U0 q: t8 S6 X) q! \2 W8 A" @
|