Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page 1 r4 N4 o8 `6 i" U8 j% _
9 r1 f, P( Q& y F$ V5 r9 y5 Y" z# Z; e# y/ G" _/ S. o9 A4 X
Sub-category:
8 h5 |& m; p( v! O" EMolecular Targets 0 Z6 y; ?8 N" F7 V4 n3 J
3 s4 h3 Y6 E$ X1 N4 m- p- W/ N/ t. ^
Category:
4 J/ I6 i5 [5 E& U1 rTumor Biology " y$ c/ p V1 \$ Y, P3 A
1 _- U6 j3 v+ Z, D7 k+ h
2 X* l- j; Q5 D e' p5 ~6 pMeeting:% N" ]* M& N; d( A9 |
2011 ASCO Annual Meeting
) w v r2 I) K2 d7 U
3 g" o; `* l3 g# q5 S& a' D& \6 h+ z# l$ J
Session Type and Session Title:5 N/ Q7 {2 f+ ^% c
Poster Discussion Session, Tumor Biology 1 t8 y; P/ ~) M2 A# A: T
Q' {1 v) l" h" T$ A; W8 m) A% j+ T! k$ C p8 \8 I9 h
Abstract No:
* e3 }9 m0 i5 k10517 0 ]; K, l# _7 b- x8 }$ z. c4 q" I
5 ? i& [; z6 C1 z: f
; h- H' H1 n; W0 J$ U7 b
Citation:
& L3 D% `1 @1 oJ Clin Oncol 29: 2011 (suppl; abstr 10517) 4 r( d4 W0 c; g* Y" ]
( k6 s( v" T2 w9 |# y" H
% G! S9 b2 m5 o5 VAuthor(s):
: [! @* F; d# y: |6 }! wJ. 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
# X8 ]+ E$ y% T
# O' y, _0 n% ?2 f5 d' |6 V
9 n) q; {6 U. `4 p) X, V- ^% t" _/ X+ u6 }7 e! C
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.& y) D& ^! ^' k; ?' s
/ H/ Z3 I% n+ Z9 ]8 w$ L
Abstract Disclosures7 h) p5 |1 ~+ z5 P; o. h
8 \2 l; F' a o* hAbstract:
4 H5 K' Y9 U8 x
9 N2 v- V1 V. Y0 U, q0 C( t
$ S7 V8 I2 O4 E( ~2 _" CBackground: 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.- r; H3 a. V+ z$ [
' b/ o$ O/ ~# x
9 K' P5 c5 y8 \' j* [, Q$ O |