Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page " i9 N( u8 I# H
( J3 g* V# i! c6 c% r
) ~! B& T9 E$ q) H$ FSub-category:
4 E3 A0 b- b* M, I# J9 oMolecular Targets / H. n+ q2 p0 `: z) M
% A/ E4 [5 o! |4 c" I9 g* Y0 Q' k+ i
* t- B, ?6 ~- @8 ]' w1 c7 `6 ?Category:
! i1 f! B: ^1 `- S5 WTumor Biology
- z5 J8 e- v7 V& x2 C: J K* t. R% {' `4 _* k6 B1 {# W/ b3 w, Q
" H! p; Y+ a% \+ u. e" w* O
Meeting:9 I( {, u5 r. h( F% s e
2011 ASCO Annual Meeting
4 s6 N s( O1 Q. F- w; a; ]
0 ?- ]' F7 K$ M* W: _
6 M/ Q& z: F( Y0 ~+ V! b) vSession Type and Session Title:/ t: \# @9 i) _' o, u
Poster Discussion Session, Tumor Biology : J5 x7 D" b D- |0 I7 f% C1 l& [
& R* ? @, j3 z E) r$ Q; [
$ ]. ?. {5 o( P0 DAbstract No:* ]5 T9 c/ [6 H; H; `, i9 z
10517 2 e" B6 t/ N( k. u& u
/ }9 y% f: L) x+ e
7 Z& [3 u# ~( ]Citation: W2 {; ?) C# Y5 m
J Clin Oncol 29: 2011 (suppl; abstr 10517)
; [2 q: h$ Z4 {. z& G! B
! V- t8 m; S; {6 b6 u# b8 ^) Z" u. h
Author(s):2 |( E, I+ c/ }$ E2 `
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 # `6 X* G: x0 z1 I1 \- \/ P
0 l/ ?# Y# T9 y+ ]" D
: k# O: k9 ^9 j0 I! |& L" s* y4 [( Q! r
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.
" Z% [! J$ S1 v% I: h
, Y! _% J! _4 r' l' |1 LAbstract Disclosures
/ z1 G6 u, H/ {" }, t7 f$ f, H H/ f# b R: t7 x# Q/ v
Abstract:
( o8 n) c2 V0 X& B) e a
3 S7 t8 B4 | L9 _
6 Q8 K5 p, f5 s/ i' l0 |; qBackground: 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.
2 V* Y1 y) ]" `) o% D- z3 K# c8 D6 ^! T/ a8 F: `9 W9 A
4 |2 i& r* C/ s9 w, T |