Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
, M5 I6 b% w* W# C( H: m; s. u3 [2 P7 v2 L& n) a) d
' |8 c8 u2 _ D7 f8 bSub-category:
+ {3 L5 ~5 A2 g$ ^$ M) ~* Z" O. E6 O, B AMolecular Targets 5 @) E& Z! ~& z( K7 G7 |
0 m( @7 D0 b; H9 q/ E! m' ~
# N' ?4 x8 W8 H$ G# VCategory:8 x# P n; _7 X* N
Tumor Biology ; d6 I$ O* \$ j% E; `
/ R; Q% g+ t0 R c+ x9 l
; z1 x" _6 C8 u9 L; J. Y7 AMeeting:, {% e' {+ z9 W5 m4 M
2011 ASCO Annual Meeting # @7 A f. Q7 H, |
# O7 c/ B/ ^3 \& |
6 r/ B0 f- u' N/ d4 G' ]3 h
Session Type and Session Title:( q8 `4 N! P# C/ Z
Poster Discussion Session, Tumor Biology
. z0 n" P! @3 E0 N7 v% O
0 ~- q# L: m% G& p; |7 s8 i9 X0 z0 g# A: ~8 b4 F4 _
Abstract No:
3 v8 `2 T- T. l8 {10517
; p5 y! P( R7 D/ F$ a& G; \% Z- p# z8 t# Q7 L; u* O6 p
) r8 D- U0 | ]/ S
Citation:
) ^& A' K! O' ` s& L, i9 ]; I7 LJ Clin Oncol 29: 2011 (suppl; abstr 10517) 9 \9 N* S% l# Z$ m
0 S ^" L% Z3 w9 r9 m; V3 F7 C- ]
/ C9 L1 ]% W% L) f
Author(s):2 H1 R+ H* j l6 d1 N+ g) P* L5 u
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
% { \2 o- j$ u; h
" H7 y$ m; p `# u* a, ^* r* x$ r( V3 r5 e9 y/ C6 l% d# j6 j4 |
% E# C b5 u! P$ L: sAbstracts 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./ t8 v5 r- n- J& {
) R! ]7 J5 f+ m K, m) D* t
Abstract Disclosures4 T: i+ Z! f: ~, J
5 z( w' W8 q: q# z+ @& Y! h/ v, p, `+ |Abstract:, k. A0 y; o, [( w' Q3 c3 ^$ {% k
/ M; x: L, X' w2 r+ Z
h! k" c' J0 ^7 C; ]: ?- x* ]; P0 TBackground: 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 k9 y' p9 C, ]3 n
( `0 F& |6 L5 P * Q- t: z, {6 g( o+ @
|