Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page ( K% D# j( f5 y' U/ Q
3 D) j0 d ]7 x
& I C' e1 q, k' p* Q1 [
Sub-category:
4 `$ ]# ~0 i& J3 \! h' oMolecular Targets - V% j$ _/ d/ w; [( V* w0 ^# W
1 }- c# c$ V9 B
' O- Z3 U& L9 E) OCategory:
0 {4 T$ W3 b# s) ^# zTumor Biology 0 J7 U# h V$ t w) D
8 I7 |, B0 _; w3 A' r) {+ y
5 J2 C1 \! Y4 [8 SMeeting:
, D7 C6 y8 d% }( ^0 w2011 ASCO Annual Meeting
7 P. D' g: B0 N+ B3 W5 I& Y6 K8 L& t$ x# B e7 r) @3 I
3 ~! \+ S( H9 c% T; E2 q4 @" [
Session Type and Session Title:
) O$ R! G, f" X1 \: ~- A) X3 M2 vPoster Discussion Session, Tumor Biology $ k( F3 G# D# u
6 ^! j$ H. h" ?
# v# q/ E6 i6 C( d$ j% s, p. B
Abstract No:
8 G$ C+ o/ j: s! _) y+ G10517
$ x& i, p- R/ H, f9 a& C
' P k1 g' E% \+ c' }" z* ]
& z( A) ?' c) X4 ^: L2 SCitation:$ G9 D' b O+ S5 ^5 W+ }) r
J Clin Oncol 29: 2011 (suppl; abstr 10517)
8 U+ u& w" I: w8 E
}/ F4 N9 D# k/ @. ?& }1 X1 \0 Y
. A w! G' p7 u, w0 ` c+ ]Author(s):
+ L) Z6 W: u8 x. O& \' J) hJ. 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
% h" {+ A) N* v6 g: Y
0 i' I; Y- A! W5 v* h& @6 j
$ F9 Y2 P* T) U& \3 R# H7 U6 _ {( ? h% R! |. D. f3 v
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.: ]! _+ m) \6 {3 K
' Q' m. a5 ?" z2 t8 ~Abstract Disclosures
1 R1 U& f8 L) [; g' n& r. e. ~& H1 W) _. z' T" O3 ~1 W9 }
Abstract:( A7 T5 D4 J" ` N/ E x
8 Z& A2 m6 y- Q2 L" B6 {, F
4 f& f) u" Y7 ~) J8 O/ O
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.
# w# }* V' b9 ?* q4 W" X# G. ]# \+ v! ^. m7 j! K5 U5 D+ Q, s
8 ~7 p( r9 b0 `& u4 S) e
|