Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page % W0 k% ?3 x6 q( _' q3 u! i. e2 g
) a. `( o& p P' e6 l7 J1 ?& K
" r- K S& S8 A+ }& \; {0 t& WSub-category:
5 b: A6 E M% NMolecular Targets
/ s7 M2 p* I$ {4 ^. y& V
" t4 H) ?; J8 o+ c- A8 H+ u
" F9 T: t- M8 L {; HCategory:+ L9 ~, M: E. q
Tumor Biology 0 _7 O# g& h6 t
( ^" |5 u& F u d3 }( g, @1 f
Meeting:, l% N! X! _! L$ L, U1 j% y/ _, K5 G
2011 ASCO Annual Meeting
$ O" c: T4 t D8 T/ A+ h' R6 o! A) e y$ d; R d( y7 v! g5 r
3 @& Y {6 x6 o9 T
Session Type and Session Title:
# u3 C. ]$ [! n& z4 N1 nPoster Discussion Session, Tumor Biology ' L3 A$ H4 ^7 ^* }, J
4 ]2 @; t' d, @. L: N4 k+ g; K! E' A, V# V# `. Q/ M1 O1 x; R
Abstract No:
( o. P$ g/ M* H/ M% [10517 . M4 g3 `' z8 V" J) D
- B+ m$ {% i4 w1 u6 d3 b5 q7 @, \/ Q
3 u7 S. _' }" V1 T: ^
Citation:$ H; X- @6 U- m
J Clin Oncol 29: 2011 (suppl; abstr 10517) " R% h: l/ ~ ~ a5 I+ ]! M
+ M) o- A/ g5 _6 ?+ @- c7 h9 h9 i$ z; ^- M: M* w" ?
Author(s):! Z! ]+ I( r7 ?
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
% |8 }# X+ k# v4 L9 D y% H2 L: \% P- U3 S2 k! t# r/ C
2 w5 A7 W8 {* w6 q l: q! [9 s* p3 l2 U; o% 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.
8 Y2 I4 w$ h' M+ E6 ]0 \2 y Y8 Q* _' n- ^
Abstract Disclosures- D8 P7 x3 k8 e) c
4 L& J. Q$ g; p. c# R6 ?
Abstract:$ s2 R1 Q% v& }4 P2 m/ A2 D, B
) Q% V& o+ Z( Q2 r6 }9 O. W
+ v# d( x# p7 i$ ^/ \/ U
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.
* u7 B; b7 n6 g5 e# x; f$ B) B9 t% h) C0 ~# d
' f8 V# z' M- q; w4 z
|