Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page 0 p7 `0 c# K9 I) r0 v$ H5 `
4 m5 n Q* I0 J9 ?% y0 k4 k# |
( s' C0 A. Y; G6 h5 M& MSub-category:
& ]1 s( m+ [ T( ZMolecular Targets
6 t* R& u( f% g" `) y
: N( |. M. ?3 l/ U" X7 G5 Q
! J! |7 Y. f& R; s4 HCategory:
7 ~! o- g3 k' s0 R6 VTumor Biology
- ` O' j8 r; l8 `! r" s7 L% r: i' B
" H) O% t3 M1 e
" |# z+ y V2 k1 K+ E. R. kMeeting:
3 U: {1 z {( I6 m5 z0 n5 d2011 ASCO Annual Meeting
+ ?+ ~! u C) c2 K) s; _- B" Q( u" f8 T! Q" ]1 H
5 d9 E' E' F; `0 `. I7 l
Session Type and Session Title:
8 f- X. y9 }1 i& b; lPoster Discussion Session, Tumor Biology 9 S8 @: g D( M ?) t0 A+ Q
$ H- {. E7 F5 v/ [% l& W" t3 c' [& G3 \7 K; P
Abstract No:; P7 ?1 X; ^; a
10517 4 I/ N1 Z8 p- P; X
4 l* k& n2 G" d; J
: W6 C9 z9 h- H7 p4 o8 ?Citation:
" U6 c4 g2 K6 `. j* ^' L8 |J Clin Oncol 29: 2011 (suppl; abstr 10517) : R8 N7 o A& h- q8 g
: n9 c9 ~8 i3 e$ }0 L5 s4 E5 ]) ^+ m, L. w6 j0 Q$ J* y
Author(s):
2 A) k' Q; o) s0 @" a9 K* L4 @9 VJ. 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
: O4 d) i0 t: H* d! k" _8 f) I8 }! o3 {3 S# @
; |" J D& V1 G& a% H) D! A$ B2 B6 c2 M" c' ~6 a! \, x
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.# g, x" E" r! A! ~4 w8 K
4 t6 [% S* T! a. N9 E
Abstract Disclosures7 U& T( w9 g! w2 k( R4 H1 z. V
6 X0 a+ F; t* A; N* y7 R& j g
Abstract:
: b: J( L1 e7 s5 R. K3 k7 A4 A7 b/ z; M! a- P
/ A2 K& S& x- e( N1 a
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.
# i, @) j* S! P$ n8 ]$ ~) M
0 r5 R* \9 U! W" [6 N8 o% Z/ t4 V/ i 1 e* H' `4 U4 J; a9 p6 ~
|
+ D7 n& b/ m5 d" Y$ Y. I( l* T
显身卡
