Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page 5 Q9 D l6 S( `" }
- `0 F5 P, A7 ~, ?2 M3 h" o, \
1 k, x$ b% n7 N6 r' V+ Z8 {
Sub-category:4 j$ O8 S( X0 ]% _; F# |% [: s
Molecular Targets
+ j! Y% t& x8 h% | n
) J% f, a% ?# ~# |( E: O# [& K0 [+ ~' U' x! O8 h& m8 \* ]
Category:* Q3 [9 s, B, ~# |/ y: S2 t
Tumor Biology
) \+ ?3 n; F/ h, A2 p" i
. U! R- y3 Y6 T" m1 [/ g
9 b3 i A2 `5 K. h5 T" PMeeting:! ?. |9 ]9 T6 S
2011 ASCO Annual Meeting
8 K3 E; j, u: z& d- _$ `
0 `5 f& M: J2 Q0 m9 c9 ]4 p# {* K* ^% H/ u% o! Z( m2 ^
Session Type and Session Title: b8 Y0 k/ e0 Y+ T L& f2 W
Poster Discussion Session, Tumor Biology 6 h. v6 p6 O9 S% y) Z
8 y# y4 a) h; ], p
! {# S' n+ N- S7 Q! M1 x) f
Abstract No:
2 C- a0 {( h0 X) q7 S10517
% R+ e5 B7 U& C! f; q
5 `2 T. `8 B! P" \ l8 l& N) \7 P4 a( d
Citation:
! [/ i# E. P) Y/ s* \J Clin Oncol 29: 2011 (suppl; abstr 10517) " D: R/ `) }/ k! e7 I' t
: H7 e) S) B3 F0 X) _% g! c: v/ `
9 m/ {* `. p% L1 Q6 d. jAuthor(s):
. T) W' q6 `3 V4 e0 C% g! h3 G: @' sJ. 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 3 z5 d+ ]+ X( O- H
! G V0 l$ j8 j4 s, B& {
2 {' \$ p4 k a8 f* h& i8 h, w& h% R5 A% c6 F
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.0 a2 p4 N% }9 T) V' u' J
5 A% }9 Q8 e1 C1 R% \- ] I: I
Abstract Disclosures
; h) ]( }: j U8 Y0 t) U. ^) B' D- Y, n
Abstract:
; g% B7 L& d9 i: ]: {% w$ V0 c" q' v$ F; z/ g. p6 f
`1 F4 [( f( Q @
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( f0 i6 h3 x1 k: A4 f1 i1 G4 d, S5 D3 D- y8 x
5 ?! Y4 G" v& n* G. u |
显身卡
