Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page ; t; z8 r$ x" m
& u$ ~9 J4 {4 H8 A! ^' S6 R4 J+ G+ {' I, H
Sub-category:7 _4 j- W7 f! w6 y
Molecular Targets ( X" B7 P. G# A& `
3 U- Z1 s" Y4 \* R4 I% x P6 Z$ q3 k4 z6 o; N! { i' u
Category:
1 A8 |5 \" Y5 r& l( }Tumor Biology
3 E" v( O4 A4 L: d s# w" U p
" x" P* T# R3 \( P' S5 X8 i7 k
) x$ |5 v$ o% Z; O2 u1 H2 GMeeting:/ S5 i9 X* b! Z
2011 ASCO Annual Meeting
$ u. {1 u# V. U* N: L
% @% A" v% w- J3 _% m* W* K
) `9 r. O/ r* tSession Type and Session Title:
1 r9 Q' l6 _/ M0 y& k% v- P* f# hPoster Discussion Session, Tumor Biology
8 E4 x3 G# S- L4 s: H- Z5 U4 c* \; {( P) N9 F$ }
' _7 {3 d6 Q$ E9 d: ]2 d
Abstract No:
/ H# ?; ^ s4 \* i) [) e: `$ H! O9 R10517
; \4 W9 C/ X$ W1 o' z, M* G3 x; |% z8 r+ V; U
( T' _' A1 U" g. [$ fCitation:
1 z n5 C: I+ E* UJ Clin Oncol 29: 2011 (suppl; abstr 10517) 0 X) R) a! o( Q6 E! i
& ?0 G+ ~* ] E2 ^7 \ q) F5 \8 d* J- G: l7 _% y y" a, F
Author(s):3 I% |+ ^) @, J8 O: H7 M# I9 l
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 : f* ]' c, e: ~/ e
# ~2 A) y# z- j% h- k( K
0 y) H Y. o" t/ |( k& x& n3 V4 u7 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.( T: u" C* ~$ @- g
$ O( W# ]# Z" X( FAbstract Disclosures
2 J# m1 `8 M K' Y
; Y$ o5 d8 G' i4 y9 ^1 gAbstract:% @4 V7 e# G+ p: o
! [; J$ K2 U) I4 f3 c" V* X" H5 {9 k2 ?7 O) e# J) z/ ?4 F3 @, L0 b
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.5 | `" E, C/ I! M( k5 \' D, I
; H( q' l# T: n- \7 Q3 Z
, `2 A/ K! K/ D$ t7 R
|
9 f, o I5 Y0 }/ o
显身卡
