Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
0 c4 ^9 p- o$ f, g; r: t2 j% u
8 ?4 Q0 c/ @9 s" B; A" J8 ?# q* u5 L
Sub-category:
I7 X5 s- {$ A: FMolecular Targets
! k+ r* Y- L& C
3 ~3 n: P' D, D* t+ w! [6 l0 ~/ z( I6 B* m$ b' Y. o# A
Category:
5 ~! z4 S9 E* b, k) `2 NTumor Biology O- X* f' _9 Q
7 ~ C% p* O! w; i, W; \' x5 T1 f, ?) [7 Y. H2 C. y
Meeting:
" d0 k# @9 I( x8 p2011 ASCO Annual Meeting , z2 a# b+ ]- f6 a ^0 o9 J
' H/ O: l2 ]' V- Q0 o/ z4 _! P
P3 U8 a! L2 n0 P* @Session Type and Session Title:+ Z9 e' G6 V" B7 O9 l$ o% k
Poster Discussion Session, Tumor Biology 8 h: X" O1 N; X
4 I0 Z& ~6 K5 N1 n
' i1 h: H, {( K& W; mAbstract No:& O% s) D9 H; k2 U( {6 _
10517
5 w S7 K3 }5 u! N2 g3 u# u4 g( [/ B7 F: w
) C7 B" y! L* Z- X0 iCitation:
+ h* `( k1 d( T, e9 UJ Clin Oncol 29: 2011 (suppl; abstr 10517) $ x2 v' g* \6 n) W5 }( U
+ A3 Q2 l% i% p0 o4 ^. n) z
5 i& F9 w) l a+ [Author(s):2 M0 |! W5 }/ e) p8 w( p, Y! w' t
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
9 {/ S3 c, j+ I% h: ~4 t# H4 x- q
n# ?% v2 e" ~, `. `+ k7 R' N6 U* [! G9 @
$ t. O, g( }, J/ g l! X0 Q
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.
5 h1 j& F0 j0 B7 v; Y% |) I- Q# S2 O( G& I0 z9 w( {' ?% ]
Abstract Disclosures4 k8 Z) f5 P6 g% v- N* W; G+ x
3 ^- ~/ \* B/ w. J+ g. {: lAbstract:# M# `& s, ^7 }
/ r k; n, X0 O% r8 W3 b- Y5 v+ K5 ?" ]* a2 b' R
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.9 Z# W. ^' N X3 Z5 B$ J
% @0 q, B) v$ B) V
) N7 H/ l7 w+ j( K |
显身卡
