Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
" U& n3 l0 N2 v+ N' \6 ]
9 e5 g. n; q1 o2 D; n- z
4 R; X3 ?: l \% [! j& V$ VSub-category:
7 r) }- F* k ~1 h& ~; zMolecular Targets " C3 r8 Z+ a2 d: m, I! m* v
1 V$ X4 o- g( N8 C( w# P
* k' r& s) k. G D# {' bCategory:# z: }( o2 ~4 U
Tumor Biology 2 ?1 a8 n9 Y4 q, @+ ?
) i9 B$ K) e! }% ]
5 _$ Y0 B4 O4 S p1 u4 m3 h
Meeting:
% h* i9 B# b, K; Q2011 ASCO Annual Meeting % F4 v; h1 T$ D: r" Q
0 G+ G6 a3 V' u3 I3 E
, k( n: ^4 g0 j$ s4 DSession Type and Session Title:
* N* Q8 i% h2 C7 @5 u- f* L' LPoster Discussion Session, Tumor Biology
& G3 k' R2 H9 _6 r* K
/ e8 H) x: x1 K. m& \% ]' n
3 d/ v! t! t T+ V5 W- a- gAbstract No:
. v5 B0 @0 O: `& Z10517 / T3 ?! ?3 t& ]4 a7 }9 V9 n/ c
+ c, k/ ^7 x/ X
; }8 j# C+ a& c1 H9 S# \Citation:
) M$ }; v- s A9 h: t) HJ Clin Oncol 29: 2011 (suppl; abstr 10517)
2 m. b/ z K+ Y9 ^7 P' h4 B& Z* b w: q" R! h$ t) ]3 }
0 M7 p% a/ h1 G
Author(s):
& W! E& E2 M& e9 Q+ 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 ! G$ h) q# L1 e) b( P
" ]+ r/ P& q9 ], r7 V8 w
2 a2 x4 }/ }9 {! X/ Z2 Q
" Z0 ^; l/ N& \) S% Q* x6 J8 g8 rAbstracts 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., `: Z3 {0 w. _' c1 G
+ v/ _' q$ c/ Z. r2 x8 n8 i, i
Abstract Disclosures; m. K2 G. a! R: H2 i) R
2 _, q) s" i: [, hAbstract:. A2 j' ~+ d# V/ B1 V( B# f, J/ v
3 w/ F6 `7 a+ O. D" ]
% [5 ]4 X: g8 `2 L; L4 t% w
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.3 U6 `* X {/ B+ M, q6 G4 r9 K3 J
3 j5 P/ n2 a# c, t) ~1 e( `, k
/ ]9 }8 y- y8 A0 X |
显身卡
