Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
" P6 m& \( r1 d+ w3 U& G9 f& u* @6 I3 @
/ x0 N0 Y& I! b- y4 k5 mSub-category:
5 \9 c8 l) O% |/ @( W QMolecular Targets ! u) q& T3 S& i7 O* E$ ^
0 |, ?5 s9 c g& T3 z4 x7 h1 i; c# @
8 R9 x- f6 l) e3 cCategory:
8 k! D. t2 k: L6 Q. dTumor Biology * d* m( h- N# w, `5 |
# `6 ~; i' O' m( Q8 P& W
' V; a' W' a) J5 ]# P5 O3 a& Z
Meeting:
- z: C% r1 D, \0 r, {% V2 b2011 ASCO Annual Meeting
" w6 s7 `3 K A, t; E$ I, v7 r+ L X. H" e
( b2 g) j u1 ~: h
Session Type and Session Title:
8 `5 Q* r0 @' h0 k, ~Poster Discussion Session, Tumor Biology
% Y0 ?$ Y- G6 g/ q
8 {+ N. w. h0 r3 _7 o! E9 p$ X5 F0 `" |. ^7 U4 u/ _
Abstract No:
D c0 C5 ]* D5 ~8 |6 Y10517
. m- }& x. u& G) J3 [" @. |# Q* l; L( I9 ~" Q# s. v, V% s
* o& U1 c5 T2 ]( O9 fCitation:
, s8 b' w, [$ a8 \J Clin Oncol 29: 2011 (suppl; abstr 10517) " A) d) Z' |8 J9 l/ _
9 k. M+ ~7 R: b2 }$ y9 x' Z' _
; U k) l5 o2 v6 K2 m, }Author(s):
/ h; v0 W1 k& M9 F9 dJ. 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 / h& d9 b# y7 e+ v: U" L
2 q8 c5 x3 a7 Z; a; I; Q5 a
# f9 W5 ^% P$ X+ n2 B+ M
" p" f: D0 J/ iAbstracts 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.
6 W- [0 m+ \, `' L5 L! O
' D( n7 X: u, Y4 s- YAbstract Disclosures, f& f0 P0 ^0 r; t; Z
. @& Q. r/ U* B9 I; S7 F# I9 ]
Abstract:3 c$ J. z& H/ o2 c6 }0 g4 J( ^
- Y5 f! D3 ~8 A0 q1 f6 j# Q5 j! ?
; D' p- k' I! m7 |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.! x" W5 @) B3 _/ F, J6 l
7 L* m; d7 j% B/ S4 i
' P: D* |# b4 U, G7 {: u3 Z |