Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
, z+ v- k& G4 X% H4 X" e% h
4 P3 b6 x& w& A- O
9 G% \# r3 p! u9 Y' j8 T7 _5 M mSub-category:* I5 E$ D: j1 k+ ^
Molecular Targets ( i; _+ K4 _8 E& [6 f
, \3 U6 `2 \( e, C
7 v) ^# A8 M% f9 x, S1 d) W
Category:
; C5 o$ i D9 i2 Q# ^4 B) jTumor Biology
; R E7 ~1 h6 i0 N( E# B
' v) d* c4 S3 y2 m" a" @$ B# H3 Y$ [. |" @' C3 K p0 l( W
Meeting:: d# k7 H$ N/ m
2011 ASCO Annual Meeting - _+ Z( z* Q4 Y: D% ^5 U% v
% O$ o, _# K6 {9 p! l) |
) C( W# t$ y( ^/ ?; I. X! qSession Type and Session Title:4 b6 W! \. J* Q
Poster Discussion Session, Tumor Biology
4 B- B4 Z* D+ k. U. B; D
9 U# m0 d3 C7 a, t* u# k+ x8 ^- z8 \/ K6 G; ?& x" ]
Abstract No:
0 J9 P4 |! A( j& E, x10517 + z4 k& I& N; N! J: K) ~0 l* d
& L, ~7 Y# H8 p/ Z$ J% w& D
2 t* U$ Y' j8 _0 H l; R- L
Citation:+ N$ i+ @$ z6 G/ e
J Clin Oncol 29: 2011 (suppl; abstr 10517)
7 y0 d4 w: t% }5 D1 \: x3 b
# t9 l8 W5 p& `
# a# P4 V. G; B, H1 ?Author(s):
+ v. V) {5 ]0 QJ. 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 _4 i$ d3 j1 U& B5 J5 x# I# G$ [& j5 x+ u5 k3 z! {, F0 Y( T
7 t, F1 t) A! R- |5 L6 [
3 O6 N% {1 V9 P1 |+ y
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.7 @! A$ C1 [( ]2 ^# n
, V" U, U4 _2 M: sAbstract Disclosures( x6 ^4 ?& a7 P% U$ o
9 c" q- c- R% g7 FAbstract:6 [) u" q6 g8 g
' u; x: F$ ^4 q }( _
" S. I5 e1 W5 y# a' }1 ~( c# xBackground: 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.
: o. P! k9 c; j0 w, G$ D
+ _3 v5 W" r' U i7 _* b7 @ ; Y3 ]3 x9 P3 A8 V5 ^6 A, j
|