Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
' w5 Y' u* g! h& i8 E: D
8 R" ~0 t7 B6 v3 }$ o, \
( [; t9 Z: Z& y% @4 W7 FSub-category:
9 A! ^9 a2 V' d& S$ t5 qMolecular Targets " \! n/ ]7 i# ?
, D9 ^. O7 y, s B+ R
3 B! O% H; y1 F% NCategory:. B: |6 U1 f; J( t8 A9 [
Tumor Biology
! p) U6 b) a0 p3 Z1 _6 J
: U" s3 r4 v$ F2 A; n. n9 R
3 U# K; X: [ M" s* @Meeting:
! ~* M% e) o/ \4 V% w2011 ASCO Annual Meeting - `0 j( S1 O9 e- G3 j' g3 q
: t( C! f3 {7 Y2 ~# o8 \
+ V0 V* e( }( U8 y0 ^9 o- q! I
Session Type and Session Title:& F# r, l" r" v a- q
Poster Discussion Session, Tumor Biology
. P0 f f+ c- l" |, x" o& t, d2 B* z( q
, {- Z8 j% G( p X2 I2 H. \
Abstract No:
) i2 F+ G/ |7 \, a& b- Y% _10517 ' y+ E' F) ?( G
- F+ w8 ~' h' \ A
! @% c/ w8 Z$ a; | z; o, NCitation: p0 o1 z1 b" A) v/ D5 }/ L- K
J Clin Oncol 29: 2011 (suppl; abstr 10517)
9 ^2 C: C# U1 c" Z' r; j
! `6 ^+ H/ q# W. C, Y+ `) F, q/ y8 h+ N" m
Author(s):! K# O2 A2 \1 d" ]6 Y
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
8 v2 j% `& t. e" r5 {+ A0 n" n( n' s* x
; f# P* A4 J1 I3 ^5 G, i! E' n7 O
9 w( e; R& x" p' M6 [! d, bAbstracts 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.: n- v( O7 d @7 k9 v
# j/ J/ [" Q2 N3 U
Abstract Disclosures
# c& c! x; b* X" i7 D% l6 C6 Q( c$ E9 g" s
Abstract:
7 f" _# M5 ?' i% B+ w. ~) K
$ g, z! ]4 u3 ]2 f1 u1 K* b0 L2 o" h: e7 I J+ j
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.
% h$ W3 O( a6 n$ j+ Q2 C" s' P( @
& E4 A: W Y: B0 S/ J; _% `
|
" q) f% A* u/ e4 |) t
显身卡
