Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page * u1 M- A$ N9 t& N7 `6 t
; r: W+ a0 m( Y' o* Y. ?7 \" k7 y# ]6 s9 x
Sub-category:
2 a; X+ W, t& b5 E8 \Molecular Targets
8 F$ C6 ?. q* \+ x2 L& l8 a
" m! g8 b4 a: L6 d# {; B8 v' d4 [2 E" q2 i7 s- a- j _
Category:
6 C, K! X! z- t3 J2 d. N$ M1 DTumor Biology
8 u0 `3 ]1 X" m; t: z) e
" I( o0 @+ S: R! q8 P" n3 R! f
0 \8 q2 a; B; `3 @ tMeeting:+ p( y) T \+ _! z7 D6 ^9 }2 y
2011 ASCO Annual Meeting ! t; z# H2 c4 y9 P5 @4 a
" B5 T; L8 T) L/ \# n* |# ~4 q% v/ i
- r/ I3 J9 ]1 j* O) o: m4 z. y$ MSession Type and Session Title:/ B# {1 P* t* S9 b; e3 w2 T
Poster Discussion Session, Tumor Biology % y3 \ ~7 ?& h, j$ q6 D r5 X
! x! h' ?! I0 ?+ p" }5 j
7 p& q0 q6 p8 {5 q" AAbstract No:
$ V o9 ~: d/ l1 J, }10517
" [# ?' N& A! s/ {$ h& t6 S
5 Y& v8 J- Y, O; ?, W, k7 f5 t/ c2 f% |) T
Citation:
4 n) M* i: ]4 mJ Clin Oncol 29: 2011 (suppl; abstr 10517)
; ?/ `; M$ h: ?$ ?$ v# y0 B9 G6 E, c3 q4 ~- B% o! j
, b' `' _5 r8 S
Author(s):
y8 `( D) s* D6 I, s4 TJ. 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 2 t' I. b Q0 J/ i: `5 z4 O# H
, t- m3 T) y5 Z2 S9 Q1 \: d$ [ l: D4 O1 o6 |$ L- w% j: B
& X1 k7 _1 S9 s: PAbstracts 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 c& M, a8 Z; `4 L# h1 h
' \. w' n; T! gAbstract Disclosures
( }/ s* T& }+ g M$ I! R5 n9 T- \! W5 }4 o1 O* m" d
Abstract:+ {. C) n1 q3 c
5 a6 p! H& B% A1 ~8 R8 ^" r
9 u9 J, K" q H" L+ ^' I8 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.$ b* s. F' U9 Y+ d3 f
1 }. S* H% x% I0 K$ N0 r0 R @( x 0 @$ f" V6 q+ P4 ?' Z$ t+ [
|
6 F& V, \8 ^$ c" y9 n' x! S
显身卡
