Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page 3 u; s# @! x0 e* i9 [# z) [9 l
% V0 B1 g1 r) h3 ^& I* E' B
7 U: l" M7 e, Q6 U& h7 P3 K( f8 P
Sub-category:
5 Z+ |& y& z m1 V# NMolecular Targets 9 e8 g1 `) |! B3 L, T" J7 z
- K- F, K+ O2 m# S% _
& d9 k3 [( U, w3 @3 z `% O+ n
Category:
& Z% A$ \7 ^$ e/ \/ lTumor Biology
* K r, S& {; Q' P0 t+ q! }# Y; U: J# K7 `& }5 j6 T+ l( o9 D
, P5 w/ a$ @$ d& f8 h3 b% jMeeting:( y$ b* `. x; u# D8 w6 P
2011 ASCO Annual Meeting
3 r, w9 l! h3 M5 _- X s$ @! J) f- j' |' L, f* D
* u. w/ P1 G/ p- `9 LSession Type and Session Title:3 {, g) r4 U& Z
Poster Discussion Session, Tumor Biology
& H! M: n7 ]0 v" t: z( s
! z2 d/ D% o3 a4 @' P
5 S, N8 _: ~ i# G0 M5 gAbstract No:7 f( r1 w6 B+ Z, z
10517 . O6 g" H0 i, a6 P. M
: k9 f/ k( c- F( w, j
+ A- m" W3 b a! n) _: ?
Citation:
0 Q5 e3 ]4 _; ^) Z% sJ Clin Oncol 29: 2011 (suppl; abstr 10517) 0 z* E+ Q8 e, ^. M b3 L
2 G" J+ B, \/ ]
$ H+ T; z; ]; y" ]- wAuthor(s):
?. i0 n+ w+ s9 C6 k5 aJ. 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 . ~& ~, i6 E5 D9 G' S
+ w* k+ }* Z( b
4 Y, l$ S% s: v. y n7 q( X
, K X- q, n& u4 \9 d1 s, dAbstracts 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.2 w! P. h. ?0 u' S8 Q- e! q- \
! o B1 C" H) nAbstract Disclosures" c* P* H, o7 o0 S% G
- n$ i0 `4 `: N' z+ l: t7 j
Abstract:& j2 D- w' B2 Y& J
, J& A# ~2 j, h3 L- ?+ r& r" _& X, ^" m. w* |4 `/ U$ j* N/ y1 g
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.1 _+ K% ~# L& {
: t K, `8 {2 b
- ]- U+ Q) _) g3 A5 K6 f8 g" B! |/ R |
显身卡
