Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page 5 f8 b- r7 D/ i% N4 }! j, r) k
$ V* L6 ~! y0 z% J4 C
8 a0 j- W* e* ^Sub-category:4 u/ z0 @7 d6 ~
Molecular Targets + U0 ^% x. X: D' @" t# S% l
- R8 E+ ?7 z' D" `( M
6 `) w, p3 S1 X9 {/ B4 a G+ @
Category:
/ J& l5 c) m8 N, X \Tumor Biology ' B, t9 D) |8 E' P+ k6 _) b, C
3 \6 f% H" x6 c2 w f% O2 ^& v
- N$ F; C- B3 M1 [2 U1 r
Meeting:
+ F/ m: m0 S% ?& V0 S$ |2011 ASCO Annual Meeting
4 e, z4 y) p( S7 i: ^& j' F7 z7 ^7 T2 H4 K: K4 ]% s. F
/ J; f) ?- O) U; l0 O5 GSession Type and Session Title:
) k! t6 P0 I, Z! i" qPoster Discussion Session, Tumor Biology 8 u3 W& } I6 l* H* x/ l+ M
' [6 b3 U* c! ?0 R, Y: H
, d, a! s# |5 d/ L6 k4 [ d& \" ^. c/ w! fAbstract No:# l, x4 b$ S9 F! p4 ^5 }) ?
10517
# q. `9 Q6 G7 M* Y
# J/ h @' v) g+ r3 W& s, s k3 t/ r
Citation:5 ]8 `# t9 o& P& Y
J Clin Oncol 29: 2011 (suppl; abstr 10517)
( P" j- {# T. k: \
7 L8 K- V5 `+ R. Z# w
$ c8 a- z. E* O; C$ u$ q) LAuthor(s):
7 b& |, r- C9 OJ. 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 , a! T0 H& _" G) p9 X, F8 _2 K
$ t0 ~) z$ N' z) O
% U8 s( M: f# W3 H
0 r7 o' s! |" }2 ^8 vAbstracts 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.
3 A/ E9 R6 G2 k
+ {* c1 p7 x7 _% o5 g7 @9 Y- M: mAbstract Disclosures* ^, b. c* Z$ p6 k( [. p8 S& K* O
, y& h' L6 o& I- E6 p9 u6 ?) g
Abstract:4 a' Z! y3 q- h. `& _
: C/ v: }1 K* h& G0 K' m
, n G F7 n4 l# DBackground: 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.
9 v- Q* v4 M% d" \' y1 b/ Q9 }( }( S
/ z0 g' s" n1 P8 E1 ]3 y
|
显身卡
