Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
5 y: C8 j/ q& X! Y" }
2 H/ K7 p3 A7 f* ]/ e& s N& C8 F; i4 l1 V
Sub-category:
6 J- U4 ?8 n' f6 C: Z$ T4 oMolecular Targets 6 z' v4 f- C' C3 g+ ?5 s
' f5 G% Z5 I& D& V
+ R: t+ i( U* L5 V1 t4 y* iCategory:
+ i; P. y3 h' b2 c! p8 J; v1 a* VTumor Biology
* s2 r5 q5 F8 d0 L. @* ?0 z2 [
/ ? x' Q5 ]/ u; z5 {6 D
5 E# _1 |; I) A" ]5 G" T& {! ]0 fMeeting:5 P6 y6 C: e7 V( ?* \ b
2011 ASCO Annual Meeting
" I1 C6 C0 @6 G& M. M& y" |& c! d6 I
# m1 `+ n; Q3 ]( v! x" C1 l" _3 B9 F6 M. k0 B6 G
Session Type and Session Title:
$ x% I3 D2 l1 @- WPoster Discussion Session, Tumor Biology
- ]) [9 q! g5 h0 O" D: T9 ^+ ]( Z) {2 G
% M' T' f) e9 A. m- Z2 t& XAbstract No:' q$ O# P, c3 c1 B2 ?! s
10517
* h; b$ ]1 D& ?% U$ t) `" i: U2 \6 Z$ ?# o' B+ r, E2 C9 D
5 _; j) Y' f8 S9 ?* _) L
Citation:9 t# B$ ]/ G% U
J Clin Oncol 29: 2011 (suppl; abstr 10517)
5 a! i* o/ X' s7 g0 I! N# h- E# |. i$ m% M& Y0 i
R e. h2 ]: @: b6 n6 gAuthor(s): y8 ?* |; t' g9 L% }- H7 V- U
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 ; G! j. U X! [( j1 z
U9 H. r0 x7 O M
, {1 v3 j' g( T3 L" _2 {
6 `0 @+ t' r0 `# J0 e0 }. \
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.
2 p1 t7 N( c% `* y% j4 B5 s4 y
/ E9 C5 U; f. m! M0 K* mAbstract Disclosures; G% K/ k$ Z: T/ g9 U
9 k9 ?9 @1 X a' j! z- b
Abstract:' O) h* G' m. c
: o0 e9 p2 d6 g3 [9 g; R
- e8 `- n: u' z+ f. z/ b! N* p
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.
. t1 K& S, H/ B; `. L9 A8 a6 J" _! g7 R4 `8 B) u6 ]
. g P" _" S H: P% r
|