Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page % Q. N% D/ j& r: M% U6 X
) L! n# I0 M9 P$ v
8 z2 p( T# g; _3 K8 kSub-category:0 S% b3 s$ [5 z4 W: F- h
Molecular Targets 7 e) z; I; N* k2 m
" V1 j( R/ E9 `6 T3 U2 R
% h8 m, [6 h3 U7 X. ~3 [- WCategory:1 C" q" l; t$ R+ d5 @7 ?. Z
Tumor Biology
. x$ Q: q F4 k* c$ K) G2 q7 |$ d9 v
\( p3 T: ~7 k8 K- d1 ^; f
Meeting:! j' F1 y( O0 Y S* T2 N
2011 ASCO Annual Meeting ! ]* c, q2 e2 d* x2 I* } x) v
9 q, G5 i$ a, `+ C" f1 _" F3 I/ F& A$ p7 j
Session Type and Session Title:
' O5 _/ C2 |4 G2 p2 [0 t# kPoster Discussion Session, Tumor Biology
. s0 f( Z! P7 p9 R, P6 S3 _5 x8 p) i2 Q' R" A& V% i4 M0 ]
; v6 X( b6 y. K, A5 \* xAbstract No:3 D5 c& P1 R3 O
10517
( o5 E, w4 O6 W% G. F9 a- ?. h
+ O, b) ^; W* ?6 J+ ~9 g0 p6 `& Q+ x b {+ k
Citation:- E: d0 F0 B$ A4 S! J. E
J Clin Oncol 29: 2011 (suppl; abstr 10517)
6 T0 H _9 A0 ?" Z0 B( ^ \" y G+ ^
" j$ X+ i0 x" g1 J2 k) AAuthor(s):
/ P# ?* r* c# t& ~$ KJ. 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 C. ~6 L& P# }# i1 ~
* B( v7 k0 \9 g3 e: m0 A: }
& N( y0 W2 Z* r+ V
/ [, ^* e3 `! v: KAbstracts 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.# ?% t3 f8 o% Y
3 h1 N/ J5 p# g- r) J! h* nAbstract Disclosures
1 S3 x' c+ q! f8 e) ]0 R/ k( C" j" `/ ?5 n) j8 f+ } q3 w
Abstract:
8 w3 C, g f' o/ H8 w* P, v: J1 i+ p, i
1 D0 d8 O4 S9 w
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.. f) k$ I) ^/ D; \6 _
! i* S( t" K$ B# n2 L U2 ]( b. e / j: w# `. {; r( a6 D1 ?
|