Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
& y0 O. U) N9 w$ O
' {7 p- l1 I$ c$ v5 c, _
3 J& n! \. z% S$ }9 r3 \$ C7 fSub-category:5 q' s; M) V; _/ @$ t! Q
Molecular Targets & _. C/ W% W L0 p6 ?; P
& T$ W+ H& w4 g% N9 N
) _3 q) M, B" q' [! L8 {' NCategory:; q- ^% }" [; A' h+ c) B% D
Tumor Biology 6 `5 i1 q/ @( v" T
* T3 V% Q6 t: B$ |6 {6 X" _
7 h, y/ i( c) e' xMeeting:
/ O+ i+ Y, W& `5 a$ w7 L* J" b2011 ASCO Annual Meeting
5 Q2 B% z7 C3 i! n8 `0 O+ v1 Z9 O _) o5 Y. W
# k& g; v* g0 ]" ^! O6 J" Y
Session Type and Session Title:
' i" m0 V) a% W# m' O- iPoster Discussion Session, Tumor Biology
# }; E0 P. t2 K6 Q5 G
2 X+ p3 z% ^5 X5 z! u& E
3 I: {0 Y: r3 u# h q& iAbstract No:
: H/ J g' A$ B( T+ W- @7 t10517
2 V, M+ J( R+ |6 j# j; U7 \! C. u5 y
# u' j$ K0 w1 e& i
Citation:
' a2 {+ w9 [8 b9 B/ NJ Clin Oncol 29: 2011 (suppl; abstr 10517) ' i5 b1 ]4 t; s8 E
( x3 _ E+ l- |* h9 N/ N
) h. \3 K! \ e3 x7 t/ ~ Y& F- kAuthor(s):8 U# i I& q% T/ I( k# `
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 1 K, Z z+ U$ g3 I* c, o
5 d0 g' D/ a* [6 f% y
& y9 e! E' y$ n, I6 ?& M2 g& e; [3 f8 w2 B, ^: ]6 V
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.) Y# Q- t u( V
( v) X. K! b3 j9 u9 d; D$ Q9 a- RAbstract Disclosures* _! L5 ]' e: j* \: z
5 z" s x7 g7 q/ b+ Z$ Y* T2 E) i
Abstract:
/ P4 D. f9 r& o; R8 X% C7 z& D$ Z, F: \- k( q2 [8 u
. F! y+ u2 Y7 L+ A& Q& wBackground: 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.
/ ` H) [0 ^* f/ ], Y& c# A0 [9 U# d3 v4 P- y. D
1 b5 e# r$ R( _7 w% I% \, B+ b |
显身卡
