Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page $ J) w& S: y5 O1 j2 Y8 |
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Sub-category:
, K* C T% Q5 \0 BMolecular Targets
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Category:4 u8 {% R/ v4 R0 x" ?
Tumor Biology : M& y q, a& d1 |
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& G6 l0 u# d$ J& q$ v& b( q+ dMeeting:
5 Y! p6 @9 q+ w7 d* I2011 ASCO Annual Meeting * I9 o. K3 z- Z4 Y
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Session Type and Session Title:
% A( C) i, Y0 q$ d! @Poster Discussion Session, Tumor Biology
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1 d) a6 {, [4 t& ?3 KAbstract No:
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. R& g7 Q- A. i1 S0 Q/ RCitation:
. d7 l. }6 j! G, N6 OJ Clin Oncol 29: 2011 (suppl; abstr 10517)
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Author(s):) m# T1 B- S, z5 Z
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
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; X8 H8 \8 B8 ^6 @' Z2 H( JAbstracts 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.
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" ^8 {8 l; z8 MAbstract Disclosures5 L8 d- p% s4 ]1 y2 j4 |7 z
. V( v' {+ ?1 K7 i& a- i. dAbstract: p7 \- L. v. W/ g
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! R& _ _4 {+ p3 Y8 q) I% eBackground: 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.
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