Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page 3 w( O4 ^+ k7 `" N8 e" i& D
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Sub-category:
1 ?1 \ E @; }+ ZMolecular Targets 2 `- |& G! j/ t; h3 J5 p
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0 o6 V2 ~0 {7 O/ b6 m' ~Tumor Biology
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Meeting: v* j" m4 ~0 F r. U( j5 ?
2011 ASCO Annual Meeting + r+ m. G& M* f7 v
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Session Type and Session Title:
+ N/ d5 |5 X# U$ K2 D, K$ lPoster Discussion Session, Tumor Biology % o" f- J* h; z
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Abstract No:& P6 D: {$ e& d+ [3 u8 T+ B" y
10517
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6 ^2 J% M( a7 X4 r3 }9 f7 l( xCitation:
4 L5 x5 E0 e, `. W8 T! g. kJ Clin Oncol 29: 2011 (suppl; abstr 10517) ( n( T& S5 s4 C W9 N) D
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Author(s):! S- z' V- B" R5 s* C
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 4 U# s$ ]) j1 a9 b3 I& i
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: P# N a/ Y# {; F/ T6 _" 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.
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9 B' Q7 T" H# F9 BAbstract Disclosures4 ?) Q9 J/ M( c% ]9 k4 O3 E1 {
8 N3 K9 |/ U+ H6 _% Z, EAbstract:$ } _9 \9 l! U4 B8 {6 U5 E
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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.
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