Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page # V# ]2 y$ V* r8 Q1 c6 E
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Sub-category:
: U* f& G% n. q# F6 aMolecular Targets
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Tumor Biology
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2011 ASCO Annual Meeting 9 e9 C0 P- j0 C: T, i8 t. I
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# W% d7 F6 J$ S0 E! oSession Type and Session Title:- q X0 ?9 ]. i8 ^+ C/ B6 X: x
Poster Discussion Session, Tumor Biology . C7 n. w7 C& F$ Q
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Abstract No:) |- a4 F0 C5 H5 N/ L1 f
10517
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Citation:
3 F( Y& s* a/ f$ D5 lJ Clin Oncol 29: 2011 (suppl; abstr 10517)
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Author(s):! N1 M" K t I( u4 W _5 {
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 ; ^2 i# N- Z/ q% s( U! I+ J
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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." |+ L* @( r4 F! m1 A. i( j
$ z% G0 C! H" M7 J& I7 c& QAbstract Disclosures
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Abstract:
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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." Z7 {/ @5 |9 m6 U9 l. z5 W
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