Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page & v2 w& ?9 E. J+ b" c: k
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, Q) C k8 N [# Q" m' e% R; aMolecular Targets
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Category:+ F& q( O% ^/ ]! \1 f9 w6 L4 K
Tumor Biology 2 E8 v4 d9 X" j8 e$ A( l/ o( S
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Meeting:/ B2 |/ M* q" _0 I* ?) |( r: b9 D
2011 ASCO Annual Meeting
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Poster Discussion Session, Tumor Biology 2 _" D: S b D# ~- Q
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Abstract No:9 |6 W( E9 n ^$ |" F
10517
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Citation:
! r9 r9 a0 ^% o8 tJ Clin Oncol 29: 2011 (suppl; abstr 10517)
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Author(s):6 S& b* |4 J8 P- m/ f$ L
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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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.
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4 G: B: i0 z4 v! {8 s t; z' FAbstract Disclosures. s9 b6 D4 _1 X* O7 d% S1 u! V
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Abstract:% }, ?( y( v* l3 b( y' v. O3 R
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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.# J+ v6 @3 `( B# f
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