Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page " {5 l+ }2 R$ S6 F( Q: [0 {* ^/ T
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Molecular Targets 8 u3 X" ^3 v, e3 f
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Tumor Biology . T: R' E# _$ }- ~1 I7 Y
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Meeting:9 l! R- g; n; H
2011 ASCO Annual Meeting ' J( y! H1 e4 S9 d- z
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k3 j" w8 A, h1 T6 l' q! nSession Type and Session Title:
- j1 ]2 r- l0 ]! ~( j$ m+ Z4 f9 RPoster Discussion Session, Tumor Biology 4 M2 n2 K4 I1 k
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Citation:
8 E$ S7 G `0 s% A* qJ Clin Oncol 29: 2011 (suppl; abstr 10517)
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Author(s):9 v8 m- T* H9 P7 S; y
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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0 W7 p" k. q5 [7 c3 XAbstracts 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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Abstract Disclosures" b3 m2 b$ y& V7 G0 h7 }
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Abstract:( M0 m7 @2 W( Q( a
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( E' ~0 B0 ~" B' dBackground: 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.0 [, f: @ U0 a! V; E+ Z
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