Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page 0 z( E8 b g3 l p2 |( @) _) F' ~
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Molecular Targets , ~% D2 N" l4 f L
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Tumor Biology
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5 C- Y: m2 S8 Q# tMeeting:
6 P2 a a) N4 O! b5 J8 q! p* d7 O2011 ASCO Annual Meeting
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& M5 n6 @, W% @5 @3 j; d$ }Session Type and Session Title:
8 A% Y/ t2 y G" Y$ K& pPoster Discussion Session, Tumor Biology % X( k0 ^: A6 i1 p9 k' C5 u4 z
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Abstract No:
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Citation:4 C8 c' @! y# @. Z4 T, ?
J Clin Oncol 29: 2011 (suppl; abstr 10517) & c* w3 Z4 [' M' r/ e! j
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$ ^7 S" H4 m3 Q, s" JAuthor(s):' g) W4 a& G5 p! v7 A/ d
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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& i5 _$ j( s/ x8 i( p' s. zAbstracts 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# j u) l2 ]( Y9 D% {+ xAbstract Disclosures& T; A( b ~" @ C: y
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Abstract:
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& v2 m+ h' l; u m' d7 PBackground: 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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