Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page 5 z& {2 ?: a9 v$ h9 z% u
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Sub-category:
]; E M! I8 T. o8 nMolecular Targets
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. o! |# u! }' v) B# LTumor Biology
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Meeting:1 g6 a5 l+ V9 k7 `( Q2 I
2011 ASCO Annual Meeting
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7 M9 }% J3 Y$ B6 U7 J( T2 \Session Type and Session Title:- D' ^5 w' M3 ^6 E* D2 U( K6 B+ I+ o2 M
Poster Discussion Session, Tumor Biology
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9 h0 v, M. U9 f3 NAbstract No:
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' ^0 ?$ F$ K- \6 J* HJ Clin Oncol 29: 2011 (suppl; abstr 10517) 7 h* }! p8 o+ V$ y9 H3 T" _
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6 l- j+ j" B7 C' J4 j/ ~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 N5 U3 y: j5 B
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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.* S |, |9 Y5 `4 Y( q" A5 ^- C0 z
) |7 c9 O- ~" ]7 J# A* ^Abstract Disclosures
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/ K/ ]2 N9 f# J ]Abstract:% e# A7 }+ B2 ]+ d1 m* q' i! o/ B
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Z6 Q4 L; k( |8 s8 @/ O3 fBackground: 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.8 u5 ?4 ~) ?; j8 l1 n; U% r
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