Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page : Q# X/ T; R# u5 M( L
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Molecular Targets 0 n: b/ J! S! R( j- t/ C
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Tumor Biology 3 F8 U/ @5 c( ^- t
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2011 ASCO Annual Meeting
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Session Type and Session Title:* O" u P* |; p2 Z5 A
Poster Discussion Session, Tumor Biology ' r; Q. f% r. h" k# t0 `
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Abstract No:
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Citation:' S: G5 P1 ^( E
J Clin Oncol 29: 2011 (suppl; abstr 10517) % X% \, ?# L' O$ j* L7 c
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Author(s):
7 ?6 J, q0 o# a0 F: C. LJ. 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 8 o8 _7 i4 e. |' g3 `
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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.! {0 [- g4 ]( {# J1 |
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Abstract Disclosures$ d! Y( H9 C, B6 b& |" O9 [6 O3 O4 L
2 r0 p t0 G u* V# p" f! |Abstract:
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' P$ r9 s- l' {$ v3 H' H+ VBackground: 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.7 i. q9 H- {& S& a7 V
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