Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page & X. h/ @6 U6 @# K) N
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Sub-category:7 C+ w s/ Y+ x5 j* W# h; S
Molecular Targets ; q4 R3 z* _: Q* g- Y$ V5 Q
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Category:
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Meeting:' M$ H3 h: d6 d& m+ P* U% n5 s* V a
2011 ASCO Annual Meeting 5 l0 Y, ?) M% I6 G* E, A& @3 _& J$ v
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Session Type and Session Title:* Q0 s1 _& Q& {; T2 h
Poster Discussion Session, Tumor Biology
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Abstract No:. V O" z% u. n/ b a* g
10517
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Citation:
. ]; M* v: ^9 N- J! _) ~; pJ Clin Oncol 29: 2011 (suppl; abstr 10517) + B! F2 W' _3 h( t6 X+ |1 s
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3 {8 u2 S0 U Y7 s1 _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.6 X2 _; j. b; ~% P
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- b9 h1 u# ?' @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.1 t- M7 o3 {& y8 v Z
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