Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page 9 i d5 D* A7 v
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Sub-category:# i6 b9 O6 O1 [, m& Z4 d* H; i/ I1 G* f
Molecular Targets 0 y2 x/ H) _8 ]8 }
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Tumor Biology
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Meeting:- j, l" R1 W- }$ p \
2011 ASCO Annual Meeting
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% B7 i5 N. E7 W' pSession Type and Session Title:
, t$ _4 f% {) }7 q0 o) nPoster Discussion Session, Tumor Biology
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# U. R9 A* }) p6 aAbstract No:
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4 _- L/ j' B+ z o8 M2 RCitation:
: s- v2 }' x; j2 u; f- [- k; pJ Clin Oncol 29: 2011 (suppl; abstr 10517) 8 e5 q# [5 _; T+ w) \' j1 `6 M G
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0 k. D' E/ g0 m' NAuthor(s):
7 P# t K9 ], @8 k f5 {& N3 T: e; jJ. 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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. q" w, T8 b1 K6 M' x! e3 w* W9 h* }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.
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Abstract Disclosures
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Abstract:' P/ A# V2 Y" w0 \' B3 u
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* ^/ I, T6 g, i: k! v6 ?1 XBackground: 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.# G3 J1 ]7 }+ Q% O9 ^7 A
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