Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
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$ g/ O+ E. k/ u! A- O! \% rMolecular Targets 6 H& l, m+ S, ?$ U. A0 h U6 J
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Category:
7 H6 l- C0 g, \4 dTumor Biology 4 g/ d0 S# [) \+ F+ _
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Meeting:
/ C' Q9 c2 o) P+ _! d# b% d# a. y2011 ASCO Annual Meeting 4 E/ p* V$ L3 z2 B p: [& ~
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Session Type and Session Title:' f: Q2 ]7 j. O- I7 w
Poster Discussion Session, Tumor Biology ! o* G7 Q# v X* _; L8 ]
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2 f) `# D/ [: s/ ?* ]5 LAbstract No:
: q( u5 H" P/ c& ? @10517 ; I& p6 K! a ]9 L0 ]7 [
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# z" B3 \% t9 v$ Y) [( QCitation:
; a7 K( E f2 }& CJ Clin Oncol 29: 2011 (suppl; abstr 10517)
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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 8 S& A% k' j i+ i0 r
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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.
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& o- y( D+ P! A0 k: B( WAbstract Disclosures+ z( Q$ i7 }1 A5 f' e. Z1 k9 R+ |
4 o% l; M0 n* E3 P6 @Abstract:3 {( L: E& P. x" [8 p6 F
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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.$ [6 i# U V3 _+ I
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