Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
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Molecular Targets
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Category:
. _& M% \' \7 p, ]7 X7 ?& R5 GTumor Biology ) d; Y I( u8 @- N$ x$ J
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; \9 l4 x2 k* B0 n. BMeeting: ^' \1 A' Z, U F; n% C6 C
2011 ASCO Annual Meeting ~8 b6 C9 C, J5 ?& q7 G7 ]4 r
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3 N2 {1 O w3 N+ D, K6 k! iSession Type and Session Title:
9 h2 g# N |2 P: Q" kPoster Discussion Session, Tumor Biology
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Abstract No:
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Citation:
6 y. k) H$ r+ JJ Clin Oncol 29: 2011 (suppl; abstr 10517) 3 z s; P' N U# P
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' d8 |0 |0 J e$ G$ P; }/ KJ. 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 * b( t: N% Z0 Q, W3 y3 B0 q8 e
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, V8 o# e% w/ T5 JAbstracts 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.5 k" h% v/ H7 U5 h1 _
t" P( P P7 k4 c2 k$ qAbstract Disclosures3 m* B" O- N! z- q" ]8 Q5 _' i
, g" s; J8 C' CAbstract:6 D+ N/ z( x4 B% ? `5 i; Y
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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.7 d5 [$ Q& F/ v0 x* y+ D
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