Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
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/ c; x# Y1 a; v( Z0 tMolecular Targets 7 q( r' d* s: ~/ I" j9 w. E
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9 @9 L, W+ \* M& t6 B1 MTumor Biology
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Meeting:
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Session Type and Session Title:/ d0 m" ?5 B% x/ b3 [1 c
Poster Discussion Session, Tumor Biology
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Abstract No:& w/ F6 F+ [1 P o ]# F/ Q1 }
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J Clin Oncol 29: 2011 (suppl; abstr 10517) ; S+ m: C& O1 s7 T% j% [
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Author(s):7 C/ Y5 E: H* M6 b( P: E
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 3 U0 o% e! c0 X- b
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9 z! I S* e" @/ X1 G& O8 AAbstracts 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.- L- {7 F$ m# m! F6 u
6 E; V; [2 H# a2 WAbstract Disclosures
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) g+ ]: d; G/ g4 ?; L% wAbstract:3 O) a4 ~' A( o k4 T! P4 W
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! k% N4 e0 _8 {/ _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.3 \5 ^# {: S5 m) [, W! @( V
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