Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page , R- M8 h3 b& M9 C( E2 {1 M, U$ @
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Molecular Targets
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s. b9 p b! BTumor Biology * a3 p3 m4 O$ ?6 |1 ?; _
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2011 ASCO Annual Meeting
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Session Type and Session Title:
/ e4 ]& d- Z- s9 rPoster Discussion Session, Tumor Biology 5 r m8 H& \5 B S( w0 q
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Abstract No:6 y u6 Q# T, _$ n, u3 u5 O" [
10517
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J Clin Oncol 29: 2011 (suppl; abstr 10517)
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1 p/ O$ W8 d3 r4 M" {, X7 gJ. 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 6 A/ H/ ]- [ h
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/ x: ]- \9 f. }" A6 oAbstract Disclosures
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1 A$ k, f$ d/ D( R3 |' UAbstract:0 k( Q0 I- u+ b' p
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" S% L4 `! N0 l3 G2 f) B. p2 }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.4 U& t! I+ i) p. Z+ e3 H! h( W
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