Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page . d$ U" q1 p3 B
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Sub-category:
1 j1 p2 Y: s+ M3 mMolecular Targets
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Tumor Biology ) _" k8 }. [6 n+ M, f
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) G& S0 ], s3 iMeeting:
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Session Type and Session Title:4 @' m. ~5 f- X4 e8 w) D% P* }: ?
Poster Discussion Session, Tumor Biology
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" Q9 i9 E g+ A, P+ d* P+ iAbstract No:1 w0 M5 F4 R8 k
10517
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Citation:: l* K" S8 \! [$ T: j7 [6 a9 t
J Clin Oncol 29: 2011 (suppl; abstr 10517)
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# v: `0 F1 P$ @* kAuthor(s):# R, ?8 N& p) G7 q# O; q. m3 ^' w2 W
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
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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., F$ Q5 p* e6 H& j/ Y- G
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Abstract Disclosures
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8 N/ h _% ?0 {3 ]9 i; mAbstract:! E. S' S0 R$ |+ `6 i. u: |
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# ^4 i; y* W9 l6 H3 I% q8 JBackground: 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 [; N8 ~) q. ?7 e
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