Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page # h7 t" Z7 `0 g( Q1 j1 `
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Molecular Targets
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Category:5 O2 i+ s( u8 i2 I* d
Tumor Biology ) Z/ b7 p$ m8 d1 E. t3 m8 D) X2 g* h
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Session Type and Session Title:% r8 \/ w2 r5 A, y% W' U) B
Poster Discussion Session, Tumor Biology - h3 A7 C& ]8 S6 u
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Abstract No:) w( v$ \$ V5 g- g' T+ K, ]
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Citation:0 `' I1 C9 r$ ?( I
J Clin Oncol 29: 2011 (suppl; abstr 10517) ' _) {: s% ~4 r' T$ ?/ d
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Author(s):) Z3 G: p9 q2 N# G+ Z
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 , m9 R0 d# u8 a) J
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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.4 r7 C. C/ k/ _$ e1 \4 M. ^$ h: |
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Abstract Disclosures
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Abstract:7 D1 |, Q/ n. K. G: L' S, q* A
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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 k9 S. D+ u+ x6 }. t3 _' k
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