Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page p4 N" @0 I! i/ g
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Sub-category:) ? l' G% U# C9 B0 Q3 B
Molecular Targets # ^! H) h1 D6 R# G
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Tumor Biology - c& ]" o+ }, u0 \: h+ ?
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Meeting:, m5 L8 f! W8 }: H& A- d' h
2011 ASCO Annual Meeting
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Poster Discussion Session, Tumor Biology 2 F) i2 R9 `, C0 x
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Citation:
9 t0 g g) ?% {% D0 VJ Clin Oncol 29: 2011 (suppl; abstr 10517) . Y+ f6 {8 [3 X" O- V, _3 F D
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Author(s):3 q3 c) R; T/ k V6 }* E" X( 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 ! f, U. `! k( L+ s1 D1 [
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. \0 i$ V2 ?2 b8 s, YAbstract:& Q5 h8 z1 l0 c# x7 Z7 \" f( L
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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.# O- ~' ?- D9 @8 `3 D
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