Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page % [& O, h0 }; E
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Sub-category:
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Category:
6 X7 l: f; P9 c* ]- V6 H4 E6 M: g( g8 ETumor Biology . g6 i( {2 P1 \" m. n P$ N% C
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, b' t2 i" y& `Meeting:$ g& R+ k& s4 S
2011 ASCO Annual Meeting
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Poster Discussion Session, Tumor Biology
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Abstract No:
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Citation:, K/ P+ A/ c! h
J Clin Oncol 29: 2011 (suppl; abstr 10517) ' O4 r! ]8 t" V6 A9 M2 H* k
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9 r: h$ I& N: s( s* V6 a( \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 * O$ u" l3 C7 z0 v" h
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Abstract Disclosures
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- `% o v6 U9 T5 R z1 f( k; SAbstract:1 ^# ^% m- S* z7 {, |) M. ^! i
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+ v+ M# H4 |: E4 b2 X! EBackground: 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.* v% Z2 z: @7 l4 k' z; o. E
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