Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page ; U# g& o, b! M2 B# D5 Q+ R0 J- p
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" U/ l0 O k* u6 rMolecular Targets
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7 J8 ?7 k5 v8 t- GTumor Biology . E4 u/ l6 L, u
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Meeting:
- x# {3 M, e B8 x2011 ASCO Annual Meeting
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Session Type and Session Title:
7 H- `1 v4 z6 H/ q+ \Poster Discussion Session, Tumor Biology
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Abstract No:7 y: t+ [4 v2 y- |! F9 H7 n, L
10517
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& t. w6 ]# b) v0 y5 ?Citation:
% Q& C" Z. D- D: p3 j" t" P" LJ Clin Oncol 29: 2011 (suppl; abstr 10517) / c4 E. w9 n2 p7 t3 d4 j
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' X( J; z' g1 u8 DJ. 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 l" R: X/ l4 T+ c1 m& A: i6 Y' f
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" A1 H8 r/ ?+ f) }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.
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Abstract Disclosures
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Abstract:$ r/ t) h* J' @) S* b& `
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0 P1 c/ ]; c7 p6 |/ o( xBackground: 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.
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