Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page : l4 D) K+ T' P3 _
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Molecular Targets * N4 I) H; j7 l- ]5 a
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Category:
# t7 c3 N: }% ~/ u+ dTumor Biology ; S7 V( x3 i+ d
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5 p* U- J5 ]9 `3 i4 vMeeting:
% P5 e" H$ F% X: G5 q; B1 j/ n2011 ASCO Annual Meeting 8 x. B2 Z {( G- W
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2 @5 m7 f" H7 D6 f) C5 ^Session Type and Session Title:
# J) W; v6 u; @5 ePoster Discussion Session, Tumor Biology
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Abstract No:
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0 R) b1 z U1 d; s6 |6 eCitation:0 O( Z8 C1 X5 W7 U
J Clin Oncol 29: 2011 (suppl; abstr 10517) 0 ~& a' r! K; v Z; Q# L8 T
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Author(s):7 |% o* o$ c* U( p3 u7 I: g) |
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 7 P* W( n# C% t; D) k# M
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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.
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Abstract Disclosures
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- e5 F+ v6 O" Q( TAbstract:# G, A; @ |+ V1 Q/ E
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; p5 t0 P2 g" f' m/ GBackground: 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.( z6 ^* Z3 N+ @1 J
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