Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page - o4 \2 i. W& W! p O; C' S
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Sub-category:" t9 _4 g+ P0 Y% @6 P! E
Molecular Targets
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Category:
; p) G0 @- ?9 kTumor Biology 0 X$ M# I% j4 j& H8 c$ |6 j- }
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Meeting:
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Session Type and Session Title:" o8 X, H- |( s$ M0 v
Poster Discussion Session, Tumor Biology
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7 G9 U' Q( c4 B4 v4 J" dAbstract No:6 N& G5 T2 s/ I; \3 n& O" G
10517
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% H; x Q9 ]5 A2 s ^Citation:
) ~( u# I. N" |1 {+ {J Clin Oncol 29: 2011 (suppl; abstr 10517)
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Author(s):% G1 ^0 x7 ^1 U4 o. D
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
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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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! q1 Z- d, [$ l6 B8 T/ DAbstract Disclosures
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7 C& P2 \* c3 m$ X7 h: HAbstract:( K6 {: d) N& n( O4 z+ Q( `' e
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& _% ?8 [6 ~& e9 iBackground: 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- W& |2 i; c* I7 D% d/ ~
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