Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page 9 S0 }. x8 N4 z' ~
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7 t8 Z- i) [# X, d/ Q+ T, K( K- q8 [Molecular Targets
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6 o+ e% t! b& U0 v; _% KCategory:
4 F5 r4 \1 r' Z- n+ STumor Biology
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2011 ASCO Annual Meeting
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. y! k3 T1 ]! K+ I t* rPoster Discussion Session, Tumor Biology - j# J1 C; ~" [& p
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6 g$ ?& l" b' Z8 K8 TAbstract No:: s) u( U. J, q( R5 E# @5 Q
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Citation:& O( K) J& n5 V% K9 r% N9 O
J Clin Oncol 29: 2011 (suppl; abstr 10517)
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Author(s):
+ ~6 S: s, g/ f7 N3 u* H* y& F1 NJ. 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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: q& K1 t" A3 x/ \5 b8 e9 sAbstracts 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.6 S& @% c! F0 [: f
6 ]2 k- A4 r0 y$ e7 Q4 @Abstract Disclosures
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: g; y& k }7 O$ f l/ EAbstract:
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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.; s+ m" f, b) A" @6 N
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