Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page 8 f, C! E J: p, H, ]9 Y8 G0 x
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# M' { p0 B6 m9 v6 bMolecular Targets . N+ E F; h0 @( l
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/ y, i- v- G* ]; k9 @8 bTumor Biology
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! F6 M+ H1 k+ q: X& s9 Z* aMeeting:; \# I, c" c5 U0 U8 O7 o; O
2011 ASCO Annual Meeting 8 D; a: o2 x& ^0 c+ L
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Session Type and Session Title:1 p& x/ ~5 Q; Y
Poster Discussion Session, Tumor Biology ) p) F/ s, k4 K- z$ p6 I& e
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7 q$ A5 G2 t* x" u( X# L3 X( ~Abstract No:3 E8 U; @ o2 D8 z
10517
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Citation:4 y$ O1 A" k8 |- f* S
J Clin Oncol 29: 2011 (suppl; abstr 10517) ' P4 H/ m3 n1 G& [. q; P
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1 I2 e1 c- m: p Z8 D n% H NAuthor(s):
8 P( D ]" J* U: jJ. 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 0 z: }, p5 s0 q d8 S" p; ?
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X# V8 I0 Z' T" ^8 ~$ |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., f# l: {& t% ^( ?$ x% x% D
7 y* @5 N3 x2 Z% w/ ~Abstract Disclosures
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Abstract:
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) ~7 S3 Y c o) ABackground: 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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