Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page ) [! [- D& _3 V5 M: G, ^# g8 I
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Sub-category:8 @/ s, |6 I& f1 L" a4 X. j: m
Molecular Targets
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. w8 f5 _) J5 i8 e% j7 LCategory:
* N0 g& F( {% ^5 I; dTumor Biology ' C) _! n% l' s
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Meeting:
' K4 N% k3 T6 I+ n0 r9 f8 K& G7 s3 ~2011 ASCO Annual Meeting 3 r+ D" J; R6 o8 w; U; P6 y0 c
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+ E# A5 Y) R9 r0 @Poster Discussion Session, Tumor Biology
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Abstract No:
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Citation:# ], s; y8 U4 `' P2 f; X
J Clin Oncol 29: 2011 (suppl; abstr 10517)
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Author(s):% g6 @5 y( G1 j6 n
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 $ f4 a" H' S* C& a0 q$ W5 C
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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. Z: L% P+ p4 p" c# u9 G
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Abstract Disclosures6 s6 c$ q0 V- |+ q. S8 \- c% f
- Y- _8 Q3 ^0 N+ h! }$ yAbstract:5 y P) X1 ?: o
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" o# B- R. A7 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.4 u, c4 c, A4 Z( ?
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