Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
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# H% N* k) h' O bMolecular Targets , T: l% u# T' H( ^
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Category:
. J% s* @5 q* g# p2 U) S* X( nTumor Biology $ M7 Z; G. t, i, c/ b0 D& H
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Meeting:
- ~5 G" O n9 p% y$ h6 I0 F2011 ASCO Annual Meeting ; R o+ L* r ?9 S
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Session Type and Session Title:
; m/ y6 C: e9 e5 @" T; M' \- L1 {Poster Discussion Session, Tumor Biology ' p M& ^0 h9 B6 c
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Abstract No:- {/ U/ Z( i$ z5 i: e X6 x
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J Clin Oncol 29: 2011 (suppl; abstr 10517) 1 ^/ C4 @0 i3 h+ y5 t
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Author(s):
1 q3 D7 l5 q& J0 ]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 5 j! n. p* @* a8 Q1 J- L3 T
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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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8 ]5 G. ] O2 Q, b8 p) p# GAbstract Disclosures. ?1 A0 T0 v) H9 x
& E1 g$ u7 ]3 g6 A, C8 q6 pAbstract:
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* A! o# U5 P7 |7 u \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.
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