Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page - x# b7 Y, A& h7 a- `1 d$ K8 l
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Sub-category:' i' Y, j9 \: }5 G7 s, [
Molecular Targets ! T4 v/ B9 h/ F) e
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Tumor Biology ! f1 i8 Q1 f# A6 m3 ~
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Meeting:
! f' R' a; S* _2011 ASCO Annual Meeting 5 w# \9 a5 {' F( q$ Y0 _. H
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" ^9 V7 M9 R3 M5 Q, eSession Type and Session Title:
% I1 o7 _9 v$ R, k% Y$ BPoster Discussion Session, Tumor Biology
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: @% i1 N" E5 }7 a, V, ?% U$ fAbstract No:9 B6 E1 \) m7 w P7 x
10517
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J Clin Oncol 29: 2011 (suppl; abstr 10517) $ ]5 e0 }! q; E- F) _
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, U) I; Y4 f! q. NAuthor(s):
; s$ e2 K% H BJ. 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 3 k6 z2 n: g+ i
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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.9 ^6 [5 G3 C/ A8 r: Q
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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.
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