Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
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- ^. X- X) v/ ~/ Q' Y& f: H& fMolecular Targets
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Category:9 p; l6 }) ?5 Q, |. b {
Tumor Biology ' |$ `% `+ J# ?) S# C+ h& O
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2011 ASCO Annual Meeting 6 v" D' k7 M6 ?
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Session Type and Session Title:' v( g- t4 Z1 W; _$ G8 m8 M
Poster Discussion Session, Tumor Biology
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Abstract No:
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Citation:; U$ a- Z* j% P5 ~* h: b
J Clin Oncol 29: 2011 (suppl; abstr 10517) ! e$ x0 v& h8 V; r$ Q$ Z- S+ D
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Author(s):
4 ~) _1 K$ B4 u7 V2 GJ. 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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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.6 U1 D, y& D( L8 \3 w. T1 C
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Abstract Disclosures o! t! L0 Z4 T4 \8 M6 r
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Abstract:
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3 ]: ?/ \) Y. H8 ~# eBackground: 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.8 G1 h4 A; K3 ^6 F0 i
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