Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
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Sub-category:
g- o7 {: [# w4 ?# x1 O% a( W) cMolecular Targets
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Category:' s9 f3 A/ Y$ X8 S: p9 `9 h4 ~0 G$ R
Tumor Biology : l3 ?2 I8 ~! [( T2 D5 s
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Meeting:
( w6 D& F& a9 y; O! \% V( u. e2011 ASCO Annual Meeting ) ~5 M7 y- ]& J3 y% B
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8 [& e5 O- q& \9 p# Q& ~7 tSession Type and Session Title:
* f" x1 n" K& {& L$ A ` bPoster Discussion Session, Tumor Biology 2 ^* }1 g3 E2 ?3 [ A% B. ^/ m
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8 B# V/ k2 V6 i% f5 PAbstract No: G( V# j9 ~* O
10517
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Citation:( L9 d" m0 b. _7 ^
J Clin Oncol 29: 2011 (suppl; abstr 10517) 2 S' y; P2 l `3 M, D2 ?
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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
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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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' H$ [; h H" X& A& S3 _Abstract Disclosures% W7 ]. s) @4 |9 G8 q
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Abstract:
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2 l i8 x8 L5 Y+ j/ {4 L1 f8 xBackground: 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. W' f1 C w0 [. N* V6 Q! } b
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