Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
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( {4 m# E V- x: `7 h3 GMolecular Targets : a/ L, l; ]0 ^! J$ O
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' J$ V C% K! O5 X( G0 L! CTumor Biology 4 e4 ]: w" ?, k$ ]8 g5 q. t
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! q$ _4 A9 ?% Z2011 ASCO Annual Meeting 2 [5 J T% w) @
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6 H }- m; d8 }" S$ n8 QPoster Discussion Session, Tumor Biology
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Abstract No:1 g( e9 B3 v, K0 z, d
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Citation:( @ j4 P7 J- I3 e" ^" _. M. n
J Clin Oncol 29: 2011 (suppl; abstr 10517)
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1 {9 m( V$ p8 Y, \9 ^ @, yAuthor(s):
, B& S& \# ]' }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 3 O4 Y( i. q* @/ H. e% B: S5 H4 l
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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 h8 J# a+ r8 i @1 {3 J
% \3 D$ g$ f" g5 `" M) ]Abstract Disclosures
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. V! d& K+ L& S9 _Abstract:
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/ x7 B8 s* _% _$ ]$ dBackground: 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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