Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page # w2 ?- o5 R. V5 [! x
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Molecular Targets
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Category:: L0 ^$ o) c( p3 L- d1 d7 T
Tumor Biology * h+ a4 ?7 D6 H, q9 C# [! f, j
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2 C, O r5 I8 B1 H* E: ]: y9 eMeeting:
& s) b% @7 B f: s T, |9 L: P2011 ASCO Annual Meeting 7 J& E7 q! X Z6 G3 p( O
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" Q |" E5 _7 V l6 bPoster Discussion Session, Tumor Biology
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+ q+ W# y W- ^/ Q7 u2 e0 I, ~3 OAbstract No:. M, [ e* X7 ^' M: a
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" q! @$ H' u l' [, ?- [. `J Clin Oncol 29: 2011 (suppl; abstr 10517)
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Author(s):$ \2 ~$ c5 U: f5 m
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 2 Q7 k5 [. ]8 M; |( E
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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.0 X5 x! Q \" P# Z: { c
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Abstract Disclosures
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Abstract:
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& Z6 x3 \: y6 X3 FBackground: 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.: N. _( H* _1 O, z- p: l/ Z
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