Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page 2 l; j5 _7 y4 e& ~/ ]; a& c9 a
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Sub-category:; S/ ] K$ E/ x9 z" M; p
Molecular Targets
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Category:
! _( M9 X* Y% J; e ?6 kTumor Biology
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Meeting:: y. A7 ?0 a% E
2011 ASCO Annual Meeting
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Session Type and Session Title:
* o' f5 K1 S1 c) W8 d" u" kPoster Discussion Session, Tumor Biology 4 U( A. t' X* O9 W9 W
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Abstract No:
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Citation:
" d9 I, C! c9 P t) y1 i/ dJ Clin Oncol 29: 2011 (suppl; abstr 10517) 3 R: y0 n6 j, \5 b7 \, _
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* h+ D5 ?6 V8 |: S$ JAuthor(s):
8 H1 A, ~* ? P& t( DJ. 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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5 c, }) w9 i1 X$ f# ~9 j4 fAbstracts 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.( K$ D6 x+ ]0 E! T' d
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Abstract Disclosures
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Abstract:
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2 w+ b9 R' |; V( X- 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.% t2 I+ V/ G5 t9 S7 F0 P
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