Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page ' V2 |' a% P+ k' \( R4 t& P# U
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Sub-category:. g1 J6 D4 w; D9 J, e- y
Molecular Targets
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Category:
- E& M6 r0 P$ \ S* r/ JTumor Biology ; E H, C+ q' Y- d9 j5 |
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Meeting:$ ~( y; J( m3 c1 ]/ T5 r
2011 ASCO Annual Meeting
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Session Type and Session Title:
; i5 F7 y# j' ~$ n* _Poster Discussion Session, Tumor Biology
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Abstract No:
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' R6 }2 }/ n" u4 e* \$ }Citation:
7 @( T. Z$ x; s$ A; g' tJ Clin Oncol 29: 2011 (suppl; abstr 10517) " u z" U* Y; j
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5 y& g) r) Y5 A/ W4 i7 BJ. 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 % Z8 G' @* O' i1 X
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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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Abstract Disclosures
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) [. `' e; R* y/ RAbstract:6 {& [# F1 z' a# k' }% T) V# R
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Background: 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 s [% b4 w. x0 {- ?2 o
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