Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page # i _& Z% b5 x7 ~) }
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Sub-category:5 {* R) _* K+ y% m* `
Molecular Targets ( Y' Y0 T* l9 n; T: Y. D
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Tumor Biology
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Meeting:
' H2 A7 Y+ _6 q6 W. B/ o2011 ASCO Annual Meeting
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Session Type and Session Title:
, V5 S/ x& P7 M+ V* ^1 dPoster Discussion Session, Tumor Biology
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5 a8 ?* v; _ e) v2 D5 c UAbstract No:# b: Z4 v0 {; l8 \" z2 }0 w
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Citation:
2 y# N+ R' d$ q7 X7 X9 rJ Clin Oncol 29: 2011 (suppl; abstr 10517) ( F- z1 {$ Q* B$ q) b1 _ T
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Author(s):
. r1 U f: Q: 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 + a; R4 |% I. J o: p
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$ U$ [0 j# _$ p5 B) }: c8 X; C4 `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.) C) M4 f' H/ `6 X0 t
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Abstract Disclosures
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Abstract:
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: N: Y+ @0 `3 j: q& a" M3 PBackground: 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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