Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page 8 U* W- Q) r' @9 ^5 n% ]+ @
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* k* q4 k! [+ m! I9 `% y; B& cMolecular Targets 5 B( @( l1 ]4 F) Y; _- n& z# \1 p
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5 {8 \1 U4 ]2 T9 jTumor Biology * W/ W' h: b+ K9 w! ]5 y
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+ y8 Y7 h. \1 Z- s& d% u# WMeeting: X/ _' h% R- U# ]( v
2011 ASCO Annual Meeting
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Poster Discussion Session, Tumor Biology & y& W7 ^ ?& Q' J, {* N! x1 c
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Abstract No:
9 G# [7 z5 E6 E& K4 L/ Q, ^# }10517
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J Clin Oncol 29: 2011 (suppl; abstr 10517) 4 t( U9 K8 a) c1 E6 ~
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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 E, d$ [% c9 K/ ~3 M
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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.& h, Z0 f- M4 O e1 [
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Abstract Disclosures
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Abstract:: ^. w8 _: j9 q" d1 g& D% B
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: G- C/ n3 N' y- v$ J1 n. y* ?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.
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