Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page 3 d) r' D/ A. V" ]! V
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Sub-category: v8 B1 d& V% W/ o) U4 e" V" p
Molecular Targets
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Category:
F/ k& V, a- `9 mTumor Biology
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; t, F+ T. F6 `. w! Z1 ]2011 ASCO Annual Meeting ( Z1 P" j2 C5 ?3 h
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7 ~4 r0 P ]1 W8 i4 \) sSession Type and Session Title:7 [8 u# ?8 Q, V3 e( ]" W- ]
Poster Discussion Session, Tumor Biology
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! `/ {2 [9 u; d9 mAbstract No:3 L& n- t" f0 [0 h5 E6 q$ I$ r
10517
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Citation:% f. u& d5 g- T8 g0 p2 c
J Clin Oncol 29: 2011 (suppl; abstr 10517) + J" K, s, B) Z5 B0 H
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3 ~+ z2 F8 |& u! ^3 \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 . ?) y, N- k- T. X" q& t/ A
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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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2 a5 ^2 \' V$ _& f1 f9 qAbstract Disclosures
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7 m/ X% h; n; z# J zAbstract:
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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. W; X3 P2 E& A6 ?+ M4 Y) O% z) s
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