Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
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5 V2 _0 `. }, P# HSub-category:
, e7 i2 R; K. w8 [" e- _( n, GMolecular Targets F2 W: v3 M3 e% V* k
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Meeting:6 c6 D/ i) `0 L( R
2011 ASCO Annual Meeting 1 g( @! m; I2 [6 N8 @$ E Y
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2 z" d, ]7 k, N8 L8 WSession Type and Session Title:8 k p4 L) M) G) m% A
Poster Discussion Session, Tumor Biology
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Abstract No:
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m: D$ S9 y5 b4 p$ oJ Clin Oncol 29: 2011 (suppl; abstr 10517) % @/ H. b7 a& ^' _' U5 G! v6 J
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# }4 C! U j0 h! S2 t t; \& OAuthor(s):
/ I/ D# Y/ e2 s. N& d- 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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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.3 i4 S% o/ q- H2 D1 C5 Q
/ \6 i7 e1 N0 U3 T9 _$ \Abstract Disclosures
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: D$ ^ y) @4 m. K# O2 c1 QAbstract:, b( T6 k$ d$ O9 ?
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O3 W# `# ?' Z3 `" O) }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 S3 z7 r0 d) x( n" `2 K) ~0 p" f
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