Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
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, H& J* A7 Z' n9 i) UMolecular Targets ! v- F! Y% ?: J! i- e% ]7 u3 C* K6 j
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Category:* p; X6 ?3 B& L( ~% V7 f
Tumor Biology
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5 J8 ]" U3 i. ?% \Meeting:
# `$ ^. ?8 P" B" `0 d6 C+ p2011 ASCO Annual Meeting
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Poster Discussion Session, Tumor Biology . a. w. n$ x1 \' V
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Abstract No:
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9 b2 Q$ b9 s( i1 w+ \& DCitation:
) }" f, k2 z3 Z) S6 EJ Clin Oncol 29: 2011 (suppl; abstr 10517) ! r3 y) ]9 w7 ^- d
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Author(s):' s: b4 b7 W% j t$ u4 d# w
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
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/ c2 v. k8 N! Y) DAbstracts 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.$ E0 M7 G6 g0 ^6 T+ }
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Abstract Disclosures+ L0 v( C$ _/ j' A z- }6 w
1 ?/ S3 W8 a* e3 r5 CAbstract:
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/ h: P/ w1 a8 l! Z5 XBackground: 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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