Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
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. H* R8 v, B1 @3 u0 gMolecular Targets . ^0 G; ^. d" |
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Tumor Biology 3 J3 a4 G' b$ i" P2 J
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+ E2 i& P! n; E0 ^! _: rMeeting:# C7 D. Z$ ~" z1 o Z! {4 k/ v
2011 ASCO Annual Meeting
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Session Type and Session Title:0 Y/ i; o, q# H0 c9 S% Q) O3 v( k+ H
Poster Discussion Session, Tumor Biology
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1 w$ j% j3 Q+ C6 X5 k+ Y2 a- b! iAbstract No:# D1 p4 s4 |4 I/ \; P
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Citation:1 g9 ? K9 t5 }3 M- ^; U
J Clin Oncol 29: 2011 (suppl; abstr 10517) 0 G" P5 p9 f1 }- j
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& t+ y* }/ U e. lAuthor(s):
X3 F! ?( e0 f" q1 q3 BJ. 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.
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Abstract Disclosures
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: U3 ~6 a3 N( VAbstract:7 M g- f% O1 Y
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9 w2 a9 {# b. Y7 P6 V. _: QBackground: 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.! h$ x% y# o: k4 Y. S. S
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