Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page 3 ]- ?2 Q# M$ p& B
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Molecular Targets
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2 f+ s' d8 K) e) L1 G4 yCategory:
$ D: ?( m7 Y O# y4 _5 ^Tumor Biology 2 Q. T: S5 V8 o
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4 w9 ^: k a0 y! Q/ BMeeting:
: r1 X3 m; a( m2 X2011 ASCO Annual Meeting
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Session Type and Session Title:
. I: e. k Q! ^, p1 UPoster Discussion Session, Tumor Biology % H4 _ x, q# Z
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( v. }: K1 G& ~2 _+ r$ r; K/ iAbstract No:. F. S; p! t5 R6 c h8 G L
10517
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Citation:/ z" y$ R) N! B9 E# `0 @
J Clin Oncol 29: 2011 (suppl; abstr 10517) % T+ l! d! g* M: v1 B9 t
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Author(s):( C2 J1 `; Z' x$ {% c3 B
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 - U- @1 w4 h8 R- D5 N9 s
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Abstract Disclosures
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7 m4 r! B$ R1 ^, LAbstract:/ [- m! H( q* x/ \- s% W0 w! B2 k
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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.
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