Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page % J8 ]7 V, Q% N1 `9 d. f2 w5 I
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Molecular Targets ) }7 U; I' {" \: R; j9 j/ k3 A1 c
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Category:2 y% ^; `# I* e" m F
Tumor Biology % l! {2 q. f. H4 H: V3 B$ e
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* m0 G6 y0 A: L9 ?$ P' Z4 KMeeting:, G9 C9 u% H* b Y8 j1 K( E
2011 ASCO Annual Meeting + B+ F4 k; z, ^3 z
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Session Type and Session Title:
0 } H8 Z: |5 \ `' t8 @2 O+ Z/ zPoster Discussion Session, Tumor Biology 0 T! |9 [6 v! `0 w: M: x: b9 B
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1 ]% I l2 S9 m+ k, DCitation:
& b9 m8 Q7 Y: U% m% H) |J Clin Oncol 29: 2011 (suppl; abstr 10517)
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$ o# U3 D) ]9 R3 X& yJ. 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 9 u" Q, z$ X \9 R5 V
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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! ^+ J; N, N+ \
8 H$ @% W; o9 f, H; zAbstract:0 v0 {! Q1 t, Z, N/ p* T; v4 a
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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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