Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page + x2 T6 b" Y2 P5 G3 Y3 p6 p
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Sub-category:$ q" F: k* E1 v2 C& D
Molecular Targets
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Category:
, u2 n$ p9 O/ m, V' a [7 u0 ATumor Biology + E, f8 N3 n. [
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Meeting:
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Poster Discussion Session, Tumor Biology
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% Z. h% k0 c, S$ H3 vAbstract No:8 {1 M7 M' \( ]- [7 S% X9 w4 j% @% _
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" C5 ~4 Q4 u! ~& g0 k! e" dCitation:
v0 |- H& l6 O: y3 b% S# jJ Clin Oncol 29: 2011 (suppl; abstr 10517) G0 k* M. o3 T( D
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9 \9 x0 h1 C7 ~2 X+ VAuthor(s):
! `, m/ G" @9 \* PJ. 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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. F4 c6 f: k, Y3 s/ A/ I- [: KAbstracts 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.! @( [, t6 I; b7 R) K) }
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Abstract Disclosures
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Abstract:7 S) J: U, \# H- L: ]
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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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