Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page : v6 U8 v* Q! P: Z$ f6 ~, R& J2 d p
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Sub-category:$ o9 A* _8 G' L6 V( |3 ^9 E: B) l
Molecular Targets
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Tumor Biology 6 {( L0 h( I" F- ?
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2011 ASCO Annual Meeting
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$ U4 c7 T5 ^5 b0 k OPoster Discussion Session, Tumor Biology / `! J: Y/ L, s! r
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Abstract No:6 ]1 o6 r) @6 F2 m
10517
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Citation:! b" [& t% t# I/ R
J Clin Oncol 29: 2011 (suppl; abstr 10517)
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Author(s):7 n* B) C4 Q" }, B: l' E) f$ 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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! B4 y4 c6 O' l6 A0 i x2 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.9 k4 P6 C& b: Q7 S6 T! d
7 Q$ ~5 Y6 T9 L4 Q1 F$ N1 aAbstract Disclosures1 W3 V9 t) m; [2 w+ ~5 g
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Abstract:2 `, A' r1 @# O2 R: G( T
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5 a- n, A. c; x, [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." f* B6 Y3 n- Q
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