Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page 2 q! B0 e Z+ p* U; s+ F" p
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6 J6 m: l' W. Q' f, x6 a- V- E5 jMolecular Targets 5 E; v# O Q4 I0 ]6 o& d5 Q
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Category:
6 o7 q% ~2 ^; `: [4 t/ aTumor Biology , }5 ~7 f( @" }0 U2 d
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9 h; I( u7 {' ?9 |! QMeeting:
' u! [! p9 @) t2 }: c2011 ASCO Annual Meeting 4 ~* n5 f3 U; L5 n( `8 e' r. x0 T
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Session Type and Session Title:6 K2 f$ ? ?' y' n( X' w
Poster Discussion Session, Tumor Biology
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Abstract No:1 e: D( I i# H( }1 C$ U5 F( v' Z9 |
10517
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J Clin Oncol 29: 2011 (suppl; abstr 10517)
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' X9 b! ^" }) O$ x7 n' O( x5 R" cAuthor(s):. ?$ {! p7 g' A4 ^$ `3 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
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8 I5 f! Z& J1 VAbstracts 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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' I1 q" t, h+ f! {, ~2 XAbstract Disclosures
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1 x: S5 L6 T/ n# \1 \Abstract:; L7 z5 v3 G% v4 P
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* A* b" i/ ` B" a$ DBackground: 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. A2 j% g" T3 f7 v/ p. `
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