Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page . W# P8 \0 W6 W
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1 s* {" n3 q1 ^5 v0 HSub-category:6 N. G% n) O n$ h& ^( Q2 B4 s
Molecular Targets
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8 o# M* f% X, E2 {# z% t9 U! qCategory:
" ^% {3 ^: B' I6 N+ O3 ?Tumor Biology
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& z0 u/ L- M( i( A& o' OMeeting: f! P; I5 ^5 V8 D6 F2 R
2011 ASCO Annual Meeting
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Session Type and Session Title:
5 y& _* ?6 @1 nPoster Discussion Session, Tumor Biology
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; ]' V. ?: R' F+ ^Abstract No:3 s6 q2 L! B. k- T9 _' l B. X. q* `9 p
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Citation:
& F2 w: h) P& DJ Clin Oncol 29: 2011 (suppl; abstr 10517) 6 ?# f9 F$ {2 |8 g1 k9 n
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5 t" G' a& b$ SJ. 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 . l% @) s5 c8 G6 `5 d: U7 m
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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.8 K; c% U; M" F1 r- z* h
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Abstract Disclosures
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& y, z7 b$ K% \) {4 EAbstract:6 d( I6 Q" i& T7 `
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% E% \9 p! R/ b+ q l6 F0 zBackground: 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. U4 C' A' n; v, x
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