Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page ; b2 Q. A5 Y4 o2 K' }+ X2 N" m K
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Sub-category:
4 f" ?3 g! V# |# V8 s) e. M* oMolecular Targets ' C4 }1 W. x+ A; j; ~
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; f0 d8 u: I) P+ C' [. tTumor Biology ! [; r$ E6 K) Q) I
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- O) ?; f# h& |. l) t, J$ u2 O, e7 lMeeting:
7 x$ y ? M# i# Q0 u: B' B2011 ASCO Annual Meeting ' d/ U. V1 R0 J" A9 N+ T1 M* _8 i+ n
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7 R( x( W7 C0 E2 Z3 ^4 K5 u' ^1 WSession Type and Session Title:
! i+ V9 Q% v" N* t; ePoster Discussion Session, Tumor Biology
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. X, Q7 K) j3 L2 F5 Z- YCitation:
" u6 x; t) K5 w2 `- J) {J Clin Oncol 29: 2011 (suppl; abstr 10517)
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0 h; X R1 `, C: O4 P6 AAuthor(s):
4 @/ w, F9 x4 Z" ^" R0 k* jJ. 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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2 ~* d1 a/ ?: mAbstracts 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.$ W2 q2 X m! s7 \/ c- `
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Abstract Disclosures
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& }. B( \ j/ v& e# jAbstract:
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5 U! R r. F; c9 SBackground: 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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