Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
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Sub-category:
5 ^3 u( l0 U8 n$ i, ` tMolecular Targets % n+ U4 A7 X$ j$ z: I/ L
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Category:
2 ?3 x4 H1 }* I6 K5 Z zTumor Biology
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+ E6 u$ I$ R; [# v5 X, oMeeting:. p) V8 v, U6 t( H, j: E3 H( ]; x/ t% l
2011 ASCO Annual Meeting 7 z7 T7 D4 Q4 s* Q
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) I, ~) T/ w. w6 [/ hSession Type and Session Title:
+ w: W7 k. W( h6 X$ J. e3 @; oPoster Discussion Session, Tumor Biology 7 [* U+ k4 O: \# _1 g( G C, C
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: ~$ A" C8 L9 z e' I5 e/ m( nAbstract No:# }2 o# W" Q% g& @$ O0 x: ^0 ?
10517
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Citation:
$ [& b8 y5 P( x2 U5 u$ g# JJ Clin Oncol 29: 2011 (suppl; abstr 10517)
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Author(s):& m# ` ?, b6 e2 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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4 l* c( Y0 t% c" l9 E- U0 wAbstracts 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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Abstract Disclosures1 P- ~% M, B8 d, X. h2 l( l
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Abstract:5 K0 F& c8 |: s$ B+ j2 N
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+ m- E: V' z: ^2 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.
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