Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
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Sub-category:6 }3 I; v2 }9 j5 G7 I% v. f
Molecular Targets ) I# \+ C/ _* V' ~. Z
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Tumor Biology # F6 q7 I2 O9 d, ^5 Z
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Meeting:
3 d3 H% K& J" T! a$ S. m+ @+ a2011 ASCO Annual Meeting : I& {) x+ s# N' J" y* P
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Session Type and Session Title:
, K3 X$ H8 E% V& {2 A. D8 jPoster Discussion Session, Tumor Biology , c3 M2 E" _! z E3 f- X& s
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Abstract No:; `" n0 ^/ u9 m6 U2 a% i% U
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Citation:$ |2 W. R4 S% E
J Clin Oncol 29: 2011 (suppl; abstr 10517) - V2 f& f7 r4 N6 q. m8 T
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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 / ^! q- M f8 e
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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.4 l- u0 u2 m, ]0 g; e
" T! X% i$ W5 N% K2 ~6 V% t5 |3 QAbstract Disclosures8 i1 v8 T* ^* X* w0 q. K
! e, E8 W0 N7 Z1 n: j6 O! @- L4 [Abstract:5 l! h% @; y u U5 Q! Z
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0 c- a/ U- o0 Q6 q7 _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.3 ?" J& e6 K* ~* W: T
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