Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page ( a- x: s7 H$ ?* D
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Molecular Targets # `2 e b1 x2 f* P
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Tumor Biology 5 d5 s3 `8 S5 V
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Meeting:
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Session Type and Session Title:8 ]9 U" V5 j2 J% t4 T- {" F
Poster Discussion Session, Tumor Biology ( r, l( H2 K" A2 v5 _5 |6 {, L
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. j* x6 @* L! X% F( L$ c5 R5 vAbstract No:% W3 a( w# z0 u2 r, |! k+ v2 s! q0 B
10517
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J Clin Oncol 29: 2011 (suppl; abstr 10517) , g* Z7 s. X: W8 [+ L6 x+ v$ }
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Author(s):4 K2 w6 w6 `/ f5 A4 d
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 $ d0 j1 C! A7 U9 i) g- D0 i' v
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. u$ f7 P- r" f ?# s# f UAbstracts 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 Disclosures* o4 {6 V* W0 D3 q2 [2 o
; A$ y; \ i; i: l' fAbstract:
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0 d$ r7 B) w# HBackground: 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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