Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
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2 z7 |# D6 x! K" K+ ~0 i% bSub-category:
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' V6 V* y/ f9 X+ K7 b2 f2 Q1 kTumor Biology
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Meeting:
% Y9 O* m `0 p1 P B, l. O" _8 O2011 ASCO Annual Meeting , K0 n6 y, c, I0 {& R/ ~& j
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2 |8 i) i' U0 `6 f0 ^0 Y6 u" bPoster Discussion Session, Tumor Biology + {+ u: v9 y m1 H* {! B, l
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9 y7 ~" Z* W" U9 p+ Y: O3 EAbstract No:
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Citation:" {( v6 n) j0 O. F7 S7 `
J Clin Oncol 29: 2011 (suppl; abstr 10517) 0 k1 i \# V6 a* h2 i) ~% R0 H
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1 p+ j, u1 F! ^. s7 nJ. 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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& {/ R2 Z# o: {" gAbstracts 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.7 ~- i% p* u& a7 Q c: D, M
, T4 h: v1 m) N% BAbstract Disclosures9 W8 w4 y# u# ?" ^: w
0 q+ B% v7 _" K3 E/ J; M- RAbstract:/ f, Q+ _& v& a1 D, ^9 a
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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.0 c; g3 _4 i- M
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