Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
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# h) u0 z" @) H$ ^, bSub-category:
. U2 }6 x8 d) V+ n2 g mMolecular Targets " U9 F- k. I3 ?% Y$ Z
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Category:
; r0 u& I& X$ E1 c3 l1 FTumor Biology
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* [, C! @) b+ ^+ Q1 ?2011 ASCO Annual Meeting , v. u. I# t) b6 |' Y2 J0 E/ N5 `) G
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" I$ ?( E& {% |2 y0 iSession Type and Session Title:, q* U7 G2 r5 M5 Z% a/ h
Poster Discussion Session, Tumor Biology - Q9 y6 M1 {1 y7 d
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Abstract No:: S5 w; J$ I' y* r$ H! R
10517
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Citation:
* l* G! ]: |3 d& l2 SJ Clin Oncol 29: 2011 (suppl; abstr 10517)
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% {& T0 B1 p6 hJ. 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 & |8 b9 _6 X! B2 i& _9 r* T, y3 c7 h
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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.
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Abstract Disclosures
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3 j9 \1 I" V1 x# X! V& e+ aAbstract:
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: Z& A% O; I, J% z5 W; \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.6 j0 N7 k! C, s. I( D% w4 ~. f$ {
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