Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
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+ S9 Y9 ^- O4 l! ^; O4 tMolecular Targets
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Tumor Biology 6 `4 l* a& X4 Q: p3 @
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Meeting:- F+ k* S- f( d- j
2011 ASCO Annual Meeting
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9 \! K( {7 |2 n' [! |Session Type and Session Title:
7 [/ s8 W, z) }5 xPoster Discussion Session, Tumor Biology , [$ d: t7 D% L a* C5 T
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Abstract No:5 P) b# W6 ~# B" S- K7 k
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Citation:
3 H# O4 \. s* S) c% `3 I# CJ Clin Oncol 29: 2011 (suppl; abstr 10517) & r" ~: V) u* G" a
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Author(s):2 K5 b2 D. i& O. {
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 9 a$ n9 l6 a9 y
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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.. {3 }$ y. R1 W# p6 w
( y- E& ^0 n4 t( yAbstract Disclosures7 t* {$ ^7 L0 Q( A* C& z
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Abstract:
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9 l( z2 q$ |' yBackground: 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./ j6 t" t+ ?# S1 P' K- H$ e6 K
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