Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page / V& F1 m& x& S5 F$ ]5 a( l
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Sub-category:
; K9 C" A/ r7 s! |' @9 S( ]Molecular Targets
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Category:
5 e& H: n. j# ~- `Tumor Biology 8 F# E8 j$ W- H% Z6 L
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Meeting:
" r2 ~5 w4 H0 G: ?( X$ h4 M2011 ASCO Annual Meeting ) S: K7 @( n$ x
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Session Type and Session Title:
/ L! y8 Q% N% m, uPoster Discussion Session, Tumor Biology / d5 w& d' [6 T! }/ b# C
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Abstract No:% W- N4 v3 w; W2 T" _9 j5 H8 @
10517
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Citation:
1 I$ f0 ~: u3 ^0 ^, M( Z @J Clin Oncol 29: 2011 (suppl; abstr 10517) # f) w X5 f# U
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Author(s):
, }1 i; S' B; W9 |1 D, u1 p# vJ. 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 q6 i% t8 x- ^- |7 w# r
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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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4 v6 A9 T7 G. ? R. |2 q! qAbstract Disclosures
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: f4 X1 {! n2 a( o& _* x+ PAbstract:
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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.3 M6 c2 O: W4 C/ h5 r- g2 v
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