Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page , R- x0 ]& v: h# l' L
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Sub-category:
v5 f' [; o Y' u# hMolecular Targets
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Category:
& z/ F9 Q7 r6 M+ d( C& g% v, JTumor Biology % O7 D& k" n/ G4 h3 Q6 D# v0 h, D% P
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; ^& K8 X0 R2 b* R* K) h2 \+ fMeeting:. x8 |! s3 h0 ~$ P5 L6 ~- v8 n
2011 ASCO Annual Meeting
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Session Type and Session Title:$ F9 q# Z: @' T# I
Poster Discussion Session, Tumor Biology 0 U, s2 w g3 J( I' u
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Abstract No:
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: ]8 N { |- _! Z' o6 t0 w, x! E& wJ Clin Oncol 29: 2011 (suppl; abstr 10517)
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Author(s):
: c: X: v2 j; E9 ~/ e1 sJ. 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 2 Z: ]& R/ S, c4 ]) l7 D# Q
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6 {. u) Z# z5 z. S \8 _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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& M* C& V4 W5 R m+ tAbstract Disclosures
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Abstract:
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1 p: g2 D: G) b% Q2 gBackground: 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./ m5 |4 Y" P8 K! Q, d9 m
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