Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page . e: v7 e9 k' W' e. W3 _
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Sub-category:" Z# G4 N$ p1 u7 d' a
Molecular Targets 4 q$ a( i7 D4 Y# y- v- B
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Tumor Biology
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Meeting:% g% m6 c; S! V5 X, |/ L
2011 ASCO Annual Meeting
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2 s1 D! \$ \5 YSession Type and Session Title:
m2 w: G- I# M4 m' Q) k3 j5 LPoster Discussion Session, Tumor Biology 4 U2 _2 J1 |1 M1 ?
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, H# L5 B$ q8 e' _6 S9 fAbstract No:
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2 a, @6 _2 r S1 P K: t$ MCitation:
5 e& t5 C! k3 [J Clin Oncol 29: 2011 (suppl; abstr 10517) # ?; _1 E) ~# P W4 i$ [
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3 ~% U( ^ O5 wAuthor(s):; N5 u; ]+ s2 t; i: }: z' r; q
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
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7 M* |, Z8 t8 nAbstracts 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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8 s% e/ d+ X) Y0 e1 N0 b/ aAbstract Disclosures
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9 f1 j) |: t: b7 c6 P6 nAbstract:4 c* G5 J/ m/ o6 h6 H
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% }. w# n/ q7 r* k% ^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.9 b* B9 C) f5 o
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