Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page , H8 {' d& v! j0 C% x
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Sub-category:
) W5 X3 N m/ JMolecular Targets
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Category:
( }" X ~6 C Q: M2 X1 e* BTumor Biology . u2 s8 m: I' j/ _5 ?6 \, I1 W
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7 i5 d7 D3 \3 ~# C) wMeeting:
3 l$ F* F2 U0 t; b1 E; b! ?! _2011 ASCO Annual Meeting + x8 K7 D5 | o" [ v
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Session Type and Session Title:+ k7 ?- R( s$ \/ i! ~5 ]2 g
Poster Discussion Session, Tumor Biology
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Abstract No:- x R" y& v% R% U# {7 E& \
10517
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J Clin Oncol 29: 2011 (suppl; abstr 10517) / A1 F! `' A/ J+ Q$ j0 [6 p/ \3 }
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Author(s):) G6 d. v- W' b& D) c7 l1 m2 b& l
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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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.- H1 W2 Y, V7 }% N; z! R( X
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Abstract Disclosures) J1 S) @, j5 o* ]( H
) I, @1 }1 ^9 I0 \& D# \Abstract:" }+ M2 m" i1 @, a# {
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& h# H) E, n. A0 mBackground: 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 A8 P4 h5 y) k- l u9 T
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