Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page ) P! S6 u' C9 c7 e$ A4 I1 Y
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Sub-category:
- J( j; o0 T2 ?- W5 [# ` ^Molecular Targets
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Category:
7 y5 v j( \3 u2 u6 ^Tumor Biology
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Meeting:4 _& O( X# s7 S/ Y
2011 ASCO Annual Meeting 1 j' V/ x& F6 v1 d5 r! U4 i
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Session Type and Session Title: \8 ^; o4 R& S
Poster Discussion Session, Tumor Biology
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+ v* `6 p9 F0 @5 z, d; Y: S/ BAbstract No:, v/ w" U& r% @! e! E
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Citation:
0 F& V! @( z+ ?- i9 R: FJ Clin Oncol 29: 2011 (suppl; abstr 10517) 1 x! `2 u4 l) |6 c" C0 U5 Y
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Author(s):0 V ] c8 [$ u
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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" k8 V5 ^$ S/ s' GAbstracts 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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Abstract Disclosures9 ?! y, s8 a4 Z& f8 T6 y! l E% F- S
/ q0 D+ v2 B, w/ yAbstract:. h& k8 _, x# ]
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* w2 l7 x5 ?, V. B8 t; w$ a. ^- lBackground: 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.8 n2 M" N( [/ N% j M6 u
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