Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page 3 j4 G! i4 m. I; o: O2 v5 g, ^6 v8 d
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Sub-category:# X$ [' F% ~) h. e
Molecular Targets
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Category:
8 G: \" x4 M5 R3 @) o: [- wTumor Biology - }9 p7 l3 ?' K& ~9 p
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Meeting: L8 g! U! P c8 ^$ z. B
2011 ASCO Annual Meeting $ o4 j! ?& d" m. [: c
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Session Type and Session Title:
4 {( R* c( K4 I1 x* P0 b0 ~7 |Poster Discussion Session, Tumor Biology
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Citation:
4 C7 ?3 H8 `# _+ x, jJ Clin Oncol 29: 2011 (suppl; abstr 10517) # x j+ _( P) s& {* S/ S: e/ n
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Author(s):. P! ~# A7 w4 k+ o3 y* T& c2 ~
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 0 J0 Q$ J& B# t( O; w+ F/ M
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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.( k" U7 `) e( y- a6 M F
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Abstract Disclosures4 B) v# M& z6 N
6 x/ z# \& T, }- P4 N$ GAbstract:) w, Q# c; U4 D
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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.
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