Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page & b( x& J! W; P7 R
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Sub-category:
7 V; {- C' J+ T& c% n4 ~8 n9 KMolecular Targets 9 L6 j: o1 }4 Z" A$ ~9 H7 l3 r
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) `: d# ~3 o6 A* ?Tumor Biology , p' d- g6 l m& c' g4 g7 v" A
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6 i; D4 K* W5 o7 p. kMeeting:( u: V% f2 ~7 i7 L. u
2011 ASCO Annual Meeting
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Session Type and Session Title:
! f O, F1 f! E1 DPoster Discussion Session, Tumor Biology
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Abstract No:
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( ?) e0 p; o/ k2 UJ Clin Oncol 29: 2011 (suppl; abstr 10517)
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Author(s):
% B \- b/ E$ GJ. 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 $ Y* [ S. j; q
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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.# E- b7 o' C9 |( E" }8 B: B
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Abstract Disclosures
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9 m" {# w: ?' A4 OAbstract:
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0 L5 H' @( i# ]. Q( dBackground: 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.! J; @' F q2 L1 K( W, b" {
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