Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page 5 o: ]7 G& [+ F$ Y; v4 [
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Sub-category:) G) [+ v( ]- y" {5 S9 o
Molecular Targets 0 U2 S7 `" P0 h8 x3 {9 b* R$ T
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0 }# k- _ }, d% kTumor Biology / n; O7 o; l0 j
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! I+ y0 {& y1 x* o1 C1 h, GMeeting:
$ p6 B: K. \ D) Z o2011 ASCO Annual Meeting
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/ V1 @+ Y: V2 O6 e6 r9 NSession Type and Session Title:
% B/ L9 h6 \: U8 f$ pPoster Discussion Session, Tumor Biology 9 A, P7 O( D7 B1 M# j( f, N
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Abstract No:
3 j P0 m; O, i$ A: X$ w3 I10517
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( @% D, h; `# X P VCitation:9 r: z5 ]* O& V D4 f; B- I
J Clin Oncol 29: 2011 (suppl; abstr 10517) ! s) h4 }, L" J; M1 L' @ v
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% i" i' p% m8 _. o1 nAuthor(s):
! p: ]. I2 w/ T% k, x$ ?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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5 t; ]" Q) p$ g( sAbstracts 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.1 f) h( e2 ^) ?6 b: h
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# D6 G, H- H5 X/ ]+ @Abstract:
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) E: M! m3 V! WBackground: 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.' }, m- _3 ~0 z
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