Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
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7 G. \1 w* n) c! o# [Molecular Targets 4 s1 B0 G: [ E9 l
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Category:
2 u, ~7 `6 V) m( l2 o4 R5 MTumor Biology : S; U+ F$ n0 }0 a& D7 c
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Meeting:& @ v- Y8 @0 y `. \
2011 ASCO Annual Meeting ! K5 r) g9 P! [* m
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Session Type and Session Title:
% n% Q# K0 V$ i1 _) jPoster Discussion Session, Tumor Biology 0 \( `0 y. Y' u+ R$ _9 l
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Abstract No:* f+ u" k R7 o- M( I5 |
10517
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J Clin Oncol 29: 2011 (suppl; abstr 10517) 6 w2 g1 S; n5 t* @! ^
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6 l7 l) k J5 s# m+ ]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 ( L: a9 R" ^) h8 \. p
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- a4 w9 d; G+ v) [% q/ L iAbstracts 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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4 x2 a8 C3 q$ ?8 CAbstract Disclosures; J$ p/ I1 x5 h* g- J/ w
; w' I+ c8 {, u7 k! @7 n# WAbstract:7 `6 N; _% E( q4 g
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$ j% t, r7 {) _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.$ N2 w6 k& ~7 _) c, b
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