Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page 0 { g R3 L1 S; E2 e# N: V
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Sub-category:6 X/ N. K" D! Z; l$ t
Molecular Targets
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8 P2 v# Y1 }2 n, X$ ATumor Biology " ^" [- ]6 |$ ^
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Meeting:' i6 W) }6 M- x7 k2 q1 n
2011 ASCO Annual Meeting & Y5 e9 N. l- i/ O" u
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Poster Discussion Session, Tumor Biology $ r# F X6 f% M2 g- f
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5 k+ S* C6 D$ J; D0 ^Abstract No:
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J Clin Oncol 29: 2011 (suppl; abstr 10517) 1 E# u+ h4 ]7 ]" g7 C: M+ ~' j
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Author(s):- l/ i9 J! s( R% F' `
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 ! v# _1 `7 F. X% z4 K! `
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- a X. F$ q0 W' {! fAbstracts 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 Disclosures1 W }( c$ k: _8 f9 S, z: o7 B6 d) r
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Abstract: f0 b8 g/ ]' {: t H/ \
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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.% f% d& U( ^" [' h; Z) ~/ b
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