Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page ' j" o1 k: c- Y: j
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0 g# e4 f$ o! ^6 l6 T+ kMolecular Targets , G8 S& T1 ^% b4 P: `+ G6 S0 w
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Category:8 E. F. w4 {3 D; F8 W7 |4 W
Tumor Biology 1 e0 L5 O* [& x% o' I
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Meeting:
/ e! A1 A, o3 k6 I2011 ASCO Annual Meeting
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Session Type and Session Title:
6 T+ M- G( ~7 } @ I, cPoster Discussion Session, Tumor Biology ) P& ~; q2 V+ L. S5 i' `
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8 L( x+ d) x J9 l( k, P, _Abstract No:: R% O! J# ]) u! P* w; l9 L
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J Clin Oncol 29: 2011 (suppl; abstr 10517) + _- G! S, G9 U4 A( @$ }: m9 R
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Author(s):- ?) c# I) F+ l) C
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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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.5 `8 G- s. v& t6 z4 I, d2 U: s. i
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Abstract Disclosures
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* u0 x% y" F* r3 g6 aAbstract:$ y: L9 S1 P4 p+ D( x, g
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8 w8 j: \7 X; z* kBackground: 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.3 e, r; I$ C# _5 ^4 l; `0 Y$ ]
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