Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page , \' G0 O& l$ j7 }, s
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Molecular Targets ( Y- }9 q+ K0 o, ^" ]
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0 Z% I: N7 P; p+ o; eTumor Biology
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7 F2 d( o" h! MMeeting:
* @3 }6 F6 M) g2 T- U- I( }2011 ASCO Annual Meeting 6 Y! Y' `' V& ^$ V" L
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Poster Discussion Session, Tumor Biology $ V0 R4 p# Y! {5 d# A* ^3 `; y
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Abstract No:
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5 a! k& j# \3 j9 P& m# Q, SCitation:
0 L' `9 [; q2 X0 M1 T. a8 _' f3 R: fJ Clin Oncol 29: 2011 (suppl; abstr 10517) 4 o% `; b; i4 [8 `& v: t
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Author(s):
, P; t/ m6 f) S- S& Z7 rJ. 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.) S: E2 Q9 p' u' H) w
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# G9 t* v3 Q& v) ]1 Q3 b. sAbstract:
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P# u7 D4 M0 c2 TBackground: 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.
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