Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page 4 }$ N/ O, }5 a- A# D
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Sub-category:
- K; R5 E% r; e ]! E- k) w7 L+ jMolecular Targets ! c( n' I4 q8 t' p2 `$ Y
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5 [* a$ T+ ^% W4 i' W6 cTumor Biology
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Meeting:1 H9 X* E7 [4 J
2011 ASCO Annual Meeting
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: k' o1 b' P/ @: { A* [Session Type and Session Title:' B$ b6 p9 ], ?& S6 j
Poster Discussion Session, Tumor Biology ( o9 Q9 w E2 a
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Citation:
H5 S R+ K( z+ o) d3 w4 R- dJ Clin Oncol 29: 2011 (suppl; abstr 10517)
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% R% h9 P' H+ r% v1 K2 `/ D }Author(s):
2 T- l8 d2 ^' L% CJ. 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 ' F& c5 C3 P% Z) K' B7 j
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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.) k! |' t$ Z+ C1 a/ z: M
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Abstract Disclosures
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9 C( P C/ `+ U$ `. F. A# H8 \Abstract:5 k' u; X; E6 a* x" O) h
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0 V+ N2 m% t. W+ x* i: X2 ~7 x1 i" W \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.
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