Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
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Molecular Targets 0 S* v$ m' |: H9 E, i
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Tumor Biology ' e1 B: D) V" ]7 Q
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Meeting:6 Z6 O) p/ o* Q) ~: B0 W- Z6 K
2011 ASCO Annual Meeting / y/ p1 A2 P I/ J, c
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Session Type and Session Title:
U& F+ f% {( a* W; G2 u+ _& q1 |. @$ APoster Discussion Session, Tumor Biology 2 \2 g* d3 P1 A" O/ P/ ?2 C% V
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# Z: f+ Q* B5 |% B2 s) ?% ~Abstract No:4 j) S/ _7 t$ u$ x+ |1 |4 z2 V
10517
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J Clin Oncol 29: 2011 (suppl; abstr 10517) , b2 Y& R+ q. N3 T/ T7 O9 ^7 ]
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( a& P& K* k# t" N/ oAuthor(s):. H' r$ D& l- n- g2 \% g/ S' j! o B
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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- C+ }4 e: a0 i3 a- O) N* n# n6 f# uAbstracts 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.9 B& i* c& d; l6 ~
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Abstract Disclosures) \# z- w d& _! s/ t6 k& b
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" \* S. x& t. e5 v4 nBackground: 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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