Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
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Sub-category:! i# x/ B! ?& _& _, O/ F' U7 D6 a
Molecular Targets
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4 T+ `' m0 a4 X; p% g4 m( ~6 [7 D. ^Tumor Biology ( G+ Y/ ~ a6 d# Y6 \$ G
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Meeting:3 J* R) ~7 p+ F2 O
2011 ASCO Annual Meeting 9 A' q5 T# V4 M5 ~; J4 ~, N: }
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Session Type and Session Title:0 F. o. S5 c8 Z) M; `
Poster Discussion Session, Tumor Biology 7 T2 `" L! N* L& d0 b9 R2 a
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Abstract No:
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' O0 I" r' E& TCitation:3 E8 a: r7 a& ]3 I& p, n* I, F
J Clin Oncol 29: 2011 (suppl; abstr 10517) , z( r9 I" `" I- T) A
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8 E+ Y7 i- w; i1 o2 Q4 R- [Author(s):6 `9 B" h; p" }' Y- A7 X, {
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 % w4 d/ a9 T$ E3 M' n+ {
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- ^3 e( K1 n- l1 G3 k0 P4 U3 jAbstracts 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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. ^: k9 U! K+ j4 xAbstract Disclosures
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5 W; {4 B3 A) M1 c2 d6 lAbstract:7 I6 _& n/ @2 o$ q+ E: R( K
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3 O; \* y" e# b: U. i" L& b8 QBackground: 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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