Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page 5 u6 J% N+ h2 T. E* h/ n# w! ^- y7 \
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Molecular Targets & r" B" ?: A9 {2 Z P3 e
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Category:
+ J% D) D$ Q' v6 F& ]1 \, M6 w4 lTumor Biology
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Meeting:
3 }+ `2 E! h! J+ b2011 ASCO Annual Meeting ' l; |4 e9 E% L+ J
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Poster Discussion Session, Tumor Biology % D/ P& Y4 i2 a5 @
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* b2 K: w6 O& N! t8 |9 t; yJ Clin Oncol 29: 2011 (suppl; abstr 10517)
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Author(s):
/ L4 l+ b: S8 R. d2 Y: l5 U* OJ. 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 % L: C y9 Y8 ]* J2 D) g
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$ d) W" v- I7 `* t- Y$ VAbstracts 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 G+ B/ R( ?/ z# ~1 F' E" X+ a, z4 Y
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Abstract Disclosures5 k. E1 e" ~& w. [, j; T3 e& L3 Q
6 ~; z- W6 Y3 y1 x3 |Abstract:
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' ^; h6 |4 n5 H- D0 i% ~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.* S* U: Y5 U% |" ^- o: z
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